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Abstract

A tendency for magnesium deficiency in patients with diabetes mellitus is well-established. Glucosuria-related hypermagnesiuria, nutritional factors and hyperinsulinaemia-related hypermagnesiuria all can contribute. The plasma magnesium level has been shown to be inversely related to insulin sensitivity. Magnesium supplementation improves insulin sensitivity as well as insulin secretion in patients with type 2 diabetes. Nevertheless, no beneficial effects of oral magnesium supplementation has been demonstrated on glycaemic control either in patients with diabetes type 1 or 2. Oral magnesium supplementation reduced the development of type 2 diabetes in predisposed rats. There are some indications that magnesium decreases blood pressure, but negative results have been observed in trials that were, however, not designed to test effect on blood pressure as primary parameter. Patients with (severe) retinopathy have a lower plasma magnesium level compared to patients without retinopathy and a prospective study has shown the plasma magnesium level to be inversely related to occurrence or progression of retinopathy. Further study on magnesium (supplementation) is warranted in the prevention of type 2 and of (progression of) retinopathy as well as a means to reduce high blood pressure.

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... The plasma magnesium concentration is inversely correlated with insulin sensitivity. Magnesium supplementation increase insulin sensitivity and also insulin discharge in type-2 diabetic patients (Valk, 1999). Magnesium deficiency results in carbohydrate intolerance, insulin resistance and dyslipidemia. ...
... With the treatment of water extract and methanol extract of Ipomoea batatas, the young and old rats showed the significant increase of magnesium level in the almost all the body organs. This increase in the magnesium level may lead to the control of hyperglycemia in diabetic rats of both groups as magnesium is linked with the control of glucose level (Valk, 1999). ...
... In the case of diabetes mellitus, its deficiency occurred due to insulin resistance and increased urinary loses. Magnesium supplementation increase insulin sensitivity and also insulin discharge in type-2 diabetic patients (Valk, 1999). ...
... [3] In past decades, it has become apparent that deficiencies of trace elements are commonly associated with T2DM. [4][5][6] Magnesium, a divalent cation is one among the common micro mineral deficiency established in DM. [7,8] Decreased serum magnesium levels and increased urinary magnesium losses have been recognized in both type 1 and type 2 DM. Decreased dietary magnesium intake has been associated with increased incidence of T2DM. ...
... [9] Hypomagnesaemia and hypermagnesuria was reported to be associated with diabetes complications. [7,10,11] Thus, magnesium has drawn considerable attention for its potential role in improving insulin sensitivity and preventing DM. ...
... [12,24,25] In diabetes, these minerals attract importance due to its association with insulin sensitivity, insulin secretion and blood glucose regulation. [7,9,15,26,27] In this study of 150 subjects, 76 DM patients on metformin treatment and 74 non diabetic controls were assessed for serum zinc and magnesium. Among the 76 patients, 20% were in good control, 47% had moderate control and 33% had poor control. ...
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In diabetes mellitus, the deficiency of trace elements is said to be linked to poorglycemic control and oxidative stress related complications. The deficiency of magnesiumand zinc accelerate the disease and its complications. Our study assessed the correlation ofserum magnesium and zinc levels with glycemic control in type 2 diabetes patients. Methods: This cross sectional study included 150 study participants. 76 type 2 diabetes patients were cases and 74 healthy participants were grouped to controls. Samples for fasting and postprandial blood glucose, HbA1c, magnesium and zinc were collected and analysed in a fully automated analyser. Data was analysed by Graph Pad Prism software. Results: Cases had higher levels of fasting, postprandial, HbA1c levels as compared tocontrols with p<0.0001. Cases had significant reduction in serum levels of zinc andmagnesium. Zinc and magnesium showed a significant inverse correlation with glycemic control with r values of -0.56 and -0.48 respectively. Conclusion: Low serum magnesium and zinc levels can worsen the complications of disease. So, early detection of its deficiency and supplementation alleviates the disease progression.
... The plasma magnesium concentration is inversely correlated with insulin sensitivity. Magnesium supplementation increase insulin sensitivity and also insulin discharge in type-2 diabetic patients (Valk, 1999). Magnesium deficiency results in carbohydrate intolerance, insulin resistance and dyslipidemia. ...
... With the treatment of water extract and methanol extract of Ipomoea batatas, the young and old rats showed the significant increase of magnesium level in the almost all the body organs. This increase in the magnesium level may lead to the control of hyperglycemia in diabetic rats of both groups as magnesium is linked with the control of glucose level (Valk, 1999). ...
... In the case of diabetes mellitus, its deficiency occurred due to insulin resistance and increased urinary loses. Magnesium supplementation increase insulin sensitivity and also insulin discharge in type-2 diabetic patients (Valk, 1999). ...
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In diabetic patients, electrolyte disorders frequently occur with the characteristic changes in minerals like calcium and magnesium etc. Several medicines are used to manage diabetes mellitus but they exert adverse effects. Plants are a valuable alternative to synthetic medicines because they are easily available, economical and have fewer side effects. Ipomoea batatas L is a well-known antidiabetic plant (sweet potato) but its effects on calcium and magnesium concentration have not studied. The prime focus of this study is to estimate the potential of Ipomoea batatas L peel-off on magnesium and calcium level in Alloxan-induced diabetic rats. Alloxan monohydrate was mixed in 0.9% NaCl solution and administrated [150 mg/kg (S/C)] to male Wistar rats to induce diabetes. After three days blood samples were collected and blood glucose level was recorded. Wistar rats having a blood glucose level of 200 mg/dl and above were selected for the study. Methanol and water extract of Ipomoea batatas L peel-off was given orally with a dose rate of 4g/day. Calcium and magnesium estimation was done using an atomic absorption spectrophotometer. Our results revealed an increase in both the calcium and magnesium level in heart, brain, liver, hind limb, and forelimb after Ipomoea batatas extract treatment. In kidneys decreased calcium level was noted as they excrete calcium. Mineral (Calcium, magnesium) level was increased in all organs except kidney after both extracts treatment. Ipomoea batatas being anti-diabetic in nature also maintain the homeostasis of calcium and magnesium in diabetes. Therefore, we propose the long-term use of such agents might help in the prevention of diabetes-associated complications. However, the validation of these results to human population needs further extensive study.
... The plasma magnesium concentration is inversely correlated with insulin sensitivity. Magnesium supplementation increase insulin sensitivity and also insulin discharge in type-2 diabetic patients (Valk, 1999). Magnesium deficiency results in carbohydrate intolerance, insulin resistance and dyslipidemia. ...
... With the treatment of water extract and methanol extract of Ipomoea batatas, the young and old rats showed the significant increase of magnesium level in the almost all the body organs. This increase in the magnesium level may lead to the control of hyperglycemia in diabetic rats of both groups as magnesium is linked with the control of glucose level (Valk, 1999). ...
... In the case of diabetes mellitus, its deficiency occurred due to insulin resistance and increased urinary loses. Magnesium supplementation increase insulin sensitivity and also insulin discharge in type-2 diabetic patients (Valk, 1999). ...
... In this study, it was observed that Magnesium in glaucoma subjects were significantly decreased when compared with control. The is in line with the work of De Valk (11) who found that patients with severe retinopathy have a lower plasma magnesium level compared to patients without retinopathy. Mg tends to play an important function in insulin homeostasis. ...
... Although, the intracellular magnesium forms a key complex with ATP and it is a crucial cofactor for a wide range of enzymes, transporters and nucleic acids required for normal cellular function, replication and energy metabolism. (11) The serum Mg play an important function in the development and normal functioning of the eye. Magnesium decrease has been linked to multifocal necrosis in the retinal pigment epithelium. ...
... Hypomagnesemia in patients with diabetes mellitus (DM) is well established, which might be due to nutritional deficiencies, glucosuria-related hypermagnesiuria, and hyperinsulinemia-induced hypomagnesemia. The plasma magnesium concentration has been shown to be inversely related to insulin sensitivity [10]. The Atherosclerosis Risk in the Community (ARIC) study found that low serum magnesium concentration was a strong, independent predictor of incident type 2 diabetes (T2DM) [11]. ...
... In this cohort, 171 individuals (54.1%) were females, with a median age of 63 years (IQR 55-68) and a median DM duration of 15 years (IQR [10][11][12][13][14][15][16][17][18][19][20][21][22]. The prevalence of hypomagnesemia among patients with DM was 17.1% (95% CI: 13.3-21.7%), ...
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Introduction: Magnesium is a vital intracellular cation crucial for over 320 enzymatic reac- tions related to energy metabolism, musculoskeletal function, and nucleic acid synthesis and plays a pivotal role in human physiology. This study aimed to explore the prevalence of dysmagnesemia in patients with diabetes mellitus and evaluate its correlations with glycemic control, medication use, and diabetic complications. Methods: A cross-sectional study was conducted at Sultan Qaboos Uni- versity Hospital, including 316 patients aged 18 years or older with diabetes mellitus. Data included demographics, medical history, medications, and biochemical parameters. Serum total magnesium concentrations were measured, and dysmagnesemia was defined as magnesium ≤ 0.69 mmol/L for hypomagnesemia and ≥1.01 mmol/L for hypermagnesemia. Results: The prevalence of hypo- magnesemia in patients with diabetes was 17.1% (95% CI: 13.3–21.7%), and hypermagnesemia was 4.1% (95% CI: 2.4–7.0%). Females were significantly overrepresented in the hypomagnesemia group, while the hypermagnesemia group showed a higher prevalence of hypertension, retinopathy, an increased albumin/creatinine ratio, chronic kidney disease (CKD), elevated creatinine levels, and a lower adjusted calcium concentration. The multinominal logistic regression exhibited that the female sex and higher serum-adjusted calcium were independent risk factors of hypomagnesemia. In contrast, the presence of hypertension, higher levels of albumin/creatinine ratio, and stage 5 CKD were independent risk factors of hypermagnesemia. Conclusions: Hypomagnesemia was common among patients with diabetes mellitus; however, hypermagnesemia was associated with microvascular complications.
... Hypomagnesemia in patients with diabetes mellitus (DM) is well established, which might be due to nutritional deficiencies, glucosuria-related hypermagnesiuria, and hyperinsulinemia-induced hypomagnesemia. The plasma magnesium concentration has been shown to be inversely related to insulin sensitivity [10]. The Atherosclerosis Risk in the Community (ARIC) study found that low serum magnesium concentration was a strong, independent predictor of incident type 2 diabetes (T2DM) [11]. ...
... In this cohort, 171 individuals (54.1%) were females, with a median age of 63 years (IQR 55-68) and a median DM duration of 15 years (IQR [10][11][12][13][14][15][16][17][18][19][20][21][22]. The prevalence of hypomagnesemia among patients with DM was 17.1% (95% CI: 13.3-21.7%), ...
Article
Full-text available
Introduction: Magnesium is a vital intracellular cation crucial for over 320 enzymatic reactions related to energy metabolism, musculoskeletal function, and nucleic acid synthesis and plays a pivotal role in human physiology. This study aimed to explore the prevalence of dysmagnesemia in patients with diabetes mellitus and evaluate its correlations with glycemic control, medication use, and diabetic complications. Methods: A cross-sectional study was conducted at Sultan Qaboos University Hospital, including 316 patients aged 18 years or older with diabetes mellitus. Data included demographics, medical history, medications, and biochemical parameters. Serum total magnesium concentrations were measured, and dysmagnesemia was defined as magnesium ≤ 0.69 mmol/L for hypomagnesemia and ≥1.01 mmol/L for hypermagnesemia. Results: The prevalence of hypomagnesemia in patients with diabetes was 17.1% (95% CI: 13.3–21.7%), and hypermagnesemia was 4.1% (95% CI: 2.4–7.0%). Females were significantly overrepresented in the hypomagnesemia group, while the hypermagnesemia group showed a higher prevalence of hypertension, retinopathy, an increased albumin/creatinine ratio, chronic kidney disease (CKD), elevated creatinine levels, and a lower adjusted calcium concentration. The multinominal logistic regression exhibited that the female sex and higher serum-adjusted calcium were independent risk factors of hypomagnesemia. In contrast, the presence of hypertension, higher levels of albumin/creatinine ratio, and stage 5 CKD were independent risk factors of hypermagnesemia. Conclusions: Hypomagnesemia was common among patients with diabetes mellitus; however, hypermagnesemia was associated with microvascular complications.
... Други изследвания базирани само на хранителни добавки обаче не показват толкова убедителни резултати и не може категорично да се каже, че ефектът се дължи само на магнезия, а не на комбинация с повишен прием с други компоненти съпътстващи магнезия в диетата (DiSilvestro, 2005b). Съществуват изследвания свързващи ниски нива на серумен магнезий с развитие на диабет тип 1 и 2 (Tosiello, 1996;de Valk, 1999). ...
... There is research linking low serum magnesium levels to the development of type 1 and type 2 diabetes (Tosiello, 1996;de Valk, 1999). ...
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Cereals of plant origin,including oats are a rich source of minerals. Three types of Bulgarian oat varieties and three new hybrid varieties imported by a Polish producer company were studied. The content of minerals – Ca, Mg, Zn, Cu, Fe and P in the six oat varieties was investigated. The aim of the present study is to determine which cultivar is optimal in terms of the lowest and highest content of mineral nutrients and their acceptable limits in the selected oat cultivars. In the 6 oat varieties studied by us, a lower content of Zn was found – 10.0 mg/kg in the Bulgarian varieties compared to the foreign ones – 18.0 mg/kg. When determining the amount of P in the analyzed varieties, concentrations of 720.0 to 900.0 mg/kg were found for the Bulgarian oat varieties and from 1080.0 to 1200.0 mg/kg for those imported by a Polish producer.
... Diabetic nephropathy patients are exposed to an acceleration of their disease due to water fluoridation. Particularly uncontrolled diabetic patients, because of polydypsia consume large volumes of water and were accumulate more Fluoride content in bones [12,7]. The mechanisms by which Fluoride induces diabetes most likely include antagonism to calcium and magnesium centered biochemistry [12]. ...
... Particularly uncontrolled diabetic patients, because of polydypsia consume large volumes of water and were accumulate more Fluoride content in bones [12,7]. The mechanisms by which Fluoride induces diabetes most likely include antagonism to calcium and magnesium centered biochemistry [12]. Insulin secretion (both basal and glucose-stimulated) by isolated islets of Langerhans in vitro is inhibited as a function of fluoride concentrations [13]. ...
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This study estimate and compare Blood Glucose and Fluoride levels within study groups and to correlate serum renal parameters with fluoride among study subjects. Diabetes mellitus (DM) and its microvascular complication; diabetic nephropathy (DN) is documented as a more prevalent disorder in fluoride endemic areas across the world. Kidneys are the major route of excretion of fluoride and are thus the primary organ affected. Fluoride in minor quantities may also be excreted through sweat, saliva and feaces. Though Fluoride in minor quantities (<1.5 ppm) is considered to be essential for dental and bone enamel mineralization which form fluroapetite. Chronic exposure (> 2ppm) is considered to be toxic leading to fluorosis. This study was conducted at Sri R.L. Jalappa Hospital attached to Sri Devaraj Urs Medical College, Constituent of Sri Devaraj Urs Academy of Higher Education and Research, Karnataka, India. Total 90 subjects with the age group 45-75 years of either gender were included. Our results showed that Fasting, post prandial blood glucose values and serum Fluoride were significantly higher (x%;179.27±53.86, 148±41.96,236.50±64.83, 250.43±72.85, 0.63±0.59, 0.52±0.3 p<0.001) in T2DM without CKD group as compared to the controls and T2DM with CKD. Renal profile when compared between three groups Urea, Creatinine and Potassium were significantly higher in T2DM with CKD as compared to controls and T2DM without CKD. We conclude that analysis of serum/ urine fluoride can be preferred for the subjects attending medicine OPD who are at risk, Installing water defluroditation plants at every village as they and livestock are mainly exposed to fluoride, Creating awareness among residents by conducting regular camps and routine medical checkups and Estimate fluoride levels of potable water at regular intervals, which 53 would help decrease its effect among living system. This study also supports the hypothesis of increase serum Fluoride increases DM and DN which is evident from the results as we observed significant increase of serum fluoride in T2DM and DN subject comparecto controls. Evaluation of these parameters may help in early diagnosis and management and may help better patient care and nation as well.
... In past decades, it has become apparent that deficiencies of trace elements are commonly associated with T2DM [4][5][6] . Magnesium, a divalent cation is one among the common micro mineral deficiency established in DM [7,8] . Decreased serum magnesium levels and increased urinary magnesium losses have been recognized in both type 1 and type 2 DM. ...
... Decreased dietary magnesium intake has been associated with increased incidence of T2DM [9] . Hypomagnesaemia and hypermagnesuria was reported to be associated with diabetes complications [7,10,11] . Thus, magnesium has drawn considerable attention for its potential role in improving insulin sensitivity and preventing DM. ...
... 18 altered magnesium status; this can be due both to urinary losses and to nutritional factors. 19 Furthermore, HF patients with DM seem to be a very particular group within patients with HF, a group in which some of the classical paradoxes do not apply. [20][21][22] Taken together, it seems plausible that the presence of DM can influence magnesium homeostasis and consequently HF prognosis. ...
... [32][33][34] Urinary magnesium losses due to both glucosuria and hyperinsulinemia and reduced magnesium intake may all contribute to this state. 19 Possible explanations for the association between higher magnesemia and worse HF outcome in patients with DM might be that the cardiac structural changes and remodeling, 35,36 autonomic dysfunction, 36,37 and slower nervous conduction velocity 36,38 seen in their hearts would render them more vulnerable to higher magnesium levels, when compared with patients without DM. This could explain why only the subgroup of HF patients with DM showed grimmer prognosis with higher serum magnesium levels. ...
Article
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Background: Hypermagnesemia predicts mortality in chronic heart failure (HF); however, in acute HF, magnesium does not seem to be outcome-associated. Diabetes mellitus (DM) frequently associates with altered magnesium status. We hypothesized that DM might influence the prognostic impact of magnesium in acute HF. Methods: This is a retrospective cohort study of hospitalized patients with acute HF. Patients without data on admission serum magnesium were excluded. Follow-up: 1 year from hospital admission. Primary end point: all-cause mortality. Patients were divided according to median serum magnesium (1.64 mEq/L). The Kaplan-Meier survival method was used to determine survival curves according to magnesium levels. The analysis was stratified according to the presence of DM. A multivariable Cox regression analysis was used to study the prognostic impact of magnesium. Results: We studied 606 patients. The mean age was 76 ± 12 years, 44.1% were male, 50.7% had DM, and 232 (38.3%) died during follow-up. Median magnesium was 1.64 (1.48-1.79) mEq/L. Patients with magnesium ≥1.64 mEq/L had higher 1-year mortality [141 (46.4%) vs 91 (30.1%), P < .001]. After adjustments for age, sex, history of atrial fibrillation, systolic blood pressure, heart rate, ischemic etiology, B-type natriuretic peptide, estimated glomerular filtration rate, alcohol consumption, antihyperglycaemic agents or glycated hemoglobin, admission glycemia, New York Heart Association class IV, and severe left ventricle systolic dysfunction, serum magnesium ≥1.64 mEq/L was associated with higher mortality only in patients with DM: HR 1.89 (95% confidence interval: 1.19-3.00), P = .007, and 1.27 (95% confidence interval: 0.83-1.94) and P = .26 for non-DM patients. The results were similar if magnesium was analyzed as a continuous variable. Per 0.1 mEq/L increase in magnesium levels, patients with DM had 13% increased risk of 1-year mortality. Conclusions: Higher magnesium levels were associated with worse prognosis only in HF patients with DM.
... It is also a cofactor for important molecules including, guanosine triphosphatase, phospholipase C, adenylate cyclase, and guanylate cyclase etc. Mg 2+ is involved in the control of muscle contraction and insulin levels in the body, as it is involve in regulating insulin action through the insulin mediated glucose uptake [43]. Moreover, Mg functions as a cofactor for more than 300 enzymes, as it is essential for all energy dependent transport system including glycolysis, oxidation, energy metabolism, neuromuscular activity and cell membrane stabilization [44]. Its deficiency is associated with hypertension, insulin resistance, which is associated with decrease in magnesium uptake [45]. ...
... Bearing the importance of Mg in-patient with diabetics, further prospective studies are needed/required-supporting role of dietary magnesium supplementation as a possible health strategy to ameliorate health effects of diabetes. Incidence of hypomagnesaemia, have been reported to be associated with diabetes and these may have resulted due to increased urinary losses [44][45] with other additional risk factors such as ketoacidosis and effects of certain medications etc. ...
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Plants contain many bioactive compounds such as nutrients (minerals and vitamins) and, which are very important for the treatment of various diseases. Delonix regia seed powder was analyzed for the vitamins and mineral contents. Using spectrophotometer combined with titration, the vitamins content of Delonix regia was analyzed. Further, Atomic absorption spectrophotometer was used to analyze the mineral contents. The plant was show to contain low amounts of vitamin B1 (0.04 ± 0.0001mg %), B 2 (0.08 ± 0.0003mg %), and B 12 (0.08 ± 0.001mg %) with high vitamin B 3 (766.66 ± 8.81mg) and B 6 (316.46 ± 6.35mg). Vitamin C (16.0 ± 0.3mg/100g) was significantly higher in the plant compare to vitamin E (0.54 ± 0.01), vitamin A (2.81 ± 0.012), vitamin B 1 , B 2 , and B 12. Delonix regia seed also contain important minerals such as Magnesium and Calcium in moderate amount (16.83 ± 8.23mg/g and 27.58 ± 0.00). Also, Chromium, Zinc, Cadmium and Iron were observed in trace amount (0.56 ± 0.0003mg/g, 0.51 ± 0.29 mg/g, 9.48 ± 0.03mg/g and 1.64 ± 0.33mg/g) respectively. In conclusion, Delonix regia seed as a phytochemical maybe necessary in the management of diseases like diabetes, Sickle cell and Aging as it may influence cellular systems with varied network, impacting on multiple targets with effects on enzymatic/or protein-protein interaction processes. Our results provide insight on the rich contents of Delonix regia extract however; further investigation on this plant is required ascertaining supplementary dosage necessary for good health in both resource poor, industrial and postindustrial environment, moving forward. Citation: Michael P Okoh and Chijoke Madu. "Phyto and Natriuretic Analysis of Delonix Regia Plant Extract for Vitamins and Mineral Contents". Nutrition and Food Toxicology 2.6 (2018): 540-548.
... Poor Mg status may also impair growth of lean body mass [24] and decrease physical performance [25]. Diabetes (both type 1 and type 2) is the most common metabolic disorder associated with Mg deficiency [26][27][28][29][30], with reported incidence rates of hypomagnesaemia in diabetics as high as 13.5%-47.7% [27]. ...
... There is evidence indicating that the relationship between Mg deficiency and type 2 diabetes is bidirectional. Mg deficiency is a common manifestation in type 1 and type 2 diabetics [26,27] and may also increase the risk of diabetes and its complications [29][30][31]. The negative associations between serum Mg and measures of glycemic regulation observed in this study are in agreement with studies indicating that poor glycemic control lowers serum Mg concentrations [33,34]. ...
Article
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Total serum magnesium (Mg) concentration (SMC) is commonly used to assess Mg status. This study reports current SMCs of Canadians and their associations with demographic factors, diabetes, and measures of glycemic control and insulin resistance using results from the Canadian Health Measures Survey cycle 3 (2012–2013). Associations were examined in adults aged 20–79 years using linear mixed models. Mean SMCs and percentile distributions for 11 sex-age groups between 3 and 79 years (n = 5561) are reported. SMCs were normally distributed and differences (p < 0.05) among sex and age groups were small. Between 9.5% and 16.6% of adult sex-age groups had a SMC below the lower cut-off of a population-based reference interval (0.75–0.955 mmol·L⁻¹) established in the United States population as part of the NHANES I conducted in 1971–1974. Having diabetes was associated with 0.04 to 0.07 mmol·L⁻¹ lower SMC compared to not having diabetes in the various models. Body mass index, glycated hemoglobin, serum glucose and insulin concentrations, and homeostatic model assessment of insulin resistance were negatively associated with SMC. This is the first study to report SMCs in a nationally representative sample of the Canadian population. A substantial proportion of Canadians are hypomagnesaemic in relation to a population-based reference interval, and SMC was negatively associated with diabetes and indices of glycemic control and insulin resistance.
... There is evidence that the relationship between magnesium deficiency and T2DM is bidirectional. Magnesium deficiency is a common manifestation in patients with type 1 and T2DM [5,6], and magnesium deficiency may also increase the risk of diabetes [7,8]. ...
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Background: Magnesium (Mg) is an essential element and participates in many metabolic pathways. Many studies have found a certain negative correlation between magnesium and blood glucose parameters, but the dose–response relationship between them is still a relatively narrow research field. We aim to explore the dose–response relationship between plasma and dietary Mg and type 2 diabetes (T2DM) among childbearing women in a nationally representative sample. And we will also initially explore the threshold of dietary and plasma magnesium in the prevention of T2DM and their consistency. Methods: A total of 2912 18–44 year-old childbearing women were recruited from the China Adult Chronic Disease and Nutrition Surveillance (2015). Multivariate logistic regression was used to explore the dose–response relationship between plasma and dietary Mg and glucose parameters. The threshold effect between Mg and T2DM was explored by a restricted cubic spline regression. Results: It was found that when plasma Mg was increased by 0.041 mmol/L, the risk of T2DM, impaired fasting glucose (IFG), and HbA1c-hyperglycemia was reduced by 18%, 19%, and 18%, respectively. The possible threshold value for plasma Mg to prevent the risk of T2DM was 0.87 mmol/L. Through the quality control of the sample dietary survey data, 2469 cases were finally included for dietary analysis. And the possible threshold value for dietary Mg to prevent the risk of T2DM was 408 mg/d. Taking the recommended dietary Mg intake of 330 mg/d as the reference group, when the Mg intake reached 408 mg/d, the risk of T2DM was significantly reduced. And the average plasma Mg level of the people whose dietary intake reached 408 mg/d was 0.87 mmol/L. Conclusions: These results indicate that dietary Mg and plasma Mg have good consistency on the threshold effect of glucose parameters in women of childbearing age.
... Гіпомагнезіємія виявляється практично в усіх хворих на діабет (Van Laecke, 2019). У разі розвитку експериментального діабету у тварин установлено аналогічні зміни концентрації магнію в крові (De Valk, 1999). Головною причиною деструкції β-клітин у ході інсулінозалежного цукрового діабету є клітинні механізми аутоімунної агресії (Roep, 2021). ...
Article
В основі цукрового діабету, що є одним із найпоширеніших захворювань ендокринної системи, лежать глибокі порушення обміну речовин, у тому числі мінерального. Актуальність досліджень умісту внутрішньоклітинного магнію зумовлена значенням цього металу для функціонування інсулярного апарату та імунної системи, а також залученням останньої у механізми розвитку інсулінозалежного цукрового діабету. Метою дослідження є вивчення змін умісту магнію в панкреатичних острівцях, тимусі та лімфоцитах крові тварин зі стрептозотоцин-індукованим діабетом під час уведення адаптивних гормонів (інсуліну, адреналіну та преднізолону). Розроблення у нашій лабораторії цитохімічної реакції люмомагнезону на магній у клітинах крові, підшлункової і вилочкової залоз дало змогу провести такі дослідження. Кореляційний аналіз проводили для оцінки ступеня зв’язку між змінами досліджених показників. Установлено, що введення діабетогенного агента стрептозотоцину призводило до розвитку дефіциту магнію в панкреатичних клітинах β, тимусних епітеліальних клітинах і лімфоцитах крові мишей і щурів. Призначення адаптивних гормонів частково корегувало магнієву недостатність у досліджених клітинах діабетичних тварин. У піддослідних мишей і щурів більш виражений ефект спостерігався у випадку сполученої дії цих гормонів. Проведений кореляційний аналіз засвідчив достовірну позитивну кореляцію змін кількості металу в досліджених клітинах тварин, що вказує на наявність тісних імунно-інсулярних взаємин. Практичне значення роботи полягає у тому, що отримані результати можуть бути використані для уточнення алгоритму діагностики цукрового діабету та подальшого проведення заходів патогенетичного лікування цього захворювання.
... Consequently, patients with diabetes and hypomagnesemia enter a vicious circle in which hypomagnesemia causes insulin resistance and insulin resistance reduces serum magnesium concentrations. It has been shown that supplementation with magnesium enhances insulin sensitivity in patients with diabetes [132]. A previous study suggested that hypomagnesemia among people with diabetes may be due to excessive urinary excretion [133]; thus, adequate dietary intake of magnesium or supplementation is recommended to maintain optimal levels [134]. ...
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Diabetes is associated with an increased risk of mental disorders, including depression, anxiety, and cognitive decline. Mental disorders can also contribute to the development of diabetes through various mechanisms including increased stress, poor self-care behaviors, and adverse effects on glucose metabolism. Consequently, individuals suffering from either of these conditions frequently experience comorbidity with the other. Nutrition plays an important role in both diabetes and mental health disorders including depression and anxiety. Deficiencies in specific nutrients such as omega-3 fatty acids, vitamin D, B vitamins, zinc, chromium, magnesium, and selenium have been implicated in the pathogenesis of both diabetes and mental disorders. While the impact of nutrition on the progression and control of diabetes and mental disorders is broadly acknowledged, there is a notable knowledge gap concerning the implications of distinct nutrients in preventing and mitigating symptoms of both conditions when they coexist. The aim of this study was to examine the role of nutrition in improving glucose homeostasis and promoting mental well-being among individuals with diabetes. Further, we evaluated the preventive or delaying effects of key nutrients on the simultaneous manifestation of these conditions when one of them is present. Our findings indicated that the use of personalized dietary interventions and targeted nutrient supplementation can improve metabolic and mental health outcomes in patients with type 2 diabetes.
... Magnesium deficiency has been linked to insulin resistance, leading to hyperglycemia [121,122]. Plasma magnesium concentrations have an inverse relationship with insulin resistance, and supplementation with magnesium enhances insulin sensitivity in people with diabetes [123]. A previous study suggested that hypomagnesemia among people with diabetes may be due to excessive urinary excretion [124]; thus, adequate dietary intake of magnesium or supplementation is recommended to maintain optimal levels [125]. ...
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Nutrition, diabetes, and mental disorders are interconnected and significantly impact an individual's overall health and well-being. This comprehensive review aims to explore the complex interplay between nutrition, diabetes, and mental disorders, highlighting the latest research findings in this field. While the influence of nutrition on the development and management of both diabetes and mental disorders is widely recognized, there remains a gap in understanding the intricate interplay between nutrition, mental health, and diabetes. Diabetes is associated with an increased risk of mental disorders, including depression, anxiety, and cognitive decline. Mental disorders can also contribute to the development of diabetes through various mechanisms including increased stress, poor self-care behaviors, and adverse effects on glucose metabolism. Thus, the mechanisms linking nutrition, diabetes, and mental disorders are complex and multi-factorial. Inflammation, oxidative stress, gut microbiota alterations, and neuroendocrine dysregulation have emerged as potential pathways that may mediate the relationship between nutrition, diabetes, and mental disorders. Additionally, deficiencies in essential nutrients such as omega-3 fatty acids, vitamin D, B vitamins, zinc, chromium, magnesium, and selenium have been implicated in the pathogenesis of both diabetes and mental disorders. Our findings indicate that the use of personalized dietary interventions and targeted nutrient supplementation can improve metabolic and mental health outcomes in patients with type 2 diabetes.
... Insulin injection can enhance renal magnesium excretion [85]. Supplementation can improve insulin sensitivity and may stimulate insulin secretion [86]. ...
Article
Globally, more than 30 million people suffer from diabetes mellitus type 1 (T1DM) characterized by pancreas producing little or no insulin hormone to facilitate glucose entering cells for energy production. T1DM patients tend to suffer a higher overall rate of atherosclerosis, cancer, and end-stage renal failure. No drug or surgical therapy seems to halt its annual upward trend amongst children and young adults. Consequently, a significant number of sufferers turn to complementary or alternative therapies for help to arrest this chronic endocrine condition. This paper discusses how a well-designed evidence-based dietary and nutritional therapy with some lifestyle modifications might offer a solution for this highly complex autoimmune disorder. The treatment outcome demonstrated a partial regeneration of pancreatic islet beta cells with substantial improvement for all relevant serum and urine markers tested.
... There is evidence that variations in Mg 2+ concentrations correlate with physiologically relevant processes (e.g. circadian rhythm 39 ) and differences in Mg 2+ levels are reported in diseases including diabetes 40,41,63 . The observations that wt IDH1 has a lower K M for Mg 2+ than R132H IDH1 (Table 1) and that the potency of the R132H inhibitors increases as the Mg 2+ concentration decreases (Fig. 6) raise the possibility of a therapy for R132H IDH1 bearing cancers in which inhibitor treatment is combined with restriction of Mg 2+ (possibly by diet therapy or inhibitors blocking Mg 2+ uptake). ...
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Cancer linked isocitrate dehydrogenase (IDH) 1 variants, notably R132H IDH1, manifest a ‘gain-of-function’ to reduce 2-oxoglutarate to 2-hydroxyglutarate. High-throughput screens have enabled clinically useful R132H IDH1 inhibitors, mostly allosteric binders at the dimer interface. We report investigations on roles of divalent metal ions in IDH substrate and inhibitor binding that rationalise this observation. Mg ²⁺ /Mn ²⁺ ions enhance substrate binding to wt IDH1 and R132H IDH1, but with the former manifesting lower Mg ²⁺ /Mn ²⁺ K M s. The isocitrate-Mg ²⁺ complex is the preferred wt IDH1 substrate; with R132H IDH1, separate and weaker binding of 2-oxoglutarate and Mg ²⁺ is preferred. Binding of R132H IDH1 inhibitors at the dimer interface weakens binding of active site Mg ²⁺ complexes; their potency is affected by the Mg ²⁺ concentration. Inhibitor selectivity for R132H IDH1 over wt IDH1 substantially arises from different stabilities of wt and R132H IDH1 substrate-Mg ²⁺ complexes. The results reveal the importance of substrate-metal ion complexes in wt and R132H IDH1 catalysis and the basis for selective R132H IDH1 inhibition. Further studies on roles of metal ion complexes in TCA cycle and related metabolism, including from an evolutionary perspective, are of interest.
... 18 Adipokines released by visceral fat negatively affects the metabolism of glucose. People having T2DM are 55% obese.19 Methodology This case control study was conducted at district Peshawar Khyber Pakhtunkhwa. ...
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Objective: To determine the genotype of Arg16Gly & Gln27Glu polymorphism in type-2 diabetes mellitus and to find possible association of ADRβ2with type-2 diabetes mellitus. Methodology: A case control study was designed and a total of 192 subjects (98 in each group) were included. After formal approval, subjects were recruited from North West General Hospital (NWGH) Peshawar. After taking consent blood samples were collected from the participants and DNA analysis was done using commercially available kits by salting out protocols, while other biochemical parameters were analyzed using normal laboratory protocols for respective tests. Results: The comparative analysis of SNP rs1042713 indicates that allele G/A was 42(49.4%) in diabetic and 43(50.6%) in non-diabetic subjects. While GG was more frequent 22(59.5%) in diabetic as compare to non-diabetic 15(40.5%). Among AA allele, 19 (65.5%) were non-diabetic while 10(34.5%) were diabetic. However the difference was not statistically significant (p=0.22). In case of "rs1042714" gene the commonest allele was C/C 80 (41.7%) out of which, 47(58.8%) was found in diabetic and 33(41.2%) were non-diabetic. Similarly CG was second common allele out of which diabetics were 27(44.3%) while non-diabetics were 34(55.7%). Allele G/G was found only among 11 subjects (p=0.085). Conclusion: Based on the result of the present study, it is concluded that polymorphism in ADRB2 genes rs1042713 (Arg16Gly) and rs1042714 (Gln27Glu) is associated with susceptibility of T2DM through alteration in BMI & HbA1c.
... Likewise, the intake of magnesium in our study was low as the intake in the national sample of African American women (median: 183 mg/day) that is below the RDA (320 mg/day) (Ford & Mokdad, 2003). Also, in Mg and glucose metabolism the results are inconsistent (De Valk, 1999 (Kao et al., 1999). ...
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Higher dietary intake of calcium (Ca), magnesium (Mg), and vitamin D has been associated with reduced risk of type 2 diabetes (T2DM), and a higher intracellular ratio of Ca to Mg leads to insulin resistance. Previous epidemiological studies did not examine the combined effects of dietary Ca, Mg, and vitamin D as well as ratio of Ca to Mg with T2DM. Therefore, we assessed the relationship between dietary intakes of Mg, Ca, and vitamin D (using 24-hr recalls) individually and in composite and T2DM in the National Health and Nutrition Examination Survey 2007–2014, which involved 20,480 adults (9,977 men and 10,503 women) with comprehensive information on related nutrients, and anthropometric, demographic, and biomarker variables using multivariable logistic regression. The results indicated that dietary calcium at Q3 (812 mg/day) was significantly linked with T2DM in women (OR: 1.30; 95% CI: 1.02, 1.65). Dietary vitamin D at Q3 (5.25 μg/day) significantly reduced the odds of T2DM by 21% in men (OR: 0.79; 95% CI: 0.64, 0.98). This is an interesting study that has important implications for dietary recommendations. It is concluded that US adults having dietary Ca below the RDA were associated with increased risk of T2DM in all population and women, while higher ratio of Ca to Mg was associated with increased risk of T2DM in all population and increased vitamin D intake is related to decreased risk of T2DM in men. Moreover, further research is needed to make more definitive nutritional recommendations. K E Y W O R D S cross-sectional study, dietary calcium, magnesium, NHANES, T2DM, vitamin D
... This effect might be mediated by Mg stimulation of the mammalian TOR complex 2 (mTORC2) [34], leading to GLUT1 phosphorylation and subsequently increased glucose uptake via this transporter [35]. This may imply that the contribution of adequate Mg supply to glucose uptake is not only dependent on the modulation of insulin action as has been proposed in human patients with diabetes mellitus [36,37], but may also include insulin-independent targets, especially in ruminants. Unfortunately, current knowledge about the Mg-insulinglucose interplay is scarce in dairy cows. ...
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At the onset of lactation, dairy cows suffer from insulin resistance, insulin deficiency or both, similar to human diabetes, resulting in lipolysis, ketosis and fatty liver. This work explored the combined effects of different levels of magnesium (0.1, 0.3, 1 and 3 mM) and insulin (25, 250 and 25,000 pM) on metabolic pathways and the expression of magnesium-responsive genes in a bovine adipocyte model. Magnesium starvation (0.1 mM) and low insulin (25 pM) independently decreased or tended to decrease the accumulation of non-polar lipids and uptake of the glucose analog 6-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-6-deoxyglucose (6-NBDG). Activity of glycerol 3-phosphate dehydrogenase (GPDH) was highest at 25 pM insulin and 3 mM magnesium. Expression of SLC41A1 and SLC41A3 was reduced at 0.1 mM magnesium either across insulin concentrations (SLC41A1) or at 250 pM insulin (SLC41A3). MAGT1 expression was reduced at 3 mM magnesium. NIPA1 expression was reduced at 3 mM and 0.1 mM magnesium at 25 and 250 pM insulin, respectively. Expression of SLC41A2, CNNM2, TRPM6 and TRPM7 was not affected. We conclude that magnesium promotes lipogenesis in adipocytes and inversely regulates the transcription of genes that increase vs. decrease cytosolic magnesium concentration. The induction of GAPDH activity by surplus magnesium at low insulin concentration can counteract excessive lipomobilization.
... Likewise, the intake of magnesium in our study was low as the intake in the national sample of African American women (median: 183 mg/day) that is below the RDA (320 mg/day) (Ford & Mokdad, 2003). Also, in Mg and glucose metabolism the results are inconsistent (De Valk, 1999 (Kao et al., 1999). ...
Article
Full-text available
Higher dietary intake of calcium (Ca), magnesium (Mg), and vitamin D has been associated with reduced risk of type 2 diabetes (T2DM), and a higher intracellular ratio of Ca to Mg leads to insulin resistance. Previous epidemiological studies did not examine the combined effects of dietary Ca, Mg, and vitamin D as well as ratio of Ca to Mg with T2DM. Therefore, we assessed the relationship between dietary intakes of Mg, Ca, and vitamin D (using 24-hr recalls) individually and in composite and T2DM in the National Health and Nutrition Examination Survey 2007-2014, which involved 20,480 adults (9,977 men and 10,503 women) with comprehensive information on related nutrients, and anthropometric, demographic, and biomarker variables using multivariable logistic regression. The results indicated that dietary calcium at Q3 (812 mg/day) was significantly linked with T2DM in women (OR: 1.30; 95% CI: 1.02, 1.65). Dietary vitamin D at Q3 (5.25 μg/day) significantly reduced the odds of T2DM by 21% in men (OR: 0.79; 95% CI: 0.64, 0.98). This is an interesting study that has important implications for dietary recommendations. It is concluded that US adults having dietary Ca below the RDA were associated with increased risk of T2DM in all population and women, while higher ratio of Ca to Mg was associated with increased risk of T2DM in all population and increased vitamin D intake is related to decreased risk of T2DM in men. Moreover, further research is needed to make more definitive nutritional recommendations. K E Y W O R D S cross-sectional study, dietary calcium, magnesium, NHANES, T2DM, vitamin D
... Grouping: The rats were divided into four (4) groups of five (5) Values are mean ± standard deviation shown chromium to act by enhancing insulin action (7). Magnesium and Zinc function as essential cofactors of several enzymes of energy metabolism (14). Since decreased levels of these elements have been shown in diabetic p a t i e n t s , C o t u r n i x j a p o n i c a e g g supplementation may increase their levels thereby increasing the chances of managing the disease. ...
Article
Background: Cases of diabetes are on the rise in almost every population and without proper management and control the burden of the disease will continue to rise globally. Vitamins and minerals play significant roles in the management of diabetes and studies have shown the hypoglycemic effect of quail's egg. Objectives: The aim of the study was to investigate the effect of Coturnix japonica (Quail) egg on serum glucose and some serum B-vitamins and mineral elements in alloxan induced diabetic rats. Methods: Rats were rendered diabetic by intravenous injection of alloxan (80mg/kg body weight). Coturnix japonica egg was administered orally at 100, 200 and 400 mg/kg body weight per day for four weeks to the experimental animal groups. Serum glucose was significantly decreased
... 66,67 Hypomagnesemia has been reported at increased frequency among patients with type 2 diabetes. 68,69 Moreover, lower serum magnesium levels were shown to significantly correlate with impaired peripheral nerve function in this cohort. 70,71 Magnesium supplementation can improve both glycemic control and insulin sensitivity 72,73 and can also favorably affect the natural evolution of DPN. ...
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Introduction: Diabetic polyneuropathy (DPN) is a debilitating condition and associated with significant morbidity, including gait disturbances, reduced quality of life, and pain, that is often resistant to conventional treatments. Treatment of DPN is based on several major approaches, including risk factor management, intensive glycemic control, and symptomatic pain management. Although some authors argue that none of the existing treatment options are satisfactory, an alternative strategy is frequently overlooked: the use of a whole‐food, plant‐based diet. The aim of this review was to systematically investigate whether a whole‐food, plant‐based diet could beneficially affect patients suffering from type 2 diabetes and DPN. Methods: The electronic databases of PubMed and Google Scholar were searched using the keywords “plant‐based,” “vegetarian,” “vegan,” “diet,” and “diabetic neuropathy.” Results: Only a handful of studies investigated the effects of a plant‐based diet on diabetic neuropathy. These studies suggest that a plant‐based diet may alleviate pain in affected patients while significantly improving glycemic control, overweight, and serum lipids at the same time. Moreover, a plant‐based diet appears to reduce the medication burden in affected patients. However, the results must be interpreted with caution, because the number of clinical trials is limited and all studies have important limitations with regard to their methodology. The dietary intervention was often combined with exercise and other supplemental factors, complicating the interpretation of results. Several potential mechanisms of action including improved blood flow and optimized intake of important nutrients were identified. These factors might complementarily contribute to improved perfusion in the endoneurial microvasculature, thus reducing local hypoxia and improving pain. Conclusion: Physicians should consider recommending a plant‐based diet to patients suffering from DPN, as current studies show favorable effects in terms of pain management, glycemic control, and reduced medication needs. Further well‐designed studies are required to confirm the results of this review.
... 4 In diabetes the various causes that can cause hypomagnesemia are mentioned in Table 1. 5 Low levels of magnesium in both intracellular and extracellular compartments interferes with enzymatic reactions involved in the production of adenosine triphosphate, thus modifying the cascade of enzymes involved in carbohydrate metabolism, triggering DM and its complications. 6 Hypomagnesemia is common in DM, is very commonly underdiagnosed and has been implicated in carbohydrate intolerance, hyperglycemia, insulin resistance and hyperlipidemia. ...
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ABSTRACT Introduction: Patients of DM are known to have low levels of serum magnesium levels as compared to non-diabetics. There is a link between the low magnesium levels and poor glycemic controls and subsequently leading to complications in diabetic patients. The aim of this study was to assess the serum magnesium levels in relation to glycemic status in diabetic patients as compared to non-diabetics. Material and Methods: 172 cases of previously diagnosed DM were taken along with the age and sex matched controls who were healthy and non-diabetic and their blood samples were analyzed for magnesium and blood sugar fasting and post prandial. Results: In our study we have found that there is a significant hypomagnesemia in diabetic cases as compared to nondiabetic controls which is in accordance with other studies. There also exists a negative correlation between mean serum magnesium levels (2.08 ± 0.4 mg/dL) and mean fasting plasma sugar (FBS) (159.72 ± 71.60 mg/dL) and mean post prandial sugar (PPS) (222.76 ± 100.86 mg/dL) levels. No significant variation as per age and sex in serum magnesium levels amongst diabetic subjects have been found in our study. Conclusion: Hypomagnesemia is common in diabetics as has been found in our study also, and it helps in regulation of glycemic levels and in turn also affects magnesium levels. Considering estimation of magnesium as a routine laboratory work up protocol in the management of diabetes may prevent various complications due to hypomagnesemia with early therapeutic intervention. Keywords: Hypomagnesemia, Poor Glycemic Control, FBS, PPS, Diabetic Complications
... In human medicine, a distinction is made between impaired glucose tolerance (IGT), impaired fasting glycaemia (IFG), also called "non-diabetic fasting hyperglycemia", and diabetes mellitus with hyperglycemia (Alberti and Zimmet 1998). In the above-mentioned studies on the relationship between magnesium and ID in humans (Paolisso and Barbagallo 1997, Pham et al. 2007, Chaudhary et al. 2010, Rasheed et al. 2012, Kao et al. 1999, de Valk 1999 patients were classified as diabetes mellitus type II. Hence, these patients showed hyperglycemia at rest and a more pronounced ID than the horses in our study. ...
... 4 In diabetes the various causes that can cause hypomagnesemia are mentioned in Table 1. 5 Low levels of magnesium in both intracellular and extracellular compartments interferes with enzymatic reactions involved in the production of adenosine triphosphate, thus modifying the cascade of enzymes involved in carbohydrate metabolism, triggering DM and its complications. 6 Hypomagnesemia is common in DM, is very commonly underdiagnosed and has been implicated in carbohydrate intolerance, hyperglycemia, insulin resistance and hyperlipidemia. ...
... It was shown that plasma magnesium level is inversely related with insülin sensitivity. Magnesium support increases both insülin sensitivity and secretion in DM patients and decreases development of Type II diabetes [36]. However, especially at long term magnesium deficiency fasting glucose or insülin concentrations increases basal glucose without changing fasting glucose or insulin concentrations [37]. ...
... Patients with severe retinopathy have a lower plasma magnesium level compared to patients without retinopathy and a prospective study has shown the plasma magnesium level to be inversely related to occurrence or progression of retinopathy. 67 Mikhail N, Ehsanipoor K (1999) concluded that their data do not support routine Mg supplementation or monitoring in type 2 diabetes. 68 Kao WH, Aoron R, Folsom H, et al (1999) concluded that low serum Mg level is a strong, independent predictor of incident type 2 diabetes. ...
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Diabetes mellitus is increasing alarmingly especially in developing country like India. The complications related to Diabetes lead to loss of life and also healthy life years lost. There are many factors contributing to the compications. The prevalance of magnisiuria in diabetics is long under reasearch. Magnesium is known to be important for endothelial function. We studied the prevalance of levels of magnesium in patients who had vascular complications associated with diabetes. We found a correlation that is not statistically significant.
... Inhibiting the enzyme cyclo-oxygenase-1 or associated with the DM chronic complications [17]. Therefore, metabolic studies have suggested that magnesium supplementation has a beneficial effect on insulin action and glucose metabolism [18,19]. It is thought that Magnesium supplementation can correct the deficit in intracellular free magnesium levels, decrease platelet reactivity, improve insulin sensitivity, protect against diabetes and its complications and reduce blood pressure. ...
... Поэтому снижение уровня Mg в сыворотке крови больных ВБП расценивается как одна из причин, предрасполагающих к развитию воспалительных заболеваний, и является усугубляющим фактором в лечении бактериальной инфекции бронхолегочной системы. В целом гипомагниемия представляет собой серьезное состояние, инициирующее процессы воспаления, клинически сопровождаемое спазмами гладкой мускулатуры, размягчением костной ткани, развитием ишемической болезни сердца, артериальной гипертензии, обострением сахарного диабета, нарушением функции центральной нервной системы и такими изменениями лабораторных показателей, как повышение уровня холестерина [33][34][35]. ...
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Background. A large amount of experimental and clinical data on the content and the role of chemical elements in the human body is accumulated by nowadays. However, the state of mineral metabolism, mechanisms of action and the role of chemical elements in the etiology and pathogenesis of infl ammatory, autoimmune and other diseases are to be studied. Objective. To examine the state of mineral metabolism (calcium - Ca, magnesium - Mg, iron - Fe, cobalt - Co, copper - Cu, zinc - Zn) in various pathogenetic variants of infl ammatory processes in the blood serum of patients with acute coronary syndrome, community-acquired pneumonia and rheumatoid arthritis.
... [21][22][23] The low magnesium level can worsen the glycaemic status in diabetes mellitus and micro and macrovascular due to persistent hyperglycemia is linked to spread of complications. 24,25 The dyslipidemia was also observed in present study population. Furthermore, Guerrero-Romero, et al and Rodriguez-Moran, et al studies found an association between low magnesium and lipoproteins. ...
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Objectives: To determine the frequency of hypomagnesemia in patients withdiabetic foot ulcer. Study Design: Cross sectional descriptive nature. Setting: Liaquat UniversityHospital Jamshoro / Hyderabad. Period: 29-09-2016 to 28-03-2017. Patients and Methods:The patients with history of diabetes mellitus (known cases) for more than 3 years durationhad diabetic foot ulcer for ≥ 02 weeks duration, of 30-60 years of age & either gender wererecruited and evaluated for serum magnesium level while the data was analyzed in SPSS 16.Results: Total 100 patients with diabetic foot ulcer were evaluated for hypomagnesaemia. Themean age ±SD of age (years), duration of diabetes (years) and foot ulcer (weeks), BMI (kg/m2),hypertension (systolic and diastolic mmHg), HBA1C and magnesium for whole population was52.86±6.87, 6.95±1.85 and 5.86±2.31, 31.92±2/43, 150.38±10.52 and 95.97±5.97, 9.96±2.73and 1.16±0.95 respectively. Out of one hundred, 55% were males and 45% were females. Thehypertension, smoking, dyslipidemia, obesity, raised HBA1C and hypomagnesemia was foundin 65%, 59%, 59%, 55%, 56% and 67%. Conclusion: Hypomagnesemia detected in subjectswith type 2 diabetes mellitus having foot ulcers.
... The mechanisms by which Fluoride induces diabetes most likely include antagonism to calcium and magnesium centred biochemistry [De Valk 1999, Simmons 2010. Insulin secretion (both basal and glucose-stimulated) by isolated islets of Langerhans in vitro is inhibited as a function of fluoride concentrations [Rigalli 1990[Rigalli , 1995. ...
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Experts in endocrinology have shown that Fluoride causes Diabetes and Obesity. This review assembles the wealth of science that shows how Fluoride damages the organs that generate or use Insulin to control Glucose metabolism and the crucial involvement of other hormone systems.
... The present study result showed the mean ( SD) value of serum Mg concentrations was nonsignificantly higher in non-diabetic group than diabetic group as shown in table (5). Diabetes mellitus, both type I and type II, are said to be the commonest causes of magnesium deficiency, with 25-39% of patients being affected [16]. A decrease in total, ultrafiltrable, ionised, red cell and white cell magnesium have been found [17,18]. ...
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ABSTRACT Megnesium depletion plays a key role in the pathphysiologic features of diabetes mellitus, hypertension, thrombosis, arrhythmias and coronary artery disease. Whether the depletion is related to the Echocardiographic parameters in an acute phase of acute coronary syndrome is not known. The objective of the study is to explore the status of serum magnesium in acute coronary syndrome patients. To investigated the association of serum magnesium levels with major risk factor, fibrinolysis and echocardiography in Patients with acute coronary syndrome. The 68 patients with were divided into three groups: STEMI, NSTEMI and unstable angina. The 24 healthy individuals matched as a control group. Serum Mg was measured in all patients groups and control group, the analysis is performed in an atomic absorption spectrophotometer (Schmiadzu AA5646). Estimation of serum glucose, urea, creatinine, lipid profile was done by colorimetric method. The mean ±SD value of serum Mg levels in patients with ACS was significantly lower than those in normal controls. ANOVA test revealed there was non significant difference in the value of serum Mg mean ±SD levels among three types of acute coronary syndrome, t- test revealed there was non significant difference in the value of serum Mg mean±SD levels in the presence or absente of diabetes millitus, Dyslipidemia, Hypertension, Smoking, Obesity and fibrinolytic treatment. The mean (±SD) value of serum Mg levels was non-significantly associated with mitral regurgitataion (MR) severity and diastolic dysfunction stages. There was non-significant correlation between the serum Mg concentration and the value of Isovolumic relaxation time, E (left ventricular inflow velocity) / e (tissue doppler velocity) ratio and Decceleration time, Age, Diameter of left atrium and Left Ventricular Ejection Fraction (LVEF). Decreases Serum magnesium level indicate ischemia severity in acute coronary syndrome patients, Serum magnesium level non significantly associated with major risk factor, fibrinolytic treatment and Echocardiographic parameter in acute phase of disease. Key Words: Magnesium, ACS, Echocardiographic INTRODUCTION Disruption of vulnerable or high-risk plaques is the common pathophysiological substrate of the acute coronary syndromes that comprise a spectrum of myocardial ischemia. Patients with an acute coronary syndrome include those whose clinical presentations cover the following range of diagnoses: unstable angina, MI without ST elevation (NSTEMI), and MI with ST elevation (STEMI) [1-3]. Patients with STEMI have a high likelihood of a coronary thrombus occluding the infarct artery. Patients presenting with persistent ST-segment elevation are candidates for reperfusion therapy (either pharmacological or catheter-based) to restore flow promptly in the occluded epicardial infarct-related artery. Patients presenting without ST-segment elevation are not candidates
... Diabetes mellitus is the also associated with secondary magnesium deficit. Plasma magnesium concentrations may correlate inversely with the degree of hyperglycemia [12]. Early recognition and treatment of severe hypophosphataemia is important to reduce the risk of neurological complications [13]. ...
... [18] Therefore, metabolic studies have suggested that magnesium supplementation has a beneficial effect on insulin action and glucose metabolism. [19,20] It is thought that magnesium supplementation can correct the deficit in intracellular free magnesium levels, decrease platelet reactivity, improve insulin sensitivity, protect against diabetes and its complications, and reduce blood pressure. ...
Article
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Objective: Recent studies have shown a rampant increase in the number of patients with diabetes around the world. This constitutes an economic burden on the resources of states and hence has prompted many international organizations to devise awareness and educational programs about the dangers of this the disease and ways to deal with it. There are serious complications to diabetes which may include; high blood pressure, heart and kidney diseases, eye problems, neuropathy, and diabetic foot. The most feared development of this disease is the diabetic foot as it may lead to amputation. This study examines the prevalence of diabetes and complementary alternative medicine in the treatment of this disease and the attitudes toward managing diabetic foot in Makkah and Taif area in Saudi Arabia. Methods: Questionnaires were distributed in the Western region of Saudi Arabia.The sample size was 750. Responses were collected and proper descriptive statistical analysis was applied. Results: An alarming 34% of respondents have diabetes, 74% of surveyed population has diabetes within family members, and 40% of respondents have had a form of foot problem with the highest incident of leg pain and numbness. The majority of examined population has chosen traditional medical intervention rather than herbal medicine in dealing with foot problems. Conclusions: The culture of interfamily marriages has to be overlooked to curb rampant increase of diabetes incidents among family members. There is lack of statistical data related to the incident rate of lower-extremity amputations LEA among patients with diabetes in Saudi Arabia. Moreover, the role of diabetic centers has to be invigorated in spreading knowledge with regards to diabetes, and in devising proper follow-up procedures to patients with diabetes after referral to other departments in hospitals.
... In another study, Al-Saleh reported that serum zinc levels in obese pregnant women with GDM compared with healthy obese women were lower, but copper levels were similar in both groups (21). Decreased serum magnesium levels and increased urinary excretion in patients with diabetes type 1 and 2 are shown in a number of studies (22)(23)(24). Similar to our results, difference in magnesium levels between diabetic patients and healthy subjects were not observed by Walter et al (16). ...
Article
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Objective: Gestational Diabetes Mellitus (GDM) is a type of diabetes that begins during pregnancy. This problem causes many complications for mother and foetus. Mineral levels in diabetic patients change and since the levels of these elements have not received much attention in patients with Impaired Glucose Tolerance test (IGT), in this study serum concentration of copper (Cu), zinc (Zn), and magnesium (Mg) were analysed in singleton pregnant women with IGT compared with euglycemic pregnant women. Methods: The subjects of this case-control study have been selected from pregnant women who referred to Rohzendeh health and therapeutic center in northwest of Iran from December 2013 - April 2014. 46 pregnant women with IGT and 35 euglycemic women were selected. The levels of hemoglobin, hematocrit, zinc, copper and magnesium in the blood samples were measured. Results: The findings of this study indicated that the difference of hemoglobin and hematocrit and magnesium levels was not significant between two groups. The difference of copper concentration in healthy pregnant women and women with IGT was statistically significant (P<0.001) which indicated a high level of copper in healthy pregnant women. Interestingly, in pregnant women with IGT plasmatic zinc level was lower than healthy women (P= 0.028). Conclusions: Pregnancy is a condition that can affect the mineral status and to achieve better results, further researches are needed with larger sample size.
Article
Анотація. Робота присвячена проведенню порівняльних досліджень вмісту магнію в панкреатичних β-клітинах, тимусних епітеліальних клітинах і лімфоцитах крові тварин за активації, пригнічення та блокування інкреторної функції підшлункової залози. Актуальність досліджень вмісту внутрішньоклітинного магнію зумовлена значенням цього металу для функціонування інсулярного апарату й імунної системи, а також залученням останньої в механізми розвитку інсулінозалежного цукрового діабету. Розробка в нашій лабораторії цитохімічної реакції люмомагнезону на магній у клітинах крові, підшлункової та вилочкової залоз дозволила провести такі дослідження. Досліди проводилися на безпородних мишах і щурах віком 6 місяців. Стан пригнічення секреторної функції β-клітин панкреатичних острівців одержували введенням тваринам атропіну, адреналіну, преднізолону та гострим голодуванням. Посилення секреторної активності цих клітин викликали ін’єкціями глюкози, пілокарпіну та холецистокініну. Експериментальні дані обробляли за допомогою t-критерію Стьюдента. Обчислювали коефіцієнт кореляції Пірсона (r) для оцінки ступеня зв’язку між змінами досліджених показників. Стан гіпофункції острівцевого апарату підшлункової залози моделювали введенням тваринам діабетогенної речовини стрептозотоцину. Було встановлено, що пригнічення секреторної активності інсулінпродукуючих клітин спричиняло збільшення вмісту магнію на 17% (Р < 0,05) – 39% (Р < 0,001), а активація цієї функції – навпаки, зменшення його вмісту на 25% (Р < 0,05) – 37% (Р < 0,001) у панкреатичних клітинах β, епітеліальних клітинах тимуса, лімфоцитах крові мишей і щурів. Блокування функції інсулярного апарату після ін’єкції стрептозотоцину призводило до розвитку вираженого дефіциту металу в досліджених клітинах, який коливався в межах 44–54% (Р < 0,001). У всіх випадках спостерігалась позитивна кореляція змін вмісту магнію у β-клітинах острівців, клітинах вилочкової залози та лімфоцитах крові піддослідних тварин, що свідчить на користь існування тісних функціональних зв’язків між інсулярним апаратом та імунною системою.
Article
Objective The prevalence of complementary and alternative medicine (CAM) usage among patients with type 2 diabetes mellitus (T2DM) in Indonesia is high. However, to date, little is known about why Indonesian T2DM patients choose CAM therapies, how their knowledge, attitude and practice (KAP) of CAM affects their choices, or how demographics correlate with patient choices. Therefore, this study aimed to investigate the KAP and predictors of CAM usage in T2DM patients in Indonesia. Methods This was an observational, cross-sectional study. Patients were interviewed using a questionnaire. Chi-square tests or Fisher’s exact tests were used to compare demographic and clinical data, as well as KAP assessments, between T2DM patients who use and do not use CAM. Multivariate logistic regression analyses were used to investigate predictors of CAM usage. Results A total of 628 T2DM patients were enrolled in the study. CAM therapies were used by 341 patients (54.3%). The most common therapies were herbs and spiritual healing, used by 100.0% and 68.3% of CAM-using patients, respectively. CAM therapies were frequently recommended by family members (91.5%), and CAM users had significantly more knowledge and more positive attitudes toward CAM therapies than nonusers. Among users, 66% said they would not follow their healthcare providers’ instructions to not use CAM therapies, and 69.5% said they would not disclose their plan to use CAM therapies with their healthcare provider. Neither demographic nor clinical characteristics were associated with CAM use. The factors that best predicted the use of CAM therapies were their availability and low cost (odds ratio [OR] = 4.59; 95% confidence interval [CI]: 3.01–7.01), the belief that CAM therapies were safe (OR = 2.04; 95% CI: 1.40–2.95), the belief that CAM therapies could help with diabetes control (OR = 1.75; 95% CI: 1.15–2.66), and the belief that CAM therapies could help maintain physical health (OR = 1.68; 95% CI: 1.13–2.49). Conclusion CAM therapy users were more knowledgeable and had more positive attitudes toward CAM, but most of them chose not to disclose their CAM use to their healthcare providers. CAM use in Indonesia was associated with its accessibility, affordability, safety and effectivity, but not with any demographic or clinical characteristics. This study provided new evidence and insights for nurses and physicians in Indonesia that will help to design educational programs about the safety and efficacy of CAM therapies. Please cite this article as: Sari Y, Anam A, Sumeru A, Sutrisna E. The knowledge, attitude, practice and predictors of complementary and alternative medicine use among type 2 diabetes mellitus patients in Indonesia. J Integr Med. 2021; Epub ahead of print.
Chapter
The Human Genome Project has provided the foundation for understanding health and disease at the molecular level. Genomes, however, respond to and interact with their environments. Nutrigenomics is an emerging field of research that examines the interactions between the nutritional environment and cellular/genetic processes. One of the primary aims of nutrigenomics is to understand the effects of diet on the activity of an individual’s genes and health.⁴⁴ Nutritional genomics is an integrative systems biology that uses tools and concepts from nutritional science, molecular biology, genetics, and genomics. Since unbalanced nutrient intake alters the equilibrium between health and disease, nutrigenomics research assesses physiologies and pathologies. Much of the current emphasis of researchers is to associate physiological measurements (such as HDL, LDL, cholesterol, height, weight, enzyme activities, protein levels, metabolite concentrations, etc.) with genotype as measured by expression analyses or, more typically, single nucleotide polymorphisms (SNPs) in genes. The field is best summarized by the following tenets⁴².
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Equine metabolic syndrome (EMS) is a worldwide disease in horses that parallels human diabetes mellitus type 2. In both diseases, patients show an altered peripheral insulin sensitivity as a key feature. In humans, multiple studies have demonstrated the beneficial effect of magnesium supplementation on insulin sensitivity. However, serum magnesium levels vary and are therefore not a reliable indicator of the patients’ magnesium status. Determining the intracellular free magnesium concentration appears to be a more sensitive diagnostic indicator. In this study, the free intracellular magnesium concentration was measured using mag‐fura 2 spectrophotometry in blood lymphocytes in 12 healthy, non‐obese horses at 9 a.m., 12 a.m. and 4 p.m. to establish reference ranges according to a protocol designed for human blood lymphocytes. Additionally, the serum magnesium concentration was measured. In all horses, the total serum magnesium concentration was within the reference range. The mean free magnesium concentration in blood lymphocytes of all horses was 0.291 ± 0.067 mmol/L with no significant difference between the time points. The reference range for the free intracellular magnesium concentration in equine lymphocytes was set at 0.16–0.42 mmol/L. The established values are slightly lower than those in healthy humans. The designed protocol for the measurement of the intracellular free magnesium concentration might be an excellent research tool to assess the cellular magnesium status and to reliably diagnose an altered magnesium homeostasis in EMS. Further studies shall elucidate possible alterations in cellular magnesium status in horses with EMS.
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Diabetes and hypothyroidism are both metabolic diseases with great incidence worldwide. Metalloproteins and metals play key roles in normal glucose metabolism and thyroid hormone synthesis, which are altered in their respective pathologies. The aim of this work was to establish the corresponding multielemental and metalloprotean profiles in a control group (n = 20) compared with a diabetic (n = 20) or hypothyroidism group (n = 20), by exploring a multivariate principal components model. Classification to discriminate these groups was possible based in the quantification of 23 elements (Mg, Al, K, Ca, V, Cr, Zn, Fe, Se, Rb, Pb, Cu, Mn, Co, Ni, U, Sr, Mo, Sb, Ba, Tl, Cd, Ag), and alternatively on the metalloprotein profiles obtained by SEC-ICPMS. Determinations were assessed by means of QQQ-ICP and SEC-ICPMS for total and metalloprotean content, respectively. Samples were classified using Principal Component Analysis chemometric tool. Results showed that there were statistical differences in transitional elements concentrations, such as Zn, Cu, Co, Mn, V, and Cr. For the metal associated protein study, the expression of the fractions of the same transitional elements also were statistically different when compared between control vs diabetic patients, and control vs hypothyroid patients. Se levels showed no differences in both studies among groups. This screening study demonstrates that mass spectrometry methods and data analysis with chemometrics tools may be valuable in order to find possible biomarkers in serum samples of diabetic and hypothyroid patients. Future proteomics analysis are necessary to complete these findings.
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To determine the relations of diet with risk of clinical noninsulin-dependent diabetes, we analyzed data from a prospective cohort of 84360 US women. During 6 y of follow-up we identified 702 definite incident cases. Because body mass index (BMI) is a powerful risk factor for diabetes, we examined the relations of fat (including type), fiber, sucrose, and other components of diet to risk of diabetes, among women with BMIs (in kg/m2) less than 29 kg/m2. After controlling for body mass index, previous weight change, and alcohol intake, we observed no associations between intakes of energy, protein, sucrose, carbohydrate, or fiber and risk of diabetes. Compared with women in the lowest quintile of energy-adjusted intake, and relative risks (and tests for trend) for those in the highest quintile were 0.61 (P trend = 0.03) for vegetable fat, 0.62 (P trend = 0.008) for potassium, 0.70 (P trend = 0.005) for calcium, and 0.68 (P trend = 0.02) for magnesium. These inverse associations were attenuated among obese women (BMIs greater than or equal to 29).
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Mg deficiency may be an important factor leading to cardiovascular disease. Diabetic subjects show an increase in platelet reactivity that can enhance the risks of vascular disease. In addition, diabetic patients have been reported to be at risk of developing extracellular Mg deficiency. However, the intracellular free Mg concentration and its role in the enhanced platelet reactivity in diabetes is not known. We evaluated the intracellular erythrocyte (RBC) Mg2+ concentration in 20 non-insulin-dependent (type II) diabetics. In addition, the effects of intravenous 3-h drip or 8 wk of oral Mg supplementation on intracellular RBC Mg2+ levels and platelet reactivity was studied. To more clearly evaluate the direct role of Mg in these effects, we induced isolated Mg deficiency in 16 nondiabetic control subjects with an Mg-free liquid diet for 3 wk. The intracellular RBC Mg2+ concentration of diabetic patients was significantly reduced compared with values in nondiabetic control subjects (166 +/- 7 vs. 204 +/- 7 microM, P less than 0.01). Serum Mg levels were also reduced in the diabetic patients compared with the control subjects (1.59 +/- 0.04 vs. 1.9 +/- 0.1 mEq/L, P less than 0.05). Oral Mg supplementation for 8 wk (400 mg/day) restored RBC Mg2+ concentration to normal without significantly changing serum Mg concentration. Both intravenous and oral Mg supplementation markedly reduced platelet reactivity in response to the thromboxane A2 analog, U46619. The Mg-free diet resulted in a significant reduction in RBC Mg2+ concentration and markedly enhanced the sensitivity of platelet aggregation to U46619 and ADP. These results suggest that type II diabetic patients have intracellular Mg2+ deficiency and that Mg deficiency may be a key factor in leading to enhanced platelet reactivity in type II diabetes. Therefore, Mg supplementation may provide a new therapeutic approach to reducing vascular disease in patients with diabetes.
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To evaluate copper, zinc, manganese, magnesium, and other indices of peroxidative status in diabetic and nondiabetic human subjects. Convenience sample of 57 insulin-dependent or non-insulin-dependent diabetic subjects recruited from the diabetes clinic of the University of California, Davis, Medical Center and 28 nondiabetic subjects recruited from the staffs of the Departments of Internal Medicine and Nutrition. Individuals conducting laboratory analyses were blind to subject group. A fasting blood sample was collected from all subjects and appropriately processed for future analyses. A 24-h urine collection was obtained in a subset of subjects. Hyperzincuria and hypermagnesuria were evident in diabetic subjects compared with control subjects. There were no differences in plasma magnesium or whole-blood manganese between groups. Plasma copper was higher and plasma zinc was lower in diabetic than in control subjects. When data were viewed with respect to specific diabetes-associated complications, diabetic subjects with retinopathy, hypertension, or microvascular disease had higher plasma copper concentrations compared with both diabetic subjects without complications and with control subjects. There were no significant differences between control and diabetic subjects in erythrocyte copper-zinc superoxide dismutase activity or whole-blood glutathione peroxidase or glutathione reductase activities. Plasma peroxide concentrations were higher in diabetic than control subjects. Diabetes can alter copper, zinc, magnesium, and lipid peroxidation status. Perturbations in mineral metabolism are more pronounced in diabetic populations with specific complications. It is not known whether differences in trace element status are a consequence of diabetes, or alternatively, whether they contribute to the expression of the disease.
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Urinary excretion of calcium, inorganic phosphorus, magnesium, glucose, and creatinine was measured in first-void spot urine samples collected 4 days apart in 220 insulin-dependent diabetic (IDDM) children (mean age 11.9 yr) attending a summer camp. A single control urine sample was obtained from 33 healthy nondiabetic siblings (mean age 11.2 yr). Mean +/- SD urinary calcium-creatinine ratios (UCa/Cr) did not significantly differ between IDDM and control subjects (0.14 +/- 0.09 vs. 0.12 +/- 0.09, respectively, P = 0.156). Mean urinary magnesium-creatinine ratios (UMg/Cr) were elevated in IDDM compared with control subjects (0.15 +/- 0.06 vs. 0.08 +/- 0.03, respectively, P = 0.0001). Similarly, mean urinary phosphorus-creatinine ratios (UP/Cr) were significantly increased over those in control subjects (1.12 +/- 0.33 vs. 0.40 +/- 0.22, respectively, P = 0.0001). UCa/Cr, UMg/Cr, and UP/Cr were correlated with increasing mean urine glucose content (P = 0.0001). No correlations were found when UCa/Cr, UMg/Cr, or UP/Cr were compared with patient age, duration of diabetes, glycosylated hemoglobin, or insulin dosage. Urine losses of phosphorus and magnesium were present even when glycemic control was considered good by several methods (glycosylated hemoglobin, short-term glycemic index, or urinary glucose content). Glomerular hyperfiltration was unable to account for increased urinary mineral content. In conclusion, the data indicate that urinary excretion of phosphorus and magnesium is elevated in children with IDDM, regardless of glycemic control. In the presence of glucosuria, this loss is further enhanced. Urinary calcium excretion is significantly higher only during periods of glucosuria. The data suggest that children with IDDM could be at risk for mineral deficiencies in the absence of intensive insulin management.
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In eight aged non-insulin-dependent diabetes mellitus (NIDDM) subjects, insulin response and action were studied before and after chronic magnesium supplementation (2 g/day) to diet. Chronic magnesium supplementation to diet versus placebo produced 1) a significant increase in plasma (0.83 +/- 0.05 vs. 0.78 +/- 0.06 mM, P less than .05) and erythrocyte (2.03 +/- 0.06 vs. 1.88 +/- 0.09 mM, P less than .01) magnesium levels, 2) an increase in acute insulin response (AIR) (4.0 +/- 0.6 vs. -1.6 +/- 0.6 mU/L, P less than .05) to glucose pulse, and 3) an increase in glucose infusion rate (GIR) (3.6 +/- 0.6 vs. 2.9 +/- 0.5 mg.kg-1.min-1, P less than .025) calculated in the last 60 min of a euglycemic-hyperinsulinemic (100 mU.m2.min-1 during 180 min) glucose clamp. Net increase in AIR, glucose disappearance rate after glucose pulse, and GIR were significantly and positively correlated to the net increase in erythrocyte magnesium content calculated after chronic magnesium supplementation to diet. In conclusion, our data suggest that NIDDM subjects may benefit from therapeutic chronic administration of magnesium salts.
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Magnesium plays a critical role in many cell functions. Hypomagnesemia may occur because of decreased intake or absorption, internal redistribution or increased loss of this element through either renal or nonrenal routes. Manifestations of magnesium deficiency include alterations in calcium, phosphate and potassium homeostasis along with cardiac disorders such as malignant ventricular arrhythmias refractory to conventional therapy, enhanced sensitivity to digoxin and, possibly, coronary artery vasospasm and sudden death. Other features of magnesium deficiency include a host of neuromuscular and neuropsychiatric disorders. In this review we detail mechanisms that may lead to magnesium deficiency, summarize the clinical features of the deficiency and provide a clinical approach to the diagnosis and treatment of this electrolyte disorder.
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Magnesium and potassium were analyzed in plasma, erythrocytes, and urine collected during 24 h and in muscle biopsies from 25 subjects with insulin-dependent, type I diabetes mellitus (IDDM). Magnesium was also measured in mononuclear cells. The results were compared with those of 28 healthy controls, and were also correlated with the degree of diabetic control as estimated by analysis of the level of glycosylated hemoglobin (HbA1c). Subjects with IDDM had significantly lower muscle (P less than 0.01) and plasma (P less than 0.001) concentrations of magnesium compared with those of healthy controls. The HbA1c levels correlated significantly with the concentrations of magnesium in muscle (r = -0.62, P less than 0.001), plasma (r = -0.62, P less than 0.001), and mononuclear cells (r = -0.47, P less than 0.05). The results indicate that some patients with IDDM have lowered contents of magnesium in striated muscular and/or plasma, and that those parameters are dependent on the degree of diabetic control.
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Fasting plasma concentrations of magnesium were measured by neutron activation analysis in 30 non-diabetics and 87 diabetics (55 non-insulin-treated, 32 insulin treated). Plasma concentrations of magnesium were lowest in the insulin treated group (mean 0.84 (SEM 0.01) mmol/1; 2.0 (0.02) mg/100 ml), intermediate in the non-diabetics (mean 0.89 (SEM 0.01) mmol/1; 2.2 (0.02) mg/100 ml), and highest in the non-insulin-treated diabetics (mean 0.95 (SEM 0.02) mmol/1; 2.3 (0.05) mg/100 ml). In all diabetics plasma magnesium concentrations were inversely related to plasma glucose values (rs = -0.33; p less than 0.01) and in non-insulin-treated patients to plasma insulin concentrations (rs = -0.28; p less than 0.05), the former confirming previous observations. In 67 of the diabetics the KG constant for disposal rate of glucose during a standard intravenous glucose tolerance test was directly related to fasting plasma magnesium concentrations, and this relation persisted after controlling for age, sex, body mass index, type of treatment, and glucose and insulin values. This direct relation of plasma magnesium concentration with glucose disposal was unexplained by its influence on insulin secretion but was related to insulin sensitivity; hence magnesium may be an important determinant of insulin sensitivity in maturity onset diabetes.
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Kidney International aims to inform the renal researcher and practicing nephrologists on all aspects of renal research. Clinical and basic renal research, commentaries, The Renal Consult, Nephrology sans Frontieres, minireviews, reviews, Nephrology Images, Journal Club. Published weekly online and twice a month in print.
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The plasma magnesium (Mg) concentrations of 582 unselected diabetic outpatients and 140 control subjects were measured by atomic absorption spectrophotometry. Mean plasma Mg (+/-S.D.) was significantly lower in the diabetic patients (0.737 +/- 0.071 mmol/l) than in the control subjects (0.810 +/- 0.057 mmol/l), and 146 (25%) diabetics had values below those of all control subjects except one. Plasma Mg correlated best with clinic blood glucose concentration (r = -0.32, p less than 0.001) and other significant associations were observed with glycosuria, age, sex, insulin therapy and biguanide therapy. Although its significance is unclear, hypomagnesaemia could conceivably predispose to ischaemic heart disease in diabetes.
Article
The serum magnesium concentration was measured in 71 insulin-treated diabetic outpatients who had had the disease for 10 to 20 years. The patients were divided into two subgroups according to the severity of their retinopathy. As a whole the patients exhibited a definite hypomagnesemia (P less than 0.001) that was most pronounced in the subgroup having the severest degree of retinopathy (P less than 0.01). The subgroups were comparable regarding known risk factors implicated in diabetic retinopathy. Thus, hypomagnesemia appears to be an additional risk factor in the development and progress of this complication.
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Intravenous infusion of adrenaline (40 microgram Kg-1 h-1 for 5 hrs) causes hypomagnesemia in ewes. Hypomagnesemia is increased by phentolamine and inhibited by propranolol. Thyroidectomy, with thyroxine supplementation, does not inhibit the hypomagnesemia caused by adrenaline and phentolamine. Sodium nicotinate (15 mg Kg-1 h-1 for 5 hrs) inhibits the increase in non-esterified fatty acids and hypomagnesemia resulting from infusion of adrenaline and phentolamine. Sodium nicotinate inhibits the increase in non-esterified fatty acids and hypomagnesemia resulting from theophylline infusion (20 mg Kg-1 h-1 for 90 min). It is concluded that an increase in the level of intra-cellular cyclic AMP due to beta adrenergic stimulation by adrenaline or to inhibition of phosphodiesterases by theophylline, results in hypomagnesemia which seems to be correlated with stimulation of lipolysis.
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We demonstrated similar plasma concentrations and urinary losses but lower erythrocyte magnesium concentrations (2.18 +/- 0.04 vs 1.86 +/- 0.03 mmol/L, P less than 0.01) in twelve aged (77.8 +/- 2.1 y) vs 25 young (36.1 +/- 0.4 y), nonobese subjects. Subsequently, aged subjects were enrolled in a double-blind, randomized, crossover study in which placebo (for 4 wk) and chronic magnesium administration (CMA) (4.5 g/d for 4 wk) were provided. At the end of each treatment period an intravenous glucose tolerance test (0.33 g/kg body wt) and a euglycemic glucose clamp with simultaneous [D-3H]glucose infusion and indirect calorimetry were performed. CMA vs placebo significantly increased erythrocyte magnesium concentration and improved insulin response and action. Net increase in erythrocyte magnesium significantly and positively correlated with the decrease in erythrocyte membrane microviscosity and with the net increase in both insulin secretion and action. In aged patients, correction of a low erythrocyte magnesium concentration may allow an improvement of glucose handling.
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Elevated fasting insulin is an independent risk factor for hyperlipidemia, hypertension, and cardiovascular disease, but determinants of insulin other than age and body mass remain poorly described. Potentially modifiable factors associated with insulin were identified by correlating anthropometric, dietary and physical activity data in the CARDIA cohort of 2643 black and 2472 white men and women aged 18-30 years. Insulin was positively correlated with serum glucose, body mass index (BMI), skinfold thickness, waist/hip ratio and sucrose intake, and negatively correlated with heavy physical activity score, treadmill exercise duration, and magnesium intake (each p less than 0.01). After adjustment for other covariates, the positive association of insulin with waist/hip ratio, skinfold thickness, and sucrose intake remained in the group as a whole, as did the negative associations with magnesium and treadmill duration. These relationships provide insight into potentially modifiable factors affecting insulin levels, and should be considered in interpreting associations between insulin levels and cardiovascular disease.
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To investigate the cellular basis linking hypertension, non-insulin-dependent diabetes mellitus (NIDDM), and obesity, we used 31P and 19F nuclear magnetic resonance spectroscopy to measure intracellular pH (pHi), free magnesium (Mgi), and cytosolic free calcium (Cai) in erythrocytes of obese and NIDDM subjects with and without hypertension. Compared with normotensive, nondiabetic controls (Cai, 25.2 +/- 1.4 nM; Mgi, 232 +/- 8 microM), Cai was elevated in both normotensive (36.8 +/- 2.7 nM, sig = 0.005) and hypertensive (43.4 +/- 2.9 nM, sig = 0.001) NIDDM subjects, and Mgi was concomitantly suppressed (normotensive: 206 +/- 11 microM, sig = 0.05; hypertensive: 196 +/- 8 microM, sig = 0.001). Similar but less striking changes were noted in obese subjects. Values of pHi were significantly lower (sig = 0.05) in all hypertensive groups compared with their normotensive controls. Continuous relations were observed for all subjects between Cai and diastolic blood pressure (r = 0.649, p less than 0.001) and body mass index (r = 0.565, p less than 0.001), between Mgi and diastolic blood pressure (r = -0.563, p less than 0.001) and fasting blood glucose (r = -0.580, p less than 0.001), and in diabetics, between pHi and diastolic blood pressure (r = -0.680, p less than 0.001). Thus, the constellation of elevated Cai and suppressed Mgi and pHi levels is characteristic of the hypertensive state. These abnormalities of cellular ion handling in whole or in part common to hypertension, diabetes, and obesity may contribute to the pathophysiology of these syndromes and may help to explain their frequent clinical coexistence.
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Metabolic and renal clearance techniques were used to examine kidney function in conscious and anesthetised streptozotocin diabetic rats. All diabetics showed an enhanced calcium and magnesium excretion compared to controls. However, the renal handling of these ions in relation to other electrolytes varied with different experiments. In non-infused conscious rats, the excretion of all ions was higher in diabetics, but the increased output of Ca2+ and Mg2+ was far greater than that of other electrolytes. In infused anesthetised diabetics only the outputs of Ca2+ and Mg2+ were significantly raised. This resulted from a significant reduction in the tubular reabsorption of both ions (% Ca2+ reabsorption: Controls 97.0 +/- 0.5; Diabetics 86.1 +/- 2.1; p less than 0.001). Insulin treatment reversed these changes. Major differences therefore exist in the renal handling of Ca2+ and Mg2+ in control and diabetic kidneys. Such differences do not simply parallel changes in the handling of other ions, and thus represent specific Ca2+ and Mg2+ lesions. Anesthetised infused diabetic rats also showed a reduced glomerular filtration rate and urine output compared to controls. Such differences may relate to an altered fluid balance in the two groups, different responses to surgery and anesthesia, or the degree of hyperglycemia in diabetic animals.
Article
To investigate the association of hypertension and insulin resistance, we utilized 31P-NMR spectroscopy to noninvasively assess intracellular free magnesium levels (Mgif) in erythrocytes of normotensive (n = 20) and essential hypertensive (n = 20) subjects given an oral 100 g glucose load. In hypertensive compared with normotensive subjects, fasting glucose and insulin levels were similar, but the integrated insulinemic responses to glucose were 45% greater (312 +/- 13.4 v 215 +/- 7.5 microU/mL, P less than .001). In hypertension, Mgif levels were significantly reduced (183 +/- 9 v 251 +/- 9 mumol/L, P less than .001), and for all subjects were closely and inversely related to systolic (r = -0.77, P less than .001) and diastolic (r = -0.81, P less than .001) blood pressures, and to the integrated insulin response (r = -0.72, P less than .001). Furthermore, while insulin responses were also related to the underlying systolic (r = 0.69, P less than .001) and diastolic (r = .73, P less than .001) pressures, these relations were no longer significant when adjusted for Mgif levels. We hypothesize that hypertension and peripheral insulin resistance may be different clinical expressions of a common abnormal intracellular ionic environment, characterized at least in part by suppressed levels of intracellular free magnesium.
Article
† Magnesium (Mg++) is a ubiquitous element in nature, playing a role in photosynthesis and many metabolic functions in humans. All enzymatic reactions that involve adenosine triphosphate have an absolute requirement for Mg++. Levels of Mg++ are controlled by the kidneys and gastrointestinal tract and appear closely linked to calcium, potassium, and sodium metabolism. The clinical manifestations and causes of abnormal Mg++ status are protean. Testing for altered Mg++ homeostasis is problematic. Serum levels, which are those generally measured, reflect only a small part of the total body content of Mg++. The intracellular content can be low, despite normal serum levels in a person with clinical Mg++ deficiency. Future directions in research related to intracellular content of Mg++ are discussed. Treatment of altered Mg++ status depends on the clinical setting and may include the addition of a potassium/Mg++ —sparing drug to an existing diuretic regimen. Guidelines for therapy are given. (Arch Intern Med 1988;148:2415-2420)
Article
Serum magnesium was measured in 100 patients of type II diabetes mellitus (40 without retinopathy, 40 with non-proliferative and 20 with proliferative retinopathy) without malnutrition, hepatic or renal disease or albuminuria and in 100 age and sex matched controls. The serum magnesium levels were lower in diabetics than in controls (P less than 0.001), and the levels in diabetics with non-proliferative and proliferative retinopathy were significantly lower than in those without retinopathy (P less than 0.001). These data seem to point towards an association between hypomagnesemia and diabetic retinopathy.
Article
Hypomagnesemia and low erythrocyte magnesium content are both common findings in non-insulin-dependent diabetic subjects. Moreover, intracellular magnesium may play a crucial role in modulating B-cell response to glucose by interfering with potassium permeability. Eight elderly, moderately obese, non-insulin-dependent diabetic subjects were treated with either magnesium supplementation (3 g/day) to the diet or placebo. Both treatment schemes lasted 4-weeks and were separated by a 'wash-out' of 3 weeks. At the end of each treatment period, in glucose test (0.33 g/kg for 3 min) and an iv arginine (5 g) test were performed to determine the B-and A-cell responses. Dietary magnesium supplementation vs placebo produced a slight but significant decrease in basal plasma glucose (8.6 +/- 0.3 vs 8.0 +/- 0.1 mmol/l, p less than 0.05) and an increase in acute insulin response after iv glucose (3.7 +/- 2.3 vs - 14.7 +/- 0.9 pmol.l 1. (10 min)-1, p less than 0.01) and after iv arginine (151 +/- vs 81 +/- 15 pmol.l-1. (10 min)-1, p less than 0.01), respectively. Plasma glucagon levels were unaffected by chronic dietary magnesium supplementation as well under basal conditions as in response to arginine. Net increase in acute insulin response after iv glucose and after iv arginine was significantly correlated to the net increase in erythrocyte magnesium content after dietary magnesium supplementation. We conclude that magnesium administration may be a useful adjuvant to the classic hypoglycemic agents in the treatment of non-insulin-dependent diabetic subjects.
Article
Intra- and extracellular levels of magnesium and potassium were determined in 16 subjects with insulin-dependent type I diabetes mellitus (IDDM) and 30 healthy controls. Subjects with IDDM had lower levels of magnesium in muscle biopsies (p less than 0.001), plasma (p less than 0.001), and mononuclear cells (p less than 0.05), and higher urinary excretions of magnesium (p less than 0.01), and lower levels of potassium in muscle biopsies (p less than 0.001), and erythrocytes (p less than 0.05), as compared with those in controls. Magnesium hydroxide (500 mg/day) was administered orally to the diabetics. The levels of magnesium and potassium in muscle biopsies increased (p less than 0.001; p less than 0.001), while the plasma levels of magnesium and the urinary excretions of magnesium increased only temporarily, during 21 weeks of treatment. The requirements of insulin were reduced (p less than 0.001) during the course of the study, whereas the levels of glycosylated hemoglobin (HbA1c) and glucose were not changed. The findings indicate that administration of magnesium hydroxide is useful to treat muscular magnesium and potassium deficiency in diabetics.
Article
Magnesium (Mg++) is a ubiquitous element in nature, playing a role in photosynthesis and many metabolic functions in humans. All enzymatic reactions that involve adenosine triphosphate have an absolute requirement for Mg++. Levels of Mg++ are controlled by the kidneys and gastrointestinal tract and appear closely linked to calcium, potassium, and sodium metabolism. The clinical manifestations and causes of abnormal Mg++ status are protean. Testing for altered Mg++ homeostasis is problematic. Serum levels, which are those generally measured, reflect only a small part of the total body content of Mg++. The intracellular content can be low, despite normal serum levels in a person with clinical Mg++ deficiency. Future directions in research related to intracellular content of Mg++ are discussed. Treatment of altered Mg++ status depends on the clinical setting and may include the addition of a potassium/Mg++-sparing drug to an existing diuretic regimen. Guidelines for therapy are given.
Article
Plasma and erythrocyte magnesium levels were measured by atomic absorption spectrometry in 12 healthy subjects and 12 moderately obese patients with Type 2 (non-insulin-dependent) diabetes mellitus. Basal plasma and erythrocyte magnesium levels were significantly lower in diabetic patients than in control subjects. In vitro incubation in the presence of 100 mU/l insulin significantly increased magnesium erythrocyte levels in both control subjects (p less than 0.001) and patients with diabetes (p less than 0.001). However, even in the presence of 100 mU/l insulin, the erythrocyte magnesium content of patients with Type 2 diabetes was lower than that of control subjects. The in vitro dose-response curve of the effect of insulin on magnesium erythrocyte accumulation was shifted to the right when red cells of diabetic patients were used, with a highly significant reduction of the maximal effect. Such reduction of the maximal effect of insulin suggests that the impairment of insulin-induced erythrocyte magnesium accumulation observed in Type 2 diabetic patients results essentially from a post-receptor defect.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
The adult human body contains approximately 24 g (1 mol) of magnesium--about half in bone and half in soft tissues. Only about 0.3% of the total body magnesium is present in serum, yet the majority of analytical data obtained is from this body fluid. Assessing the magnesium status of an individual is difficult, there being at present no simple, rapid, and accurate test to determine intracellular magnesium, but determination of total and free magnesium in tissues and physiological tests provide some information. Changes in magnesium status have been linked to cardiac arrhythmias, coronary heart disease, hypertension, and premenstrual syndrome. A better understanding of magnesium transport and of factors controlling magnesium metabolism is needed to elucidate the role of magnesium in disease processes.
Article
Plasma and erythrocyte magnesium levels were measured by atomic absorption spectrophotometry in 10 healthy volunteers during an oral glucose tolerance test and during an euglycaemic hyperinsulinaemic glucose clamp. At min 180 and 210 of the oral glucose tolerance test, a significant decline in plasma magnesium levels (p less than 0.01 and p less than 0.05 respectively) and a significant increase in erythrocyte magnesium levels (p less than 0.01 and p less than 0.05 respectively) were observed. Similar changes were seen during the second hour of the glucose clamp, during which euglycaemia (4.1 +/- 0.4 mmol/l) was maintained despite hyperinsulinaemia (110-130 mU/l). During in vitro incubations, glucose (5 mmol/l) did not modify erythrocyte magnesium levels. In contrast, erythrocyte magnesium levels were significantly increased (p less than 0.01) by insulin (100 mU/l), an effect entirely abolished by ouabain (5 X 10(-4) mol/l). These results suggest that insulin induces a shift of magnesium from the plasma to the erythrocytes both in vivo and in vitro. These data may help to interprete the abnormalities in magnesium circulating levels frequently reported in diabetic patients.
Article
Magnesium is the fourth most abundant cation in the human body and the second most common cation in the intracellular fluid. The abundance and distribution of this divalent cation implies an essential role of magnesium in intracellular metabolism. Although no single homeostatic control has been demonstrated for magnesium, the cellular availability of this cation is closely regulated by the gastrointestinal tract, kidney and bone. The purpose of this review is to survey some of the events involved in renal magnesium handling. The excretory side of magnesium balance involves appropriate changes in renal magnesium handling. Present evidence suggests that the renal handling of magnesium is normally a filtration-reabsorption process. Experimental support for secretion remains unconvincing. Renal magnesium reabsorption has distinctive features when compared with that of sodium and calcium. The concentration of magnesium in the proximal tubule rises 1.5 times greater than the glomerular filtrate. Some 20-30% of the filtered magnesium is reabsorbed in the proximal tubule compared to the fractional absorption of sodium or calcium of 50-60%. Although the fractional reabsorption of magnesium is only half that of sodium, it changes in parallel with that of sodium in response to changes in extracellular fluid volume. The major portion of filtered magnesium (some 65%) is reabsorbed in the loop of Henle, mainly in the thick ascending limb. Recent evidence suggests that magnesium reabsorption in the ascending limb may be voltage-dependent and secondary to active sodium chloride reabsorption. Evidence also suggests an important competition between magnesium and calcium for transport at the basolateral surface of the ascending limb cell. The loop of Henle appears to be the major nephron site where magnesium reabsorption is controlled. The principal factors which alter magnesium reabsorption in the loop include parathyroid hormone, changes in plasma magnesium and calcium concentration and the loop diuretics. About 10% of the filtered magnesium is delivered into the distal nephron where only a small fraction of the filtered magnesium is reabsorbed and the transport capacity is readily exceeded with increased magnesium delivery. A number of drugs have been shown to alter magnesium handling; these include antibiotics such as gentamicin, antineoplastic agents such as cisplatin and immunological suppressive drugs such as cyclosporin. The cellular alterations of these diverse drugs leading to renal magnesium wasting are not well understood.
Article
Plasma ultrafiltrable (MgUF) and total magnesium concentrations were measured in 60 insulin dependent diabetics and compared with values in an age matched control group. Although the diabetic patients had lower plasma albumin concentrations (p less than 0.05), both ultrafiltrable and total magnesium concentrations were significantly decreased by 6.8% and 7.6%, respectively, compared with those of the controls (p less than 0.001). In the diabetic group MgUF varied inversely with fasting plasma glucose (r = -0.269, p less than 0.05). In 14 patients with significant hypomagnesaemia, fasting plasma glucose concentration was higher (p less than 0.01) and the diabetes was of shorter duration (p less than 0.05) than in 46 patients with an MgUF in the control range. The fasting urinary magnesium creatinine ratio was greater in the diabetic patients (p less than 0.05). Patients with retinopathy did not have lower plasma magnesium values than those without retinopathy.
Article
The magnesium content of mononuclear blood cells may provide a better assessment of intracellular magnesium or total body magnesium status than does measurement of magnesium in plasma or erythrocytes. We describe a method for determining this, and report results for 20 normal volunteers. The mononuclear cells are separated with a discontinuous Ficoll-Hypaque gradient, washed, centrifuged at 400 X g, and lysed by sonication in 10 mmol/L NaCl. The magnesium in the cell lysate, with 2.93 g of added lanthanum oxide per liter, is determined by atomic absorption spectrometry. The mean mononuclear cell magnesium content in our volunteers was 70.7 (SD 14.1) fg per cell and 9.29 (SD 1.85) mg/g of DNA. The CVs for the determinations of magnesium, DNA, and cell count were 3.0%, 5.0%, and 8.7%, respectively. There was a significant correlation (r = 0.67, p less than 0.001) between results by the two methods of expressing magnesium content of mononuclear cells. However, by either method there were no significant correlations among results for magnesium concentration of mononuclear cells, plasma, or erythrocytes.
Article
Muscle, erythrocyte, and bone magnesium was studied in patients with reduced, normal, and increased serum magnesium levels. Muscle magnesium content was shown to vary directly with muscle potassium levels and independently of other body magnesium stores. In contrast to the fact that serum magnesium did not consistently reflect muscle magnesium concentration there was a highly significant correlation between serum and bone magnesium levels. It would appear from these results that bone and extracellular fluid magnesium are the major magnesium pools in man increased during magnesium excess and decreased during magnesium depletion. Changes in muscle magnesium reflect changes in total body potassium and are not a valid indicator of total body magnesium.
Article
States of K and Mg deficiency, deprivation or depletion, are difficult to detect by determining serum concentrations, since both cations are concentrated intracellularly. The intestinal absorption of K is rather quick and complete; the uptake of Mg probably comprises two mechanisms and proceeds continuously, although incomplete. The resulting different pharmakokinetic behavior must be kept in mind when K and Mg are supplemented by the oral route. Favorable effects of oral K and Mg supplementation are reviewed, and the fact is stressed that the body cannot retain K, unless the Mg status is adequate. Therefore, K should be supplemented together with Mg. Drugs like amiloride not only spare K, but at the same time prevent renal losses of other important electrolytes, especially of chloride and Mg.
Article
Micropuncture studies were performed on 27 thyroparathyroidectomized dogs to determine the segmental reabsorption of magnesium before and after graded magnesium infusion. Overall kidney reabsorption, as determined by the difference between filtered magnesium and urinary excretion, initially increased with elevation of plasma magnesium up to 3.5 meq/liter. Further elevation of plasma magnesium resulted in the appearance in the urine of all additional increments in filtered magnesium. Thus, renal magnesium reabsorption followed a pattern characteristic of a maximal transport rate (Tm). Evaluation of the proximal tubule by micropuncture demonstrated that net reabsorption of magnesium rose proportional to the increase in filtered magnesium and accounted for a constant fractional reabsorption of 14%. In contrast, magnesium reabsorption in Henle's loop initially increased with low delivery rates but peaked and fell with high plasma magnesium concentrations. Little magnesium reabsorption was observed between the distal collection site and final urine. Accordingly, the overall urinary excretion pattern was a summation of the different effects occurring in the proximal tubule and Henle's loop. Thus, renal magnesium reabsorption is not characterized by a Tm process but is a composite of distinct transport properties of the proximal tubule and the loop of Henle.
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