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Abstract

Objectives: Recent studies have demonstrated that minerals play a role in glucose metabolism disorders in humans. Magnesium, in particular, is an extensively studied mineral that has been shown to function in the management of hyperglycemia, hyperinsulinemia, and insulin resistance (IR) action. The aim of this study was to investigate the effect of magnesium supplementation on IR in humans via systematic review of the available clinical trials. Methods: This review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) recommendations. A survey was conducted to select clinical trials related to the effects of this mineral in insulin sensitivity using the following databases: PubMed, SciVerse Scopus, ScienceDirect, and SciVerse Cochrane. Results: After the selection process, 12 articles were identified as eligible, representing different clinical conditions and being free of restriction with regard to sex, age, ethnicity, and differential dosing/shape of magnesium. The results of eight clinical trials showed that supplementation with magnesium influences serum fasting glucose concentrations, and five trials determined an effect on fasting insulin levels. The results of seven studies demonstrated that mineral supplementation reduced homeostasis model assessment for IR values. Conclusions: The data of this systematic review provide evidence as to the benefits of magnesium supplementation in reducing IR in patients with hypomagnesemia presenting IR. However, new intervention studies are needed to elucidate the role of the nutrient in protection against this metabolic disorder, as well as the standardization of the type, dose, and time of magnesium supplementation.

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... The inter-relationships between disrupted secretion and function of insulin and reproductive complications in PCOS may also explain the implications of decreased Mg status on hyperandrogenism and ovarian dysfunction; hyperinsulinemia and insulin resistance impair ovarian follicologenesis, stimulate ovarian steroidogenesis, and inhibit the hepatic production of sex hormone-binding globulin [54]; thereby, increasing the bio-availability of free androgens [54]. A decline in insulin resistance has been proposed in response to Mg supplementation in the general population with hypomagnesemia [55]. Recent evidence has also shown the benefits of Mg supplementation on metabolic phenotype in women with PCOS. ...
... In addition to metabolic homeostasis, Mg has antioxidant properties and can attenuate the detrimental effects of oxidative stress [55]. Magnesium deficiency of cells makes them more susceptible to oxidative damage through pre-defined mechanisms [57]. ...
... Magnesium deficiency of cells makes them more susceptible to oxidative damage through pre-defined mechanisms [57]. Oxidative stress, secondary to hypomagnesemia, has been associated with reduced activity of antioxidant enzymes, activation of inflammatory pathways, increased intracellular calcium concentration, and endothelial dysfunction [55]. Hypomagnesemia has been also associated with the increased activity of (NF-kB) signaling [58]; (NF-kB) is a ubiquitous transcription factor and a key regulator of inflammatory responses which triggers the production and release of pro-inflammatory cytokines through activation of calciumchannels [59]. ...
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Magnesium (Mg) is the second most frequent intracellular cation in humans with a critical role in insulin metabolism and glucoregulation. Women with polycystic ovary syndrome (PCOS) often present with insulin resistance and impaired glucoregulatory status; however, their Mg status remains unclear. Therefore, we aimed to conduct a systematic review and meta-analysis to evaluate serum Mg concentration in women with PCOS and compare it with that of controls without PCOS. Online databases of PubMed, Scopus, Cochrane Library, and ISI Web of Science were searched for studies evaluating the relationship between Mg concentrations and PCOS status until October 2019. Pooled weighted mean differences (WMDs) of serum Mg levels were calculated using random effects models. A total of eight studies (10 arms; n = 2026 women) were included. Pooled effect sizes, expressed as WMD and 95% CI, revealed decreased serum Mg concentrations in women with PCOS compared with controls (− 0.09 (− 0.17, − 0.02) mmol/L; P = 0.01). However, significant heterogeneity was detected across the studies (I 2 = 98.0%, P < 0.001). Despite the classification of studies based on baseline BMI classes, we did not detect the potential source of the observed heterogeneity. Subgroup analysis showed that overweight and obese women (BMI ≥ 25 kg/m2, 0.07 mmol/L (− 0.14, − 0.01); P = 0.02) with PCOS had lower magnesium concentrations than normal women (BMI < 25 kg/m2, − 0.11 (− 0.25, 0.04) mmol/L; P = 0.14) compared with the control group. Serum Mg concentrations appear to be declined in overweight or obese women with PCOS, which may warrant screening and management of Mg status in this clinical population. High-quality studies are needed to elucidate the relationship between Mg concentrations and the development of PCOS.
... [2,3] Hence, IR and type 2 diabetes in rodents and humans are associated with defects at the level of GLUT4 content in skeletal muscles and adipose tissue [2,3] that leads to enhancing the concentration of insulin in the circulatory system as a compensatory mechanism. [4,5] Following these conditions, IR occurs with downregulating INR and desensitizing postreceptor pathways. [6] IR is widely recognized as an important risk factor for cardiovascular disease, metabolic syndrome (MetS), obesity, cancer, and T2D. ...
... [6] IR is widely recognized as an important risk factor for cardiovascular disease, metabolic syndrome (MetS), obesity, cancer, and T2D. [5,7] Diabetes Mellitus DM is a common metabolic disorder that can change people's life due to high morbidity and mortality. This disease is associated with pancreatic dysfunction in insulin secretion or low insulin-directed fostering of glucose by target cells which cause hyperglycemia in the blood. ...
... [1] Mg 2+ involves in more than 300 enzymatic reactions and numerous physiological processes by acting as a cofactor for many enzymes such as energy metabolism, glucose transport across cell membrane, hepatic gluconeogenesis, pancreatic functions, insulin secretion, and action in pancreatic cells and target tissues through interaction with receptors of this hormone. [5,[15][16][17] On this basis, intracellular Mg 2+ balancing is vital for adequate carbohydrate metabolism. [10,18] Studies have indicated that daily Mg 2+ supplements may improve glycemic response among T2D patients [10] and also prevent MetS. ...
Article
Insulin resistance (IR) is a chronic pathological condition that is related to reduce the rates of glucose uptake, especially in the liver, muscle, and adipose tissue as target tissues. Metabolic syndrome and type 2 diabetes mellitus can occur following progression of the disease. The majority of prior research has applied that some cations such as magnesium (Mg2+) have important physiological role in insulin metabolism. Mg2+ is the fourth most abundant mineral in the human body that gets involved as a cofactor of various enzymes in several metabolic events, such as carbohydrate oxidation, and it has a fundamental role in glucose transporting mechanism of the cell membrane. This cation has numerous duties in the human body such as regulation of insulin secretion in pancreatic beta-cells and phosphorylation of the insulin receptors in target cells and also gets involved in other downstream signal kinases as intracellular cation. On this basis, intracellular Mg2+ balancing is vital for adequate carbohydrate metabolism. This paper summarizes the present knowledge about the therapeutic effects of Mg2+ in reducing IR in liver, muscle, and pancreases with different mechanisms. For this, the search was performed in Google Scholar, PubMed, Scopus, and Web of Science by insulin resistance, skeletal muscle, liver, pancreases, magnesium, Mg2+, and inflammation keywords.
... Magnesium is closely associated with type-2 diabetes and other metabolic diseases. This element plays an essential function in glucose metabolism, acting as a cofactor for many enzymes, as well as being part of the Mg 2 + -ATP complex [50]. Mg also affects the activity of insulin [51]. ...
... It is believed that magnesium deficiency can cause oxidative stress [19,45]. Hypomagnesaemia reduces the sensitivity of peripheral tissues to insulin by diminished autophosphorylation of tyrosine kinase, a component of the insulin β subunit of which magnesium is a cofactor [50]. Hypomagnesaemia may also be associated with decreased β-cell proliferation, thus affecting insulin production [51,52]. ...
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Polycystic ovary syndrome (PCOS) is a common disease in women of childbearing age. It is characterized by excessive androgen production, ovulation disorders, and developing metabolic syndrome. The aim of the study was to check whether selected minerals were related to the pathophysiological mechanisms of PCOS. The concentrations of minerals were determined using an inductively coupled atomic plasma-emission spectrometer (ICP-AES Jobin Yvon JY-24). Blood samples from PCOS and control women were collected, processed, and digested with a microwave system in women with PCOS with and without insulin resistance and in the control group. It was found: zinc (Zn)-10.14 ± 2.11, 9.89 ± 1.44 and 10.30 ± 1.67; nickel (Ni) 0.001 ± 0.0009, 0.001 ± 0.0006 and 0.002 ± 0.00001; iron (Fe) 868.0 ± 155.8, 835.3 ± 156.4 and 833.0 ± 94.6; manganese (Mn) 0.017 ± 0.006, 0.017 ± 0.008 and 0.020 ± 0.009; copper (Cu) 0.714 ± 0.129, 0.713 ± 0.114 and 0.761 ± 0.146; magnesium (Mg) 48.4 ± 8.3, 50.0 ± 8.4 and 45.3 ± 10.7; sodium (Na) 374.3 ± 84.3, 396.3 ± 66.6 and 367.9 ± 88.9; potassium (K) 2541.8 ± 330.9, 2409.6 ± 347.1 and 2336.9 ± 211.4 (µg/g). Some micronutrient deficiencies may have a negative effect on the lipid profile in PCOS patients (Ni, Na). Further studies are needed to better understand dependencies.
... In addition, magnesium is a cofactor of enzymatic pathways involved in the modulation of glucose transport across cell membranes. Hypomagnesemia is highly prevalent in patients with diabetes, and magnesium supplementation has been shown to help stabilize blood glucose levels in these patient populations [6][7][8]. Therefore, perioperative magnesium treatment may also help stabilize postoperative blood glucose levels in patients with diabetes. However, to our knowledge, there are currently no clinical studies investigating the effects of intraoperative magnesium administration on postoperative glucose control in surgical patients with diabetes. ...
... Furthermore, magnesium levels are frequently lower in patients with diabetes than in those without. Additionally, magnesium supplementation is known to improve insulin sensitivity and metabolic control in patients with diabetes [6,[22][23][24]. Therefore, according to the results of this study, intraoperative magnesium sulfate administration should have helped to increase blood magnesium concentrations, avoid hypomagnesemia, and potentially assist with glucose control in patients with diabetes. ...
Article
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Magnesium deficiency, which is known to be highly prevalent among patients with diabetes, has been associated with insulin resistance and poor glucose control. Here, we aimed to investigate the effects of intraoperative magnesium administration on postoperative glucose control in patients with diabetes. We retrospectively reviewed the medical records of patients with type 2 diabetes who had undergone total joint arthroplasty at a tertiary hospital, where intraoperative magnesium sulfate injections were frequently performed for postoperative analgesia. The patients were grouped based on whether treated with magnesium or not (magnesium vs. control groups). We investigated postoperative blood glucose levels and sliding scale insulin requirements. After propensity matching, 170 patients were allotted to each group. Both the mean glucose level and the incidence of a mean glucose level of >200 mg/dL were significantly lower in the magnesium group than in the control group (p = 0.040 and 0.013, respectively). There was also a lower insulin requirement in the magnesium group (p = 0.043). Multivariate logistic regression revealed that magnesium treatment was significantly related to a less frequent incidence of a mean blood glucose level of >200 mg/dL (p = 0.047). This study demonstrated that magnesium sulfate infusion was associated with an improved postoperative blood glucose profile in patients with diabetes.
... As listed in Table 1, other magnesium measuring methods, including the magnesium loading test, may improve identification of magnesium-deficient individuals. Health care providers should take the initiative to increase awareness of magnesium deficiency and encourage the general population to consume magnesium-containing foods to reduce disease burden [55][56][57]. ...
Article
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Magnesium is essential for maintaining normal cellular and organ function. In-adequate magnesium balance is associated with various disorders, such as skeletal deformities, cardiovascular diseases, and metabolic syndrome. Unfortunately, routinely measured serum magnesium levels do not always reflect total body magnesium status. Thus, normal blood magnesium levels eclipse the wide-spread magnesium deficiency. Other magnesium measuring methods, including the magnesium loading test, may provide more accurate reflections of total body magnesium status and thus improve identification of magnesium-deficient individuals, and prevent magnesium deficiency related complications.
... Reduced magnesium intake and augmented magnesium urinary loss cause magnesium deficiency in diabetics, which is very common (11,42,43). Magnesium could regulate insulin sensitivity via its involvement in the regulation of insulin signalling, the phosphorylation of insulin receptor kinase, the post-receptorial action of insulin, and insulin-mediated cellular glucose uptake, thereby regulating blood glucose (12,43).Dietary magnesium deficiency may cause insulin resistance, as shown by several studies both in humans and in experimental animals (44).The intake of magnesium has been shown to improve FPG levels and insulin sensitivity in hyperglycaemic subjects (45,46) and to improve insulin sensitivity in healthy subjects (47); these findings are consistent with our research results. However, new intervention studies are needed to elucidate the standardization of the type, dose, and time of magnesium supplementation, thus making robust guidelines for clinical practice. ...
Article
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Background: Hyperglycaemia and diabetes have become major public health problems worldwide. There is increasing evidence that minerals and the vitamin B group might play specific roles in hyperglycaemia and the pathogenesis and progression of diabetes or metabolic complications. Objectives: The main aim of this study is to investigate the effect of mineral and vitamin B group supplementation on the blood glucose levels of different populations. Design: This was a cross-sectional study. Data from the National Health and Nutrition Examination Survey (NHANES) 2007-2014 were used in this study. A total of 8,322 participants (4,169 men and 4,153 women) were included in the study. Quantile regression (QR) was performed to identify the influence of mineral and vitamin B group intake on the level of fasting plasma glucose (FPG) in individuals in different quantiles of FPG. Results: After adjusting for age, income, education, race, smoking, and alcohol consumption, FPG had a negative association with folic acid in individuals with normal or high FPG, with calcium in individuals with normal FPG, and with magnesium in males. FPG was negatively associated with folic acid and calcium in individuals with normal FPG, and magnesium in most of the quantiles for females. Discussion: Hyperglycaemia and diabetes are currently becoming popular research topics. However, little is known about how the whole continuum of blood glucose is associated with commonly researched nutrient supplementation in terms of hyperglycaemia and diabetes. Conclusions: The intake of calcium, folic acid and magnesium was negatively associated with blood glucose levels in individuals in different quantiles of FPG. Appropriate prevention and treatment strategies should be developed for people with different blood glucose levels.
... Mg directly influences glucose metabolism by acting as a cofactor for many enzymes involved in energy metabolism as well as being part of the Mg 2+ -ATP complex (21). Beyond the role as a cofactor for over 300 enzymes, Mg is essential for both aerobic and anaerobic energy production by glycolysis and oxidative phosphorylation via the Mg-ATP complex or directly as an enzyme activator (12,16). ...
Article
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Polycystic ovary syndrome (PCOS) affects ∼1 in 10 women worldwide. Hypomagnesemia may worsen insulin resistance (IR) due to the role magnesium (Mg) plays in glucose metabolism. This review explores the relation between serum Mg and IR among women with PCOS. A review of primary research focusing on both serum Mg and women with PCOS was conducted from 2011 to 2019. Studies reviewed included human subjects, written in the English language, and limited to community-dwelling women aged ≥18 y. A total of 7 articles were reviewed. The findings from 4 epidemiological analytic studies evaluating serum Mg status suggest there may be a relation between serum Mg concentrations and IR among women with PCOS. However, among the 3 experimental trials, Mg supplementation inconsistently impacted IR among women with PCOS. Women with PCOS are more likely to underconsume Mg-rich foods and have a greater likelihood of lower serum Mg concentrations. Although it remains unclear if dietary Mg and/or supplementation should be a nutritional strategy for all women with PCOS, current research indicates an association between adequate Mg status and improved IR. Further research evaluating dietary interventions and supplementation is warranted.
... mmol/L) was associated with increased risk of developing diabetes among Mexican adults aged 20-65 years [25]. Randomized clinical trials found that magnesium supplementation improves insulin sensitivity [26]. ...
Article
Aim: We aimed to examine the association between serum magnesium and diabetes and hypertension among Qatari adults. Methods: In the cross-sectional study, we used data from 9693 Qatari participants) aged 20 years and above attending the Qatar Biobank (QBB) Study. Blood samples were analyzed in a central lab. Habitual food consumption was assessed by a food frequency questionnaire. Reduced rank regression was used to construct magnesium related dietary pattern (MRDP) using serum magnesium as a response variable. Diabetes was defined by blood glucose, HbA1c or known diabetes. Prediabetes was defined as HbA1c between 5.7% and 6.4%. Subclinical magnesium deficiency was defined as serum magnesium <0.85 mmol/L. Results: The prevalence of diabetes, prediabetes and subclinical magnesium deficiency was 18.9%, 11.5% and 59.5%, respectively. Across the quartiles of serum magnesium from high to low, the prevalence ratios (PR 95%CI) for diabetes were 1.00, 1.35, 1.88, and 2.70 (95%CI 2.38-3.05), respectively (p for trend <0.001). The presence of hypertension significantly increased the probability of diabetes along a wide range of low serum magnesium. A low intake of MRDP was also positively associated with diabetes and high HbA1c. Conclusion: Subclinical magnesium deficiency is common in Qatar and associates with diabetes, prediabetes and hypertension in Qatari adults.
... Some lifestyle and dietary-related interventions have been linked with improvement of insulin sensitivity in insulin-resistant and/or metabolic syndrome and/or type 2 diabetic patients. These include exercise [22,23], healthy/Mediterranean diet (generally known to be rich in monounsaturated fatty acids) [24][25][26][27], hygienic/regulated sunlight exposure [28,29], probiotics [30][31][32], magnesium supplementation [33,34], vitamin D supplementation [35,36] and zinc supplementation [37][38][39][40][41]. Although, at present, there is still controversy (due to conflicting results from relevant clinical studies) regarding the insulin sensitivity-enhancing effect of omega (n)-3 polyunsaturated acids (PUFA), the potential beneficial effect on insulin resistance has been linked with its well-known anti-inflammatory and triglycerides-lowering properties [42]. Indeed, higher omega-3 index has been found to be associated with increased insulin sensitivity and more healthy metabolic profile in some overweight men [43]. ...
Article
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Background: Depression is the leading cause of disability worldwide and is known to be associated with insulin resistance (IR). Insulin resistance worsens the symptoms of depression and reduces the effectiveness of antidepressant medications in some depressed patients. Many studies have assessed the effect of adjunctive exercise, vitamin D supplementation, zinc supplementation, magnesium, probiotics, unsaturated fatty acids, and hygienic-dietary recommendations (sleep hygiene, healthy diet, physical activity, and sunlight exposure, combined or singly used), individually, on antidepressant treatment response. However, despite the reported insulin sensitivity-enhancing potential of these adjuncts, no systematic review has collectively analysed their antidepressant effect with regards to insulin sensitivity. Methods/design: In this systematic review, we will analyse the effect of the above-stated adjuncts on antidepressant treatment response (primary outcome) in comparison with treatment as usual with or without adjunctive placebo after identifying the relevant trials from a systematic literature search. Randomised controlled trials involving clinically depressed patients with diagnosis of major depressive, dysthymic or bipolar disorder will be considered. Changes in insulin sensitivity parameters, following treatment, will also be analysed as the secondary outcome. Effect estimates of the included trials will be combined using random-effects meta-analysis, while addressing risk of bias issues. Any significant heterogeneity between studies will be explored using sensitivity and subgroup analyses. Discussion: The findings of this review will contribute to the evidence base regarding the utility of non-pharmacological insulin-sensitising treatments in enhancing conventional antidepressant treatment response.
... A meta-analysis of 12 articles supported the beneficial effect of magnesium supplementation in reducing insulin resistance in patients with hypomagnesemia presenting insulin resistance [85]. A systematic analysis of 18 RCTs supported modest improvement of fasting blood glucose and HbA1c with oral magnesium supplementation [86]. ...
Article
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COVID-19 and metabolic syndrome, though seemingly different disorders, appear to share certain common pathogenic components, especially in the development of COVID-19-associated diabetes mellitus. The similarities include impairment in immunoendothelial, gastrointestinal, pancreatic, adipose and mitochondrial functions, with several critical micronutrients undergirding the intricate interactions among these dysfunctions. This discussion aims to highlight the parallels between COVID-19 and metabolic syndrome and to propose the possibility of SARS-CoV-2 being a prototype of an acquired etiological agent which can eventually lead to the development of classical metabolic syndrome. Based on the proposed model, the discussion will include the implication for early management of COVID-19 and metabolic syndrome.
... Magnesium Magnesium is a cofactor in metabolic pathways and insulin secretion. A systematic review (12 studies) described that magnesium deficiency was associated with hyperglycemia, hyperinsulinemia and insulin resistance, and an increase processed food diet will decrease the intake of magnesium-rich foods [115]. Subanalysis of these studies showed that magnesium supplementation had a beneficial effect on the serum fasting glucose concentrations and fasting insulin levels in patients with hypomagnesemia and insulin resistance. ...
Article
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Purpose of Review The current approach to diabetes in the elderly incorporates components from the comprehensive geriatric approach. The most updated guidelines from the American Diabetes Association reflect influence from the consensus made in 2012 with the American Geriatrics Society. Notably, the framework included the evaluation for geriatric syndromes (falls and urinary incontinence), functional and cognitive abilities. The goal for this review is to provide an updated summary of treatment strategies for community-dwelling older adults. We identified the need to expand our approach by addressing innovative approaches and scientific concepts from telemedicine, functional medicine, and geriatrics. Recent Findings Findings on cardiovascular protection with sodium-glucose co-transporter 2 inhibitors (SGLT-2i) and some glucagon-like peptide 1 receptor agonists (GLP-1RA) support their use for older patients with diabetes. However, careful consideration for agent selection must incorporate the presence of geriatric issues, such as geriatric syndromes, or functional and cognitive decline, as they could increase the risk and impact adverse reactions. Telemedicine interventions can improve communication and connection between older patients and their providers, and improve glycemic control. Functional medicine concepts can offer additional adjuvant strategies to support the therapeutic interventions and management of diabetes in the elderly. Summary A systematic review confirmed the efficacy and safety of metformin as first-line therapy of type 2 diabetes in the older adult, but multiple reports highlighted the risk for vitamin B12 deficiency. Randomized controlled trials showed the efficacy and safety of antihyperglycemic agents in the elderly, including some with longer duration and lesser risk for hypoglycemia. Randomized clinical trials showed cardiovascular protection with SGLT-2i (empagliflozin, canagliflozin) and GLP-1RA (liraglutide, semaglutide). The most current guidelines recommend addressing for geriatric syndromes, physical and cognitive function in the elderly, in order to individualize targets and therapeutic strategies. Clinicians managing diabetes in the elderly can play a major role for the early detection and evaluation of geriatric issues in their patients. Telemedicine interventions improve glycemic control, and certain functional medicine strategies could be adjuvant interventions to reduce inflammation and stress, but more studies focused on the elderly population are needed.
... Type 2 diabetes mellitus, previously referred to as noninsulin-dependent diabetes, or adultonset diabetes, encompasses individuals who have insulin resistance (IR) and usually have relative insulin deficiency (6). IR is a pathological situation characterized by impairment of insulin-mediated glucose transport to peripheral cells, which is due to the lack of physiological response of peripheral tissues to insulin action and leads to the metabolic and hemodynamic disturbances known as metabolic syndrome (7). Increasing attention has been given to the role of certain elements in the pathogenesis of diabetes mellitus, and recent studies have demonstrated the participation of minerals in glucose metabolism disorders in humans (8). ...
Article
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Objectives: Diabetes mellitus has been suggested to be the most common metabolic disorder associated with magnesium deficiency. This study aimed to investigate the effects and mechanisms of magnesium supplementation on insulin receptor activity in elderly type 2 diabetes using a rat model and to provide experimental evidence for insulin resistance improvement by magnesium supplementation. Materials and methods: Rat model of type 2 diabetes was developed using a high-fat diet along with low dose streptozotocin (STZ) treatment. Magnesium supplement was given orally by mixing with the high-fat diet. Serum insulin level, insulin sensitivity, and insulin receptor affinity were assessed using radioimmunoassay (RIA). Insulin receptor, insulin receptor substrate (IRS-2), and β-Arrestin-2 gene and protein expression levels were measured using immunohistochemistry and RT-PCR. Xanthine oxidase assay, thiobarbituric acid reactive substance assay (TCA method), colorimetric assay, and ELISA were used to determine the serum SOD, MDA, T-AOC, and ox-LDL levels, respectively. Results: Magnesium supplementation enhanced insulin sensitivity and decreased insulin resistance in diabetic rats mainly through increasing insulin receptor expression, affinity, and augmenting insulin receptor signaling. Magnesium supplementation also inhibited lipid peroxidation in diabetic rats and protected against pancreatic cell injury in diabetic rats. In addition, we found that β-arrestin-2 gene expression was suppressed in diabetes, which was possibly attributed to gene methylation modification, as β-arrestin 2 promotor was rich in methylation-regulating sites. Magnesium supplementation could affect β-arrestin-2 gene expression and methylation. Conclusion: Magnesium supplementation has a positive effect on insulin receptor activity and insulin sensitivity in type 2 diabetes.
... Mg is vital for activation of the insulin receptor β-subunit, and patients with type 2 diabetes are reported to have lower serum Mg concentrations compared to controls [13]. Additionally, Mg supplementation is considered to have a beneficial effect on insulin resistance [14]. ...
... Mg is vital for activation of the insulin receptor β-subunit, and patients with type 2 diabetes are reported to have lower serum Mg concentrations compared to controls [13]. Additionally, Mg supplementation is considered to have a beneficial effect on insulin resistance [14]. ...
Article
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Serum magnesium (Mg) is reported to be reduced in individuals with obesity, hypertension, and diabetes mellitus and has been suggested as a marker for metabolic syndrome. We have studied changes in serum Mg concentrations in a group of obese patients (n = 92) with and without diabetes mellitus after weight loss induced by dieting and bariatric surgery. At inclusion, 11% (10/92) of the population had severe Mg deficiency (< 0.75 mmol/L) and median serum Mg was lower in diabetic (n = 20) compared to non-diabetic (n = 72) patients (p = 0.002). A weight loss of 10 kg after 8 weeks of lifestyle interventions was accompanied by increased serum Mg of about 5% in both diabetic and non-diabetic patients. Serum Mg remained stable thereafter in the non-diabetic patients, while it continued to increase in the diabetic patients after bariatric surgery. Six months after bariatric surgery, there was no significant difference in serum Mg concentration between the groups (p = 0.08). The optimal range of circulating Mg concentration is not known, but as even small increments in serum Mg are reported to lower the risk of cardiovascular and ischemic heart disease, our results are interesting in a public health perspective.
... Research conducted by these authors was compared and verified in equivalence of search and selection of items. The search strategy was similar to that used by Morais et al. [20]. ...
Article
Background Many studies have investigated the influence of minerals on the control of changes in lipid metabolism in obese individuals. The objective of this study was to describe, in a systematic review, the clinical trial outcomes of zinc supplementation and lipid profiles of obese participants. Methods This review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) recommendations. A survey was conducted for selecting clinical trials related to the effects of zinc supplementation on lipid profiles in obese people, using the following databases: PubMed, SciVerse ScienceDirect and Cochrane. Results After the selection process, five articles were identified as eligible for this review and it was observed that the clinical trials included adults and children of both sexes, in three different countries, and with zinc supplementation doses ranging from 20 to 100 mg/day. None of the studies observed changes in High-Density Lipoprotein (HDL-c) with zinc supplementation. On the other hand, three studies observed a positive effect of zinc supplementation on triglycerides, and two found an effect on Low-Density Lipoprotein (LDL-c) and total cholesterol. Conclusion The results of this systematic review provide evidence on the benefits of zinc supplementation on lipid profiles in obese individuals. However, new intervention studies are needed to elucidate the function of the nutrient in protection against disorders related to lipid metabolism, as well as the standardization of the type, dose, and time of zinc supplementation.
... The finding that low serum magnesium is associated with several adverse CVD risk factors is supported by randomised control trials. Systematic reviews of magnesium supplementation trials provide evidence as to the benefits Serum magnesium and risk of incident heart failure in older men: The British Regional Heart… 879 of magnesium supplementation in reducing metabolic CVD risk factors including blood pressure and glucose as well as CRP levels [39][40][41]. Two recent trials have shown magnesium supplementation to improve vascular function [42,43]. ...
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To examine the association between serum magnesium and incident heart failure (HF) in older men and investigate potential pathways including cardiac function, inflammation and lung function. Prospective study of 3523 men aged 60–79 years with no prevalent HF or myocardial infarction followed up for a mean period of 15 years, during which 268 incident HF cases were ascertained. Serum magnesium was inversely associated with many CVD risk factors including prevalent atrial fibrillation, lung function (FEV1) and markers of inflammation (IL-6), endothelial dysfunction (vWF) and cardiac dysfunction [NT-proBNP and cardiac troponin T (cTnT)]. Serum magnesium was inversely related to risk of incident HF after adjustment for conventional CVD risk factors and incident MI. The adjusted hazard ratios (HRs) for HF in the 5 quintiles of magnesium groups were 1.00, 0.72 (0.50, 1.05), 0.85 (0.59, 1.26), 0.76 (0.52, 1.11) and 0.56 (0.36, 0.86) respectively [p (trend) = 0.04]. Further adjustment for atrial fibrillation, IL-6, vWF and FEV1 attenuated the association but risk remained significantly reduced in the top quintile (≥ 0.87 mmol/l) compared with the lowest quintile [HR 0.62 (0.40, 0.97)]. Adjustment for NT-proBNP and cTnT attenuated the association further [HR 0.70 (0.44, 1.10)]. The benefit of high serum magnesium on HF risk was most evident in men with ECG evidence of ischaemia [HR 0.29 (0.13, 0.68)]. The potential beneficial effect of high serum magnesium was partially explained by its favourable association with CVD risk factors. Further studies are needed to investigate whether serum magnesium supplementation in older adults may protect from the development of HF.
... Nevertheless, a recent systemic review evaluated the effect of magnesium supplementation on insulin resistance. Twelve studies were identified, and it was concluded that oral magnesium supplementation had beneficial effect on insulin resistance in patients with hypomagnesemia compared to patients with normal serum magnesium [89]. Moreover, oral magnesium supplementation may have positive effect on lipid profile in individuals with and without diabetes [90,91]. ...
Article
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Magnesium is the fourth most abundant cation in the body. It has several functions in the human body including its role as a cofactor for more than 300 enzymatic reactions. Several studies have shown that hypomagnesemia is a common electrolyte derangement in clinical setting especially in patients admitted to intensive care unit where it has been found to be associated with increase mortality and hospital stay. Hypomagnesemia can be caused by a wide range of inherited and acquired diseases. It can also be a side effect of several medications. Many studies have reported that reduced levels of magnesium are associated with a wide range of chronic diseases. Magnesium can play important therapeutic and preventive role in several conditions such as diabetes, osteoporosis, bronchial asthma, preeclampsia, migraine, and cardiovascular diseases. This review is aimed at comprehensively collating the current available published evidence and clinical correlates of magnesium disorders.
... • Improves insulin resistance 317 • Reduces incidence of hypertension and hyperlipidemia 318 • Increases function of vitamin D and its activation 319 dysfunction and inflammation, including increased TNF-α, IL-6, and IL-1 production in rats. [398][399][400] Studies show that magnesium plays a vital role in preventing bacterial, viral as well as fungal infections by enhancing immunity and by decreasing pro-inflammatory mediators. ...
Article
Over‐nutrition and its late consequences are a dominant theme in medicine today. In addition to the health hazards brought on by over‐nutrition, the medical community has recently accumulated a roster of health benefits with obesity, grouped under “obesity paradox”. Throughout the world and throughout history until the 20th century, under‐nutrition was a dominant evolutionary force. Under‐nutrition brings with it a mix of benefits and detriments that are opposite to and continuous with those of over‐nutrition. This continuum yields J‐shaped or U‐shaped curves relating body mass index to mortality. The overweight have an elevated risk of dying in middle age of degenerative diseases while the underweight are at increased risk of premature death from infectious conditions. Micronutrient deficiencies, major concerns of nutritional science in the 20th century, are being neglected. This “hidden hunger” is now surprisingly prevalent in all weight groups, even among the overweight. Because micronutrient replacement is safe, inexpensive, and predictably effective, it is now an exceptionally attractive target for therapy across the spectrum of weight and age. Nutrition‐related conditions worthy of special attention from caregivers include excess vitamin A, excess vitamin D and deficiency of magnesium.
... These effects are generally attributed to improved insulin-elicited glucose uptake because magnesium is essential for optimal coupling and signaling through the insulin receptors. A recent review on magnesium and insulin resistance confirmed that magnesium supplementation assists in the control of insulin resistance in patients with hypomagenesemia [162]. Regarding dyslipidemia, magnesium has been shown to reduce serum triglycerides, apolipoprotein B, LDL cholesterol, total cholesterol, and to increase HDL cholesterol concentrations in patients with ischemic heart disease [163][164][165]. ...
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Postprandial plasma glucose and triglyceride concentrations are predictive of relative cardiovascular disease (CVD) risk, and the pathogenesis of both insulin resistance and atherosclerosis has been attributed to acute states of hyperglycemia and hypertriglyceridemia. Postprandial lipemia and hyperglycemia suppress vascular reactivity and induce endothelial dysfunction. Epidemiological studies suggest that chronically-high consumption of milk and milk products is associated with a reduced risk of type 2 diabetes, metabolic syndrome, and CVD. The addition of dairy products to meals high in carbohydrates and fat may lessen these risks through reductions in postprandial glucose and triglyceride responses. Purported mechanisms include dairy proteins and bioactive compounds, which may explain the inverse relationship between dairy consumption and cardiometabolic diseases. The current review evaluates the available literature describing the relationships between metabolic dysfunction, postprandial metabolism, and vascular dysfunction and discusses the potential role of milk and dairy products in attenuating these impairments.
... 34 Another study revealed that supplementation with trace minerals like Mg has some positive effect on symptomatic relief of polycystic disease. 35 Delayed menstruation is a sign of altered ovarian activity. 36,37 Traditionally, PCOS is one of the causative factors for type 2 diabetes. ...
... Magnesium (Mg) plays an important role in insulin and glucose homeostasis [7,8]. Both animal and human studies indicate that insulin sensitivity is improved by Mg administration or supplementation [9,10]. In addition, oxidative damage and/or chronic inflammation are involved in the pathogenesis of NAFLD [5]. ...
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PurposeHuman data are limited linking magnesium (Mg) intake to the risk of non-alcoholic fatty liver disease (NAFLD). We aimed to examine the association between Mg intake and the risk of NAFLD among young adults in the US with a 25-year follow-up. Methods This study included 2685 participants from the Coronary Artery Risk Development in Young Adult (CARDIA) study. Diet and dietary supplements were assessed at baseline (1985–1986) and exam years 7 and 20 using an interview-based dietary history. NAFLD, defined as liver attenuation ≤ 51 Hounsfield Units excluding secondary causes of liver fat accumulation, was identified by non-contrast-computed tomography scanning at exam year 25. Multivariable-adjusted logistic regression model was used to examine the associations between cumulative average total intake of Mg (dietary plus supplemental) and NAFLD odds.ResultsA total of 629 NAFLD cases were documented. After adjustment for potential confounders, an inverse association between total Mg intake and NAFLD odds was observed. Compared to participants in the lowest quintile of total Mg intake, the odds of NAFLD was 55% lower among individuals in the highest quintile [multivariable-adjusted odds ratio (OR) = 0.45, 95% confidence interval (CI) (0.23, 0.85), p for trend = 0.03]. Consistently, whole-grain consumption, a major dietary source of Mg, was inversely associated with NAFLD odds (p for trend = 0.02).Conclusions This study suggests that higher cumulative intake of Mg throughout adulthood is associated with lower odds of NAFLD in midlife. Future studies are needed to establish a possible causal relationship.
... Similarly, FGF19 treatment resulted in the reduced lipid accumulation and increased survivability in the liver organoids from patients with Wolman disease compared with untreated liver organoids 101 . In contrast, magnesium treatment, which is a highly controversial clinical therapy for treating T2DM and liver metabolic discorders 144 , has proven ineffective in this 3D system 101 . Moreover, sorafenib was shown to reduce steatosis-induced fibrogenesis in a human 3D co-culture model of NAFLD 145 . ...
Article
Metabolic diseases, including obesity, diabetes mellitus and cardiovascular disease, are a major threat to health in the modern world, but efforts to understand the underlying mechanisms and develop rational treatments are limited by the lack of appropriate human model systems. Notably, advances in stem cell and organoid technology allow the generation of cellular models that replicate the histological, molecular and physiological properties of human organs. Combined with marked improvements in gene editing tools, human stem cells and organoids provide unprecedented systems for studying mechanisms of metabolic diseases. Here, we review progress made over the past decade in the generation and use of stem cell-derived metabolic cell types and organoids in metabolic disease research, especially obesity and liver diseases. In particular, we discuss the limitations of animal models and the advantages of stem cells and organoids, including their application to metabolic diseases. We also discuss mechanisms of drug action, understanding the efficacy and toxicity of existing therapies, screening for new treatments and pursuing personalized therapies. We highlight the potential of combining stem cell-derived organoids with gene editing and functional genomics to revolutionize the approach to finding treatments for metabolic diseases.
... Thus, Mg 2 + deficiency in the development and persistence of T2DM. Although Mg 2 + deficiency has been widely studied in T2DM [4][5][6][7][8][9] , the molecular clinical and molecular mechanisms are poorly reviewed. This review ex- Fig. 1. ...
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Type 2 diabetes mellitus (T2DM) is one of the most common chronic diseases, affecting hundreds of millions of people worldwide. Environmental factors influence the progressive development of diabetes, the main ones being obesity, hypertension, dyslipidemia, and genetic factors. In addition to the above factors, magnesium (Mg 2 +) deficiency has been linked to an increased risk of developing T2DM in the general population. The homeostasis of this ion is highly regulated by absorption in the intestine, storage in bone, and renal excretion. However, Mg 2+ content in the diet, the primary source for the body, and the content of Mg 2+ in fruits and vegetables have progressively decreased, so Western-style diets currently contain between 30 and 50% of the minimum recommended magnesium. Since Mg 2 + deficiency has been associated with higher fasting glucose concentrations, glycosylated hemoglobin, or higher insulin resistance rates in patients with T2DM, Mg 2 + supplementation may be a potential therapy to treat T2DM. Although Mg 2 + deficiency has been widely studied in T2DM, the molecular clinical and molecular mechanisms are poorly reviewed. This review examines the recent literature linking T2DM to altered Mg 2 + homeostasis, from experimental observations and clinical trials to the molecular mechanisms by which Mg 2 + influences glucose homeostasis in T2DM.
... It is worth mentioning that dietary factors such as high-fat diets, sources of phytates and oxalates, and alcohol intake can hinder magnesium absorption. In contrast, high-protein diets in fluoride and lactose favor magnesium absorption [6,7]. ...
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Several studies have demonstrated the participation of various minerals in mechanisms involving insulin. Magnesium, in particular, plays an important role in the secretion and action of this hormone. Therefore, this review aimed to examine the latest insights into the biochemical and molecular aspects of the participation of magnesium in insulin sensitivity. Magnesium plays a vital role in the activity of intracellular proteins involved in insulin secretion in β-pancreatic cells, such as glucokinase, ATPase, and protein kinase C. In addition, evidence suggests that this mineral participates directly in insulin sensitivity and signaling in peripheral tissues, acting in the phosphorylation of the receptor tyrosine kinase and the insulin receptor substrates 1, insulin receptor substrates 2, phosphatidylinositol 3-kinase, and protein kinase B, and indirectly by reducing oxidative stress and chronic low-grade inflammation, which also lead to insulin resistance. Thus, magnesium deficiency is associated with glucose intolerance, while magnesium supplementation stimulates insulin secretion in pancreatic cells and improves insulin sensitivity in peripheral tissues. However, studies must consider assess short- and long-term nutritional status of mineral before performing intervention, the relevance of the balance of other nutrients that influence hormone secretion and sensibility, and health status of the assessed population.
... Analyzing the hormonal profile of women with PCOS, a negative correlation between Mg and estradiol was found in nonobese women. Magnesium supports the detoxification of estrogens by directly increasing the activity of glucuronyl transferase [56]. Ovarian hormones affect magnesium levels by causing magnesium levels to drop at certain times in the menstrual cycle and by changing the calcium-magnesium ratio. ...
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Introduction: Polycystic ovary syndrome (PCOS) is one of the most commonly recognized endocrinopathies in women. The literature lacks clear data that allow any meaningful conclusions to be drawn about the influence of trace elements in erythrocytes on the biochemical parameters of PCOS. Materials and methods: This study was conducted among 47 women meeting the Rotterdam criteria for the diagnosis of polycystic ovary syndrome. The research groups included women with PCOS with different BMI values (body mass index): obese women with PCOS (PCOS with BMI ≥ 30, mean BMI index 35.4 ± 4.4 kg/m2), nonobese PCOS women (PCOS with BMI < 30, mean BMI index 25.2 ± 2.8 kg/m2), and healthy control group (CG) with a mean BMI of 23.57 ± 0.9 kg/m2. The contents of trace elements in erythrocytes were determined with an inductively coupled plasma atomic emission spectrometer. Results: The only trace element showing significant differences in concentration between the studied groups was nickel (Ni). The level of nickel in the obese women with PCOS (BMI ≥ 30) was significantly higher than in nonobese women (BMI < 30). The content of other trace elements in erythrocytes did not differ significantly between the studied groups. Several significant correlations were found within each of the studied PCOS groups: in the group of obese women, the content of zinc (Zn) in erythrocytes positively correlated with prolactin, the content of magnesium (Mg) positively correlated with testosterone, and the content of manganese (Mn) negatively correlated with thyroid-stimulating hormone. In the group of nonobese women, Zn content correlated positively with testosterone, Ni with luteinizing hormone (LH) and estradiol, and Mg negatively correlated with estradiol. Conclusions: The relationship between the level of trace elements and the level of hormones suggests that, in obese women with PCOS, nickel may play a role in inhibiting the processes of folliculogenesis and ovulation. Research on trace elements and their relationship to ovulatory cycles and the development of PCOS may contribute to reducing the consequences of PCOS and, therefore, should be extended.
... In many studies, researchers have linked high magnesium diets with diabetes. Jennifer Beatriz et al., [32] reviewed the effect of magnesium supplementation on insulin resistance in humans suggests that taking magnesium supplements can also improve insulin sensitivity in people with low magnesium levels. This study observed that P.semisulcatus has the highest value of magnesium content and leading by P.indicus. ...
Article
The present study was carried out to evaluate the proximate and mineral composition of wild catch available marine Penaeus species, for their nutritive importance. The proximate composition was determined by BIS method and the minerals such as Calcium, Sodium and Potassium were estimated by AAS method. All the experiments were replicated. The results showed significant difference (p < 0.05) in all the parameters, such as moisture content ranges from (3.83 to 19.31%), highest crude protein was observed in Metapenaeus monoceros. The crude fat content varies from (0.74 to 3.54 %) were P.monodon showed the highest lipid content (3.54 %). The average total ash content was observed in Penaeus species ranges from (4.07 to 8.77 %), two species, P. indicus and P. semisulcatus showed highest values of (8.36 and 8.77%), crude fiber content was observed as 1.85% in P.indicus and 1.93% in Metapenaeus monoceros. Among the species P. semisulcatus shows Calcium (1664 mg/100g) followed by sodium (919 mg/100g) and potassium (699 mg/100g). Most of the Penaeus species are rich sources of protein and calcium and vital trace minerals (Fe, Zn, and Cu). Among the study, Metapenaeus monoceros recorded with high amount of protein. P. semisulcatus and P.indicus were recorded for macro minerals, whereas the concentration of micro minerals are in permissible limits the range of FAO. Thus from the results the study revealed, the analyzed shrimp species were good sources of nutrients and minerals which could provide health benefits on dietary supplements.
... Mg supplementation significantly improved HbA1c, insulin levels, and HOMA-IR (homeostasic model assessment of insulin resistance) in patients with type 2 diabetes [35]. In the review of 12 randomized controlled trials (RCTs), Morais et al. showed that the positive effect of Mg supplementation on several parameters, such as HbA1c, fasting insulin and glucose, and HOMA-IR, was more pronounced in hypomagnesemic patients [36]. Only a few studies assessed glycemic control in nondiabetic patients with normal Mg levels, with no clear consensus in results [37][38][39]. ...
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Magnesium (Mg) supplementation was shown to improve metabolic syndrome (MetS) parameters in hypomagnesemic patients. The current study evaluated the role of Mg in normomagnesemic individuals with MetS. Patients were randomly assigned to 400 mg Mg as Mg citrate or placebo daily for 12 weeks. Blood pressure (BP), HbA1c, plasma concentrations of glucose, Mg and Ca, blood-ionized Mg, serum concentrations of cholesterol, triglycerides, vitamin D, creatinine, interleukin-6, and C-reactive protein were measured at baseline and after 12 weeks. Data were obtained from n = 13 in the Mg supplemented and n = 11 in the placebo group. Mg supplementation led to a significant increase in plasma Mg concentration (0.78 ± 0.07 mmol/L to 0.83 ± 0.07 mmol/L) and a decrease in systolic and diastolic BP (baseline: 145 ± 10/85 ± 3 mmHg; 12 weeks: 121 ± 5/79 ± 3 mmHg). HbA1c decreased significantly in the Mg group (6.43 ± 0.64% to 6.15 ± 0.55%), and the difference in change between placebo and Mg group was significant. Serum vitamin D levels significantly increased only in the Mg group. In normomagnesemic individuals with MetS, oral Mg citrate supplementation reduced HbA1c and BP.
... It is now established that diabetes can induce hypomagnesemia and that hypomagnesemia can in turn induce or deteriorate this disease [7]. In addition, several studies have shown that magnesium supplementation has a beneficial effect on insulin action and glucose metabolism [12,13]. To our best knowledge, this is the first reported study in the African continent to estimate the prevalence of magnesium deficiency in a population of Tunisian outpatients with T2DM and to evaluate the association between magnesium status and intake, glycemic control and diabetes microvascular and macrovascular complications. ...
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(1) Background: Magnesium deficiency is usually associated with type 2 diabetes mellitus (T2DM). Individuals living with T2DM with hypomagnesemia show a more rapid disease progression and have an increased risk for diabetes complications. (2) Methods: This is a cross-sectional and descriptive study in the National Institute of Nutrition and Food Technology of Tunis in Tunisia, including all adult outpatients (≥18 years old) with a diagnosis of T2DM from 1 September 2018 to 31 August 2019. The aim of this study was to evaluate the prevalence of plasmatic magnesium deficiency in a Tunisian population of T2DM and to study the relationship between magnesium status and intake, glycemic control and long-term diabetes-related complications. (3) Results: Among the 101 T2DM outpatients, 13 (12.9%) presented with a plasmatic magnesium deficiency. The mean age was 56 ± 7.9 years with a female predominance (62%, n = 63). The mean of the plasmatic magnesium level was 0.79 ± 0.11 mmol/L (0.5–1.1), and the mean of 24 h urinary magnesium excretion was 87.8 ± 53.8 mg/24 h [4.8–486.2]. HbA1c was significantly higher in the plasmatic magnesium deficiency group than the normal magnesium status group (10% ± 1.3 vs. 8.3% ± 1.9; p = 0.04), with a significant difference in participants with a poor glycemic control (HbA1c > 7%) (100%, n = 13/13 vs. 53%, n = 47/88; p = 0.001). A weak negative relationship was also found between plasmatic magnesium and HbA1c (r = −0.2, p = 0.03). Peripheral artery disease was more commonly described in individuals with low plasmatic magnesium levels than in individuals with normal levels (39%, n = 5 vs. 0%, n = 0; p < 0.001). The mean plasmatic magnesium level in participants without diabetic nephropathy and also peripheral artery disease was significantly higher compared to individuals with each long-term diabetes-related complication (0.8 mmol/L ± 0.1 vs. 0.71 mmol/L ± 0.07; p = 0.006) and (0.8 mmol/L ± 0.1 vs. 0.6 mmol/L ± 0.08; p < 0.001), respectively. (4) Conclusions: Hypomagnesemia was identified in individuals with T2DM, causing poor glycemic control and contributing to the development and progression of diabetes-related microvascular and macrovascular complications.
... Similarly, in the research of Jastrzębska-Mierzyńska et al. [13] and Hosseini-Esfahani et al. [14], deficiencies in magnesium intake were observed in 90% to 100% of respondents. Magnesium deficiencies may cause neuromuscular and cardiovascular disorders, insulin resistance, and impaired secretion of this hormone [19,35]. In our own research, supplementation with this element also turned out to be insufficient, especially in women whose dietary magnesium intake was below 200 mg/day and the magnesium supplement intake below 100 mg in a daily dose. ...
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Purpose Most of the research indicated that daily dietary intake of minerals in SG patients was lower than the current recommendations. The aim of the study was to assess the need and safety of a mineral supplementation practice in adults with obesity, at 3, 6, and 9 months post bariatric surgery—sleeve gastrectomy (SG). Methods The study included 24 women and 6 men. Based on a 4-day food record questionnaire, mineral and calorie intake was calculated at 3, 6, and 9 months after bariatric surgery (SG). Furthermore, an interview on supplement intake was also conducted. Results It was found that in both men and women, there was a dietary intake deficiency of calcium (97% of respondents), potassium (97%), magnesium (83%), sodium (60%), and zinc (53%). In women, the deficiencies also included iron (50%) and copper (29%). Only 72% of the patients took dietary supplements. The applied supplementation did not adjust for the required intake of calcium in all of the patients, as well as the intake of magnesium in the male patients. Low intake of sodium and potassium were not supplemented and should be corrected by diet modification. The patients did not require supplementation of phosphorus or manganese, while male patients did not require iron or copper supplementation. The dietary and/or supplemental intake of minerals did not exceed the tolerable upper intake level (UL). Conclusion The results of the study confirm the need to implement personalized mineral supplementation for bariatric surgery patients. Graphical abstract
... Rice bran is also rich in potassium, and diets low in potassium have been associated with an increased risk of diabetes in epidemiological studies [46]. Magnesium, zinc, and calcium supplementation has been shown to improve glycemic control, and cellular pathways involving these minerals have been linked to glucose and insulin homeostasis [47][48][49][50]. ...
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The regular consumption of soy products is associated with inverse incidence of type 2 diabetes, and there has been an increasing interest in the glycemia reducing potential of rice bran and its components. In this study, we investigated whether consuming soymilk with the addition of rice bran (fiber) can reduce the glycemic response of a carbohydrate meal. Seventeen healthy Asian men (BMI: 18.5-29 kg/m²) participated in this randomized crossover trial. On four occasions, they consumed white bread (two times) and white bread with two different soymilks differing in protein and rice bran content. Blood samples were taken to measure glucose and insulin response over a period of 3 hours. Taking the glycemic index (GI) value of white bread as a reference value of 100, the GI of white bread when co-ingested with rice bran soymilk (RBS) was 83.1 (±7.7) and sugar-free soymilk (SFS) was 77.5 (±10.1), both were lower than white bread (p< 0.05). The insulin response of both soymilk treatments was similar to white bread (p> 0.05). The glucose/insulin ratio of RBS and SFS were respectively 43.1 (± 6.1) and 60.0 (± 17.0) and were lower (p< 0.05) than white bread (123.5 ± 21.1) during the first 30 min. In conclusion, co-ingestion of low amounts of soy protein with a carbohydrate meal stimulated early-phase insulin secretion and thereby increased blood glucose clearance effectiveness. Furthermore, rice bran-fortified soymilk reduced the glycemic response similarly to soymilk with a greater dose of soy protein. Rice bran and its components offer therapeutic potential for glycemic and insulinemic control.
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Human organoid systems recapitulate in vivo organ architecture yet fail to capture complex pathologies such as inflammation and fibrosis. Here, using 11 different healthy and diseased pluripotent stem cell lines, we developed a reproducible method to derive multi-cellular human liver organoids composed of hepatocyte-, stellate-, and Kupffer-like cells that exhibit transcriptomic resemblance to in vivo-derived tissues. Under free fatty acid treatment, organoids, but not reaggregated cocultured spheroids, recapitulated key features of steatohepatitis, including steatosis, inflammation, and fibrosis phenotypes in a successive manner. Interestingly, an organoid-level biophysical readout with atomic force microscopy demonstrated that organoid stiffening reflects the fibrosis severity. Furthermore, organoids from patients with genetic dysfunction of lysosomal acid lipase phenocopied severe steatohepatitis, rescued by FXR agonism-mediated reactive oxygen species suppression. The presented key methodology and preliminary results offer a new approach for studying a personalized basis for inflammation and fibrosis in humans, thus facilitating the discovery of effective treatments.
Chapter
Electrolytes are involved in numerous intracellular and extracellular biological and physiological functions, including maintenance of cell volume, cellular ionic strength, and enzymatic activities, critical for sustaining life. Hyponatremia is by far the most common electrolyte disorder encountered in practice. This chapter explores the existing and new advances in electrolyte alterations. Hyponatremia is the most common electrolyte disorder in both the community‐dwelling population and in hospitalized patients. Hypernatremia is less common than hyponatremia, with a reported incidence of 1–3% in hospitalized patients. The chapter outlines the management of potassium disorders. Hyperkalemia is the most common electrolyte disorder in patients with chronic kidney disease (CKD). Hypokalemia is also associated with an increased risk of developing CKD and CKD progression. Management of acute and symptomatic hyperkalemia requires cardiovascular monitoring. The chapter provides the major causes of hypomagnesemia and hypermagnesemia. Both hypomagnesemia and hypermagnesemia adversely impact patient outcomes, including increased mortality and duration of hospital stay.
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Evidence suggest that magnesium dietary supplementation has several health benefits including lowering blood pressure, reducing insulin resistance, and improving symptoms of depression, anxiety, and migraine. Here, we aimed to study the effect of chronic magnesium supplementation on anxiety-like behavior in rats by supplementing with magnesium their drinking water for 30 days. Anxiety-like behavior was induced by subcutaneous injection of veratrin 30 minutes before performing elevated plus maze and open field tests to measure anxiety levels and locomotion, respectively. We quantify the concentration of magnesium in plasma and cerebrospinal fluid. We used diazepam to compare the efficacy of magnesium supplementation as an anxiolytic agent. Our results show that rats supplemented with magnesium had a statistically significant decrease in anxiety levels with not effects on locomotion and a statistically significant increase in concentration of magnesium in plasma and cerebrospinal fluid. However, the anxiolytic effect of magnesium supplementation washes-out in 12 days. We discuss the advantages of using supplemental magnesium as anxiolytic.
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The global prevalence of diabetic kidney disease is rapidly accelerating due to an increasing number of people living with type 2 diabetes. It has become a significant global problem, increasing human and financial pressures on already overburdened healthcare systems. Interest in diabetic kidney disease has increased over the last decade and progress has been made in determining the pathogenic mechanisms and patient-related factors involved in the development and pathogenesis of this disease. A greater understanding of these factors will catalyse the development of novel treatments and influence current practice. This review summarises the latest evidence for the factors involved in the development and progression of diabetic kidney disease, which will inform better management strategies targeting such factors to improve therapeutic outcomes in patients living with diabetes.
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Objective Mineral nutrients play an important role in maintaining material and energy metabolism. Reports on mineral nutrient intakes and body mass index (BMI) and waist circumference (WC) are rare in the United States. This study examined the relationship between BMI, WC and dietary mineral intakes. Method We used the data from National Health and Nutrition Examination Survey 2007–2014. Nutrient intakes were adjusted for energy according to the residual adjustment method. We used the quantile regression model to analyze the relationship between BMI, WC under different distributions and the average daily mineral intakes. Result A total of 19,952 people were included in the study, including 9,879 men and 10,073 women (≥20 years old). The median BMI was 27.935 kg/m ² and the median WC was 97.700 cm. The results of quantile regression showed that calcium, magnesium, potassium, copper, zinc and iron intakes were negatively correlated with BMI and WC, after adjusting for age and gender. Sodium and phosphorus intakes were positively correlated with BMI, sodium intakes were positively correlated with WC. This correlation was enhanced with increasing quantiles of risk levels. In high BMI or high WC populations, mineral intakes had a greater impact on BMI and WC. The quantile regression coefficients of selenium intakes were not statistically significant at each quantile. Conclusion Our results suggested that the mineral nutrient intakes were associated with BMI and WC in American adults. However, we also need to further study the longitudinal effects of mineral intakes and obesity.
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Os hábitos alimentares dos ser humano do ser humano são modificados ao longo dos anos, conforme a evolução tecnológica. Com a troca de alimentos in natura pelos industrializados, cujo valor nutritivo são mínimos, os níveis desejados para consumo de micronutrientes não são suficientes o que leva o indivíduo a apresentar deficiências nutricionais. A carência em micronutrientes leva a um quadro de desequilíbrio funcional do organismo, podendo o tornar suscetível a doenças crônicas não transmissíveis, além de alterações metabólicas e hiperglicemia. Assim, este trabalho teve como objetivo apresentar os nutrientes fundamentais cromo e magnésio e a ação no tratamento da hiperglicemia. Os principais micronutrientes envolvidos com o metabolismo da glicose e da insulina são as vitaminas lipossolúveis (A, D, E, K), vitamina C, cromo, folato, magnésio, vanádio e zinco. O cromo pode ser encontrado no organismo humano em pequenas quantidades, porém este tem um papel fundamental na homeostase da glicose, pois atua no aumento da sensibilidade insulínica. O magnésio por sua vez quando em concentrações inadequadas pode resultar em um desequilíbrio nos receptores de insulina, podendo desencadear uma resistência insulínica. Ambos os micronutrientes têm uma ação fundamental em nosso organismo a níveis metabólicos, pois ausência ou excesso dos mesmos interfere na homeostase da glicose.
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Background and Aims Results of in vitro and in vivo studies showed that green leafy vegetables (GLV) could attenuate liver steatosis. However, little is known regarding the association between GLV intake and nonalcoholic fatty liver disease (NAFLD) in human. We examined the association of GLV intake with NAFLD in a large-scale adult population. Methods and Results This cross-sectional study investigated 26,891 adults in China who participated in health examinations from 2013 to 2017. Newly diagnosed NAFLD was detected by liver ultrasonography. Dietary intake was assessed by using a validated and standardized food frequency questionnaire. Multivariable logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) across categories of GLV intake. After adjustment for sociodemographic characteristics, lifestyle factors, and other dietary intakes, the OR (95% CI) for comparing the highest vs. lowest GLV intake categories (≥7 times/week vs. almost never) was 0.72 (0.59, 0.90) (P <0.0001). In addition, a linear inverse association was demonstrated between GLV intake and NAFLD in women (P for trend = 0.04), but ORs for any intake category did not reach significance. Stratified analyses suggested a potential effect modification by obesity status; the ORs (95% CIs) for comparing the highest vs. lowest GLV intake categories was 0.72 (0.54, 0.97) in normal/overweight individuals and 1.04 (0.65, 1.65) in obese individuals (P-interaction < 0.0001). Conclusion This large population-based study shows that high GLV intake is inversely associated with NAFLD, particularly in women and non-obese participants.
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У статті наведені дані щодо ролі магнію в забезпеченні життєдіяльності людського організму, репродукції і розвитку акушерських ускладнень. Розглянуті методи діагностики та препарати для корекції магнієвого дефіциту. Метою дослідження стало вивчення ефективності застосування комплексного водорозчинного засобу, що містить цитрат магнію і вітамін В6, в профілактиці ускладнень вагітності, індукованої в циклах допоміжних репродуктивних технологій (ДРТ). Матеріали та методи. Під наглядом перебувало 215 жінок із вагітністю, індукованою в циклах ДРТ, які були рандомізовані на дві групи: основна група (110 жінок) отримувала з профілактичною метою комплексний водорозчинний препарат Метіда, що містить 1970 мг цитрату магнію (в перерахунку на елементарний магній 300 мг) і 30 мг вітаміну В6, 1 раз на добу з 1 по 36 тижні вагітності. Група порівняння (105 жінок) препарат магнію не отримувала. Групу контролю склали 53 умовно здорові жінки з вагітністю після природного зачаття. Вивчали рівні сироваткового і еритроцитарного магнію в 6–8, 18-20 і 30-32 тижні гестації. Оцінювали клінічний перебіг вагітності і пологів. Параметри магнієвого дефіциту слід визначати за вмістом магнію в еритроцитах, оскільки його рівень у сироватці крові при цьому є ще нормальним, тобто знаходиться в межах референтного інтервалу. Результати. Застосування препарату Метіда в жінок із індукованою вагітністю в циклах ДРТ порівняно з групою, в якій препарати магнію не призначалися, привело до зниження числа випадків загрози передчасних пологів у 2,62 разу, дисфункції плаценти – в 2,24 разу, гестаційного цукрового діабету – в 2,62 разу, передчасних пологів – у 2,28 разу і до збільшення числа своєчасних пологів у 1,12 разу. Висновок. Застосування магнієвмісного препарату Метіда з найбільш ранніх термінів дозволило оптимізувати перебіг і результат вагітності, знизити число випадків загрози викидня та низки ускладнень, а також збільшити число своєчасних пологів. Важливими властивостями препарату Метіда є безпека і біодоступність магнію, який міститься в ньому. Препарат має максимальний комплаєнс – високу ефективність і засвоюваність.
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Background: Depression is associated with insulin resistance (IR). However, the potential beneficial effect, on antidepressant treatment response, of adjunctive therapy with insulin sensitivity-enhancing lifestyle and dietary interventions (exercise; supplementation with: vitamin D, magnesium, zinc, probiotics or omega-3 fatty acids) has not been systematically explored. Aims: To determine the effect of the above stated adjuncts on antidepressant treatment response in clinically depressed patients via a systematic review and meta-analysis. Methods: RCTs which assessed the effect, on antidepressant treatment response of adjunctive therapy with any of the interventions in comparison with treatment as usual were included. Results: The interventions had a significant antidepressant effect, with SMD for follow-up (end of study) scores and change (from baseline) scores being -0.88, [95% CI: -1.19 to -0.57; P < 0.001] and -1.98 [95% CI -2.86 to -1.10; P < 0.001], respectively. The odds ratio (OR) for remission was 2.28 (95% CI 1.42 to 3.66; P < 0.001). The number-needed-to-treat (NNT) for remission was 6. Subgroup analysis of the follow-up scores revealed age effect: SMD significant in those with mean age ≤50 (-1.02 SMD; 95% CI: -1.40 to -0.64; p < 0.001) and insignificant in those with mean age >50 (-0.38 SMD (95% CI: -0.82 to 0.05; P = 0.08)). Also, the interventions were more beneficial among outpatients- SMD: -0.97 (95% CI: -1.32 to -0.62; P < 0.001) compared to inpatients- SMD: -0.34 (95% CI: -0.88 to 0.20; P = 0.22). Sensitivity analysis did not change the results. Conclusion: The finding that antidepressant treatment response may be improved using insulin sensitivity-enhancing lifestyle and dietary adjuncts is worthy of further exploration.
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A growing understanding of antioxidant mechanisms and insulin-like actions of trace elements selenium and zinc has rekindled researchers’ interest towards their role in diabetes mellitus, nutritional management of which concentrates predominantly on macronutrient intake. However, selenium studies limiting largely to diabetes have yielded inconsistent results with sparse knowledge in the pre-diabetes population. This hospital-based cross-sectional study screened 300 people who came to the institutional hospital laboratory with fasting plasma glucose and glycosylated haemoglobin requisition over a period of 6 months. Thirty-five pre-diabetes subjects aged 25–45 years and 35 age-matched healthy controls were selected as per inclusion criteria and clinical history. Serum selenium was estimated by inductively coupled plasma-mass spectrometry, zinc and magnesium by colorimetric end-point methods and insulin by enzyme-linked immunosorbent assay, and insulin resistance was calculated using a homeostasis model assessment (HOMA) 2 calculator. Data analysis was done using SPSS ver. 16 employing an independent sample t test for intergroup comparison of means and Pearson’s correlation for correlation analysis. Serum mineral levels in the pre-diabetes group (selenium 63.01 ± 17.6 μg/L, zinc 55.78 ± 13.49 μg/dL, magnesium 1.37 ± 0.38 mg/dL) were significantly reduced (p < 0.05) in comparison to the healthy controls (selenium 90.98 ± 15.81 μg/L, zinc 94.53 ± 15.41 μg/dL, magnesium 2.12 ± 0.22 mg/dL). A significant negative correlation was seen with glycaemic indices and insulin resistance. This study conducted in pre-diabetes subjects highlights a considerable deficiency of serum selenium, zinc and magnesium observed at a much earlier pre-clinical phase. This coupled with the evidence of a strong inverse association with glycaemic indices and insulin resistance postulates the role of mineral alterations in the pathophysiology of hyperglycaemia and insulin resistance.
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Background: Insulin resistance (IR) is the key pathophysiological defect that leads to the development of type 2 diabetes mellitus. The purpose of this study was to estimate serum magnesium level and insulin sensitivity indices among type 2 diabetes mellitus patients and to see an association between them. Methods: This study was carried out among 38 type 2 diabetic patients and forty age and sex matched controls. Serum fasting glucose, magnesium, insulin, urea, and creatinine levels were estimated. Insulin sensitivity indices, homeostasis model assessment for insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI) levels were calculated as per formulae. Results: A highly significant low serum magnesium level was found in diabetic subjects as compared to the controls. Statistically significant high HOMA levels (>2.6) and low QUICKI levels (<0.33) were found among the case group. An inverse, statistically significant correlation was found between serum magnesium and fasting insulin level. A highly statistically significant inverse correlation was found between serum magnesium and HOMA level, and a positive correlation was found between serum magnesium and QUICKI level, that is, serum magnesium level decreases with increase in IR. A strong association was also found between fasting serum insulin level and insulin sensitivity indices. Conclusion: This study showed a lower serum magnesium level in diabetic patients compared to control. A strong association was also found between serum magnesium level and insulin sensitivity indices. For proper management of type 2 diabetes, it may, therefore, be necessary to treat hypomagnesemia in these patients.
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Background: Magnesium is the second most abundant intracellular cation. It plays an important role in insulin homeostasis and glucose metabolism through multiple enzymatic reactions. With increasing data on magnesium deficiency in diabetic patients and epidemiological studies demonstrating magnesium deficiency as a risk factor for diabetes, it is logical to search for its possible beneficial effects on diabetes control and prevention. We aimed to determine whether oral magnesium supplementation improves metabolic control, lipid profile and blood pressure in patients with type II diabetes. Methods: Fifty four patients with type II diabetes were included in a randomized double blind placebocontrolled clinical trial.Patients received either placebo or 300 mg elemental magnesium (as magnesium sulfate -MgSo4-) daily, for 3 months. Metabolic control, lipid profile, blood pressure, magnesium status, hepatic enzymes, hemoglobin concentration, and anthropometric indices were determined in the beginning and at the end of the study. Results: Daily administration of 300 mg elemental magnesium for 3 months, significantly improved fasting blood glucose (183.9±15.43 to 125.8±6.52 vs. 196.5±28.12 to 136.5±7.94, p< 0.0001), 2-hour post prandial glucose (239.1±74.75 to 189.1±60mg/dl vs. 246.4±97.37 to 247.8±86.74mg/dl, p< 0.01), lipid profile, blood pressure and hepatic enzymes. Conclusion: Oral magnesium supplementation with proper dosage has beneficial effects on blood glucose, lipid profile, and blood pressure in patients with type II diabetes.
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There are limited and conflicting data from clinical trials concerning the beneficial effects of magnesium supplementation on diabetic patients. We investigated the effects of magnesium supplementation on metabolic control and insulin sensitivity in type 2 diabetic patients with normomagnesemia. A total of 98 normomagnesemic subjects with type 2 diabetes were enrolled in a randomized, crossover, double-blind, placebo-controlled trial. Participants were randomly assigned to receive magnesium lactate (360 mg elemental magnesium) or placebo for three months, followed by a three-month washout period. Treatment assignments were then reversed over an additional three months of follow-up. The primary endpoint was a reduction in fasting glucose and HbA1c. A total of 56 subjects completed the follow-up in the magnesium and placebo supplementation groups. Urinary magnesium excretion was increased following magnesium supplementation in the intervention group compared with the placebo group (p = 0.0002). Fasting glucose, HbA1c, insulin and HOMA-IR, as well as lipid profile, did not change significantly during treatment. We concluded that magnesium supplementation does not improve metabolic control or insulin sensitivity in diabetic subjects with normomagnesemia.
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The present study evaluated the influence of magnesium on insulin resistance in obese women. A case-control study involving 114 women on the age between 20 and 50 years old, divided into two groups: control (eutrophic women, n = 59) and case (obese women, n = 55). The analysis of magnesium intake was carried out through the 3-day food record and also NutWin software version 1.5. The plasma, erythrocyte, and urinary magnesium concentrations were determined by flame atomic absorption spectrophotometry. The determinations of serum glucose and serum insulin were performed by enzymatic colorimetric method and chemiluminescence, respectively. The insulin resistance was assessed by homeostasis model assessment insulin resistance (HOMA-IR). The mean values of magnesium intake were lower than those recommended, without difference between groups (p > 0.05). All the patients who were evaluated showed adequate mean concentrations of magnesium in the plasma and erythrocyte. The urinary excretion of this mineral was lower than the reference values in both groups and did not show significant difference (p > 0.05). The values of serum glucose, serum insulin, and HOMA-IR were higher in obese women compared to the control group. A negative correlation was observed between erythrocyte magnesium and glycemic parameters (p < 0.05). Obese patients take in foods with low dietary magnesium content, and they show hypomagnesuria as a compensatory mechanism to keep the plasma concentration of this mineral in adequate levels. The correlation between the erythrocyte magnesium concentration and the parameters of glycemic control suggests the influence of this mineral on the index of insulin resistance in obese women.
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There have been few studies to examine the effect of magnesium (Mg) supplementation on liver enzymes. The aim of this study was to evaluate the effect of Mg supplementation and weight loss on liver enzymes, lipid profile, and fasting blood sugar in patients with nonalcoholic fatty liver disease (NAFLD). This study was a double-blind, placebo-controlled, randomized clinical trial. Ultrasonography was used to diagnose fatty liver in patients with alanine aminotransferase (ALT) ≥ 40 U/L and without other hepatic diseases. A total of 68 participants (18-59 years) with NAFLD were randomly divided into two groups to receive either Mg supplement (350 mg elemental Mg per day) or placebo for 90 days. At baseline and at the end of the intervention serum ALT, aspartate aminotransferase (AST), alkaline phosphatase (ALP), total cholesterol (TCHO), high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), blood sugar and serum insulin, and Mg levels were measured in fasting state. Low-density lipoprotein cholesterol (LDL-C) and insulin resistance (IR) were calculated using Friedewald formula and homeostasis model assessment of insulin resistance (HOMA-IR), respectively. All participants received lifestyle recommendations including low calorie diet and physical activity. Significant decreases within the intervention and placebo groups were observed in ALT (57.00 (25) to 41.82 ± 19.40 U/L, P = 0.000; 68.50 ± 26.96 to 40.17 ± 19.40 U/L, P = 0.000 in Mg and placebo groups, respectively). Similar significant decreases were observed in AST and fasting serum insulin within the study groups. The decrease in weight was also significant in both groups (91.05 ± 13.77 to 87.60 ± 14.37 kg and 94.59 ± 16.85 to 91.45 ± 16.39 kg in Mg and placebo groups, respectively). LDL-C and TCHO were decreased significantly in placebo group but not in the intervention group. Serum Mg was increased significantly in the intervention group. No statistically significant differences were observed between the two study groups at baseline and after intervention. According to the findings of this study, Mg supplement does not affect liver enzymes but weight loss may have an important role in improving fatty liver disease.
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Many cross-sectional studies show an inverse association between dietary magnesium and insulin resistance, but few longitudinal studies examine the ability to meet the Recommended Dietary Allowance (RDA) for magnesium intake through food and its effect on insulin resistance among participants with metabolic syndrome (MetS). The dietary intervention study examined this question in 234 individuals with MetS. Magnesium intake was assessed using 24-h dietary recalls at baseline, 6, and 12 months. Fasting glucose and insulin levels were collected at each time point; and insulin resistance was estimated by the homeostasis model assessment (HOMA-IR). The relation between magnesium intake and HOMA-IR was assessed using linear mixed models adjusted for covariates. Baseline magnesium intake was 287 ± 93 mg/day (mean ± standard deviation), and HOMA-IR, fasting glucose and fasting insulin were 3.7 ± 3.5, 99 ± 13 mg/dL, and 15 ± 13 μU/mL, respectively. At baseline, 6-, and 12-months, 23.5%, 30.4%, and 27.7% met the RDA for magnesium. After multivariate adjustment, magnesium intake was inversely associated with metabolic biomarkers of insulin resistance (P < 0.01). Further, the likelihood of elevated HOMA-IR (>3.6) over time was 71% lower [odds ratio (OR): 0.29; 95% confidence interval (CI): 0.12, 0.72] in participants in the highest quartile of magnesium intake than those in the lowest quartile. For individuals meeting the RDA for magnesium, the multivariate-adjusted OR for high HOMA-IR over time was 0.37 (95% CI: 0.18, 0.77). These findings indicate that dietary magnesium intake is inadequate among non-diabetic individuals with MetS and suggest that increasing dietary magnesium to meet the RDA has a protective effect on insulin resistance.
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As a cofactor in numerous enzymatic reactions, magnesium fulfils various intracellular physiological functions. Thus, imbalance in magnesium status—primarily hypomagnesaemia as it is seen more often than hypermagnesaemia—might result in unwanted neuromuscular, cardiac or nervous disorders. Measuring total serum magnesium is a feasible and affordable way to monitor changes in magnesium status, although it does not necessarily reflect total body magnesium content. The following review focuses on the natural occurrence of magnesium and its physiological function. The absorption and excretion of magnesium as well as hypo- and hypermagnesaemia will be addressed.
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Background: Epidemiological studies have associated low dietary Mg2+ intake with insulin resistance (IR) and increased risk for metabolic syndrome; however, the effect of Mg2+ supplementation on IR has not been adequately investigated. This study aimed to investigate the effects of oral Mg2+ supplementation on insulin sensitivity (IS) and serum lipids. Material/Methods: Forty-eight patients with mild uncomplicated hypertension participated in the study. Among them, 24 subjects were assigned to 600 mg of pidolate Mg2+ daily in addition to lifestyle recommendations for a 12-week period, and another 24 age- and sex-matched controls were only given lifestyle recommendations. At baseline and study-end, blood sampling for determination of fasting glucose and insulin levels, serum lipids and other standard laboratory tests, as well as an oral glucose tolerance test (OGTT) for estimation of IS indices, were performed in all subjects. Results: In the Mg2+ supplementation group the OGTT-derived IS indices of Stumvoll, Matsuda and Cedercholm in were increased between baseline baseline and study-end. In contrast, none of these parameters were changed in the control group. Reductions in total cholesterol, LDL-cholesterol and triglyceride levels, along with a parallel increase in HDL-cholesterol levels, were evident at study-end in the intervention group, but not in the control group. Conclusions: This study suggests that oral Mg2+ supplementation improves IS and lipid profile in mildly hypertensive patients. These potential beneficial effects of Mg2+ on associated metabolic factors could be helpful for patients with hypertension in terms of overall cardiovascular risk reduction.
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Morbid obesity may be accompanied by diabetes and painful diabetic neuropathy, a poorly understood condition that is manifested by mechanical or thermal allodynia and hyperalgesia. Recent studies have highlighted the importance of T-type calcium channels (T-channels) in peripheral nociception; therefore, our goal was to examine the function of these channels in the pathophysiology and development of painful diabetic neuropathy. In vivo testing of mechanical and thermal sensation, morphometric peripheral nerve studies, and electrophysiological and biochemical measurements were used to characterize the role of T-channels and the development of painful diabetic neuropathy in leptin-deficient (ob/ob) mice. We found that ob/ob mice developed significant mechanical and thermal hypersensitivity early in life that coincided with hyperglycemia and was readily reversed with insulin therapy. These disturbances were accompanied by significant biophysical and biochemical modulation of T-channels in dorsal root ganglion neurons as measured by a large increase in the amplitude of T-currents and the expression of mRNA. The most prevalent subtype, alpha1H (Ca(v)3.2), was most strongly affected. Moreover, (3beta,5alpha,17beta)-17-hydroxyestrane-3-carbonitrile (ECN), a novel neuroactive steroid and selective T-channel antagonist, provided dose-dependent alleviation of neuropathic thermal and mechanical hypersensitivity in diabetic ob/ob mice. Our results indicate that pharmacological antagonism of T-channels is potentially an important novel therapeutic approach for the management of painful diabetic neuropathy.
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Enzyme and or hormone actions have not been shown to be consistently changed by consuming a low-magnesium diet similar to one that may occur in the general population. Thus, a human metabolic study was performed to determine whether deficient intakes of magnesium similar to those that occur naturally have pathophysiological effects through altering calcium retention and the metabolism of other minerals (sodium, potassium, phosphorus) involved in cellular ionic balance. Fifteen postmenopausal Caucasian women were recruited by advertisement throughout the United States. Eleven women (ages 49 to 71 years) completed the study as designed. The women resided in a metabolic research unit and consumed a basal Western-type diet that resulted in a mean intake of 4.40 mmol (107 mg) magnesium/d. The women were fed the basal diet supplemented with 9.05 mmol (220 mg) magnesium/d for 18 d (equilibration) before being assigned to one of two groups in an experiment with a double blind, crossover design. One group was fed the basal diet and supplemented with a lactose placebo while the other group continued consuming the basal diet supplemented with 9.05 mmol magnesium/d for 72 d, then each group switched to the other's diet, which they consumed for 72 d. Magnesium was supplemented as magnesium gluconate. Magnesium deprivation resulted in a non-positive magnesium balance (-0.21 mmol or -5 mg/d) that was highly positive during magnesium supplementation (+2.22 mmol or +54 mg/d). Magnesium deprivation decreased red blood cell membrane magnesium (2.5 versus 2.7 nmol or 0.061 versus 0.065 microg/mg protein; p < or = 0.05). Magnesium deprivation increased calcium balance (+0.82 mmol or +35 mg/d versus -0.02 or -1 mg/d; p < or = 0.009); decreased the fecal excretion of phosphorus (28.9% versus 32.3% of intake; p < or =0.0001); increased the urinary excretion of phosphorus (73.4% versus 71.0%; p < 0.003); and decreased the urinary excretion of potassium (40.4 mmol or 1.58 g/d versus 41.9 mmol or 1.64 g/d; p < 0.04). Non-positive magnesium balance and decreased red blood cell membrane magnesium concentration apparently are indicators of magnesium deprivation. Moderate magnesium deprivation achieved through diet alone results in increased calcium retention. Magnesium deprivation also alters phosphorus and potassium excretion. The changes indicate that an intake of 4.40 mmol (107 mg) magnesium/d is inadequate for postmenopausal women because of changes in cellular ionic balance that may lead to pathophysiological conditions.
Article
A systematic review and meta-analysis was conducted to evaluate the effect of oral magnesium supplementation on insulin sensitivity and glucose control in both diabetic and non-diabetic individuals. PubMed-Medline, SCOPUS, Web of Science and Google Scholar databases were searched (from inception to November 25, 2015) to identify RCTs evaluating the effect of magnesium on insulin sensitivity and glucose control. A random-effects model and generic inverse variance method were used to compensate for the heterogeneity of studies. Publication bias, sensitivity analysis, and meta-regression assessments were conducted using standard methods. The impact of magnesium supplementation on plasma concentrations of glucose, glycated hemoglobin (HbA1c), insulin, and HOMA-IR index was assessed in 22, 14, 12 and 10 treatment arms, respectively. A significant effect of magnesium supplementation was observed on HOMA-IR index (WMD: −0.67, 95% CI: −1.20, −0.14, _p_ = 0.013) but not on plasma glucose (WMD: −0.20 mmol/L, 95% CI: −0.45, 0.05, _p_ = 0.119), HbA1c (WMD: 0.018 mmol/L, 95% CI: −0.10, 0.13, _p_ = 0.756), and insulin (WMD: −2.22 mmol/L, 95% CI: −9.62, 5.17, _p_ = 0.556). A subgroup analysis comparing magnesium supplementation durations of <4 months versus ≥4 months, exhibited a significant difference for fasting glucose concentrations (_p_<0.001) and HOMA-IR (_p_ = 0.001) in favor of the latter subgroup. Magnesium supplementation for ≥4 months significantly improves the HOMA-IR index and fasting glucose, in both diabetic and non-diabetic subjects. The present findings suggest that magnesium may be a beneficial supplement in glucose metabolic disorders.
Article
To our knowledge, prior research has not examined the effects of magnesium supplementation on metabolic status and pregnancy outcomes in maternal-child dyads affected by gestational diabetes (GDM). This study was designed to assess the effects of magnesium supplementation on metabolic status and pregnancy outcomes of magnesium-deficient pregnant women with GDM. A randomized double-blind placebo-controlled clinical trial was performed among 70 women with GDM. Patients were randomly assigned to receive either 250 mg magnesium oxide (n = 35) or a placebo (n = 35) for 6 wk. Fasting blood samples were taken at baseline and after a 6-wk intervention. The change in serum magnesium concentration was greater in women consuming magnesium than in the placebo group (+0.06 ± 0.3 vs. -0.1 ± 0.3 mg/dL, P = 0.02). However, after controlling for baseline magnesium concentrations, the changes in serum magnesium concentrations were not significantly different between the groups. Changes in fasting plasma glucose (-9.7 ± 10.1 vs. +1.8 ± 8.1 mg/dL, P < 0.001), serum insulin concentration (-2.1 ± 6.5 vs. +5.7 ± 10.7 μIU/mL, P = 0.001), homeostasis model of assessment-estimated insulin resistance (-0.5 ± 1.3 vs. +1.4 ± 2.3, P < 0.001), homeostasis model of assessment-estimated β-cell function (-4.0 ± 28.7 vs. +22.0 ± 43.8, P = 0.006), and the quantitative insulin sensitivity check index (+0.004 ± 0.021 vs. -0.012 ± 0.015, P = 0.005) in supplemented women were significantly different from those of women in the placebo group. Changes in serum triglycerides (+2.1 ± 63.0 vs. +38.9 ± 37.5 mg/dL, P = 0.005), high sensitivity C-reactive protein (-432.8 ± 2521.0 vs. +783.2 ± 2470.1 ng/mL, P = 0.03), and plasma malondialdehyde concentrations (-0.5 ± 1.6 vs. +0.3 ± 1.2 μmol/L, P = 0.01) were significantly different between the supplemented women and placebo group. Magnesium supplementation resulted in a lower incidence of newborn hyperbilirubinemia (8.8% vs. 29.4%, P = 0.03) and newborn hospitalization (5.9% vs. 26.5%, P = 0.02). Magnesium supplementation among women with GDM had beneficial effects on metabolic status and pregnancy outcomes. This trial was registered at www.irct.ir as IRCT201503055623N39. © 2015 American Society for Nutrition.
Article
This study evaluated the efficacy of oral magnesium supplementation in the reduction of plasma glucose levels in adults with prediabetes and hypomagnesaemia. A total of 116 men and non-pregnant women, aged 30 to 65years with hypomagnesaemia and newly diagnosed with prediabetes, were enrolled into a randomized double-blind placebo-controlled trial to receive either 30mL of MgCl2 5% solution (equivalent to 382mg of magnesium) or an inert placebo solution once daily for four months. The primary trial endpoint was the efficacy of magnesium supplementation in reducing plasma glucose levels. At baseline, there were no significant statistical differences in terms of anthropometric and biochemical variables between individuals in the supplement and placebo groups. At the end of follow-up, fasting (86.9±7.9 and 98.3±4.6mg/dL, respectively; P=0.004) and post-load glucose (124.7±33.4 and 136.7±23.9mg/dL, respectively; P=0.03) levels, HOMA-IR indices (2.85±1.0 and 4.1±2.7, respectively; P=0.04) and triglycerides (166.4±90.6 and 227.0±89.7, respectively; P=0.009) were significantly decreased, whereas HDL cholesterol (45.6±10.9 and 46.8±9.2mg/dL, respectively; P=0.04) and serum magnesium (1.96±0.27 and 1.60±0.26mg/dL, respectively; P=0.005) levels were significantly increased in those taking MgCl2 compared with the controls. A total of 34 (29.4%) people improved their glucose status (50.8% and 7.0% in the magnesium and placebo groups, respectively; P<0.0005). Our results show that magnesium supplementation reduces plasma glucose levels, and improves the glycaemic status of adults with prediabetes and hypomagnesaemia. Copyright © 2015. Published by Elsevier Masson SAS.
Article
Post-transplantation hypomagnesemia is common and predicts diabetes. Magnesium improves glycemic control in diabetics and insulin sensitivity in insulin resistant subjects. We aimed to assess the effectiveness of oral magnesium for improving glycemic control and insulin sensitivity at 3 months post-transplantation. We conducted a single-center, open-label, randomized parallel group study. We included adults with serum magnesium <1.7 mg/dl within 2 weeks after kidney transplantation. We randomized participants to 450 mg magnesium oxide up to three times daily or no treatment. The primary endpoint was the mean difference in fasting glycemia. Secondary endpoints were the mean difference in area under the curve (AUC) of glucose during an oral glucose tolerance test and insulin resistance measured by Homeostasis Model of Assessment-Insulin Resistance (HOMA-IR). Analyses were on intention-to-treat basis. In patients randomized to magnesium oxide (N = 27) versus no treatment (N = 27), fasting glycemia on average was 11.5 mg/dl lower (95% CI 1.7 to 21.3; P = 0.02). There was no difference between the two groups neither for 2 h AUC, where the mean value was 1164 mg/dl/min (95% CI -1884 to 4284; P = 0.45) lower in the treatment group nor for HOMA-IR. Magnesium supplements modestly improved fasting glycemia without effect on insulin resistance. Higher baseline glycemia among patients in the control group may have driven the positive outcome (ClinicalTrials.gov number: NCT01889576).
Article
Background and Aims Magnesium plays an important role in the modulation of vascular tone and endothelial function and can regulate glucose and lipid metabolism. Patients with hypertension, metabolic syndrome (MetS) and diabetes mellitus (T2DM) have low body magnesium content; indeed, magnesium supplementation has been shown to have a positive effect on blood pressure (BP) and gluco-metabolic parameters. The aim of our study was to evaluate the effect of magnesium supplements on hemodynamic and metabolic parameters in healthy men with a positive family history of MetS or T2DM. Methods and Results In a randomized, double-blind, placebo-controlled 8-week crossover trial with a 4 week wash-out period, oral supplements of 8.1 mmol of magnesium-pidolate or placebo were administered twice a day to 14 healthy normomagnesemic participants, aged 23 to 33 years. The primary endpoint was office BP, measured with a semiautomatic oscillometric device. Secondary endpoints included characteristics of the MetS, namely endothelial function, arterial stiffness and inflammation. Plasma and urinary magnesium were measured in all participants while free intracellular magnesium was measured only in a subsample. There was no significant difference in either systolic and diastolic BP in participants post-magnesium supplementation and post-placebo treatment when compared to baseline BP measurements. Further, the metabolic, inflammatory and hemodynamic parameters did not vary significantly during the study. Conclusions Our study showed no beneficial effect of magnesium supplements on BP, vascular function and glycolipid profile in young men with a family history of MetS/T2DM (trial registration at clinicaltrial.gov ID: NCT01181830; 12th of Aug 2010).
Article
We undertook this study to determine the efficacy of oral magnesium supplementation in the improvement of the metabolic profile and blood pressure in metabolically obese, normal-weight (MONW) individuals. A total of 47 MONW individuals with hypomagnesemia were enrolled in clinical a randomized double-blind placebo-controlled trial. Individuals in the intervention group received 30 mL of MgCl2 5% solution (equivalent to 382 mg of magnesium) and individuals in the control group 30 mL of placebo solution, once daily during 4 months. In the absence of obesity or overweight, the presence of fasting glucose levels ≥100 mg/dL, HOMA-IR index ≥3, triglyceride levels ≥150 mg/dL and/or systolic and diastolic blood pressure ≥140 and 90 mmHg defined the presence of the MONW phenotype. Hypomagnesemia was defined by serum magnesium concentration ≤1.8 mg/dL. At basal conditions there were no significant differences between groups. At the end of follow-up, changes in the mean of systolic (-2.1 vs. 3.9% mmHg, p <0.05) and diastolic (-3.8 vs. 7.5% mmHg, p <0.05) blood pressures, HOMA-IR index (-46.5 vs. -5.4%, p <0.0001), fasting glucose (-12.3 vs. -1.8% mg/dL, p <0.05) and triglyceride levels (-47.4% vs. 10.1% mg/dL, p <0.0001) were significantly lower in the subjects who received MgCl2 compared with individuals in the control group. Oral magnesium supplementation improves the metabolic profile and blood pressure of MONW individuals.
Article
Given that role of magnesium in insulin secretion is uncertain, our objective was to determine whether oral supplementation with magnesium chloride (MgCl(2)) improves the ability of beta-cells to compensate for variations in insulin sensitivity in non-diabetic individuals with significant hypomagnesaemia. Eligible individuals were non-diabetic, normo-tensive men and non-diabetic, normo-tensive, non-pregnant women with serum magnesium levels ≤0·70 mM/L; they were enrolled in a randomized double-blind clinical trial to receive either 50 mL of 5% MgCl(2) solution or 50 mL of inactive solution daily for 3 months. The primary trial end point was a change in the AUC of the hyperbolic model of beta-cell function (HMbCF) derived from the fasting state. Individuals, caregivers and personnel who assessed the outcomes were all blinded to the group assignments. A total of 54 and 52 individuals were assigned to the MgCl(2) and placebo groups, respectively; five individuals in the MgCl(2) group and four in the placebo group dropped out. There were no serious adverse events or side effects because of MgCl(2) or placebo. At the beginning of the study, the AUC of the HMbCF was similar in both groups (AUC = 7·591 and 7·895 cm(2)); at the end of follow-up, the curve of the MgCl(2) group showed a hyperbolic distribution (AUC = 18·855 cm(2)), whereas in the placebo group, there were no changes (AUC = 7·631 cm(2)). MgCl(2) 2·5 g daily improves the ability of beta-cells to compensate for variations in insulin sensitivity in non-diabetic individuals with significant hypomagnesaemia.
Article
The incidence of insulin resistance and metabolic syndrome correlates with the availability of magnesium (Mg). We studied the effect of oral Mg supplementation on insulin sensitivity and other characteristics of the metabolic syndrome in normomagnesemic, overweight, insulin resistant, non-diabetic subjects. Subjects were tested for eligibility using oral glucose tolerance test (OGTT) and subsequently randomized to receive either Mg-aspartate-hydrochloride (n = 27) or placebo (n = 25) for 6 months. As trial endpoints, several indices of insulin sensitivity, plasma glucose, serum insulin, blood pressure and lipid profile were determined. Mg supplementation resulted in a significant improvement of fasting plasma glucose and some insulin sensitivity indices (ISIs) compared to placebo. Blood pressure and lipid profile did not show significant changes. The results provide significant evidence that oral Mg supplementation improves insulin sensitivity even in normomagnesemic, overweight, non-diabetic subjects emphasizing the need for an early optimization of Mg status to prevent insulin resistance and subsequently type 2 diabetes.
Article
Little is known about the effect of magnesium on insulin sensitivity and BP in healthy individuals. Therefore, we investigated whether magnesium could improve insulin sensitivity and blood pressure (BP) in normo-magnesemic nondiabetic overweight adults. In a double-blinded, placebo-controlled, randomized trial, a total of 155 participants (BMI > or = 23 kg/m(2)) received either 12.3 mmol (300 mg) of elemental magnesium in the form of magnesium oxide (n=75) or placebo (n=80) each day for 12 weeks, constituting the intent-to-treat population. A repeated-measures ANOVA was used to evaluate the between-group changes in variables during the study. The baseline characteristics between the intervention and control groups were similar. There were no significant differences between the groups in the pattern of change of the homeostasis model assessment insulin resistance index, BP over time during the 12-week study. In subgroup analysis, magnesium supplementation (n=8, 27, and 24, respectively) lowered BP much more than placebo (n=16, 29, and 25, respectively) in those subjects whose systolic BP > or = 140 mmHg, diastolic BP 80-90 mmHg, and diastolic BP > or = 90 mmHg at the start of the study (P=0.016, 0.043, and 0.023, respectively); in comparison, those subjects whose initial BP reading was low at baseline did not show a change in BP. No significant adverse events related to magnesium supplementation were recorded. These results suggested that magnesium supplementation does not reduce BP and enhance insulin sensitivity in normo-magnesemic nondiabetic overweight people. However, it appears that magnesium supplementation may lower BP in healthy adults with higher BP.
Article
To determine whether oral magnesium supplementation (as magnesium chloride [MgCl(2)] solution) improves both insulin sensitivity and metabolic control in type 2 diabetic subjects with decreased serum magnesium levels. This study was a clinical randomized double-blind placebo-controlled trial. A total of 63 subjects with type 2 diabetes and decreased serum magnesium (serum magnesium levels </=0.74 mmol/l) treated by glibenclamide received either 50 ml MgCl(2) solution (containing 50 g MgCl(2) per 1,000 ml solution) or placebo daily for 16 weeks. Chronic diarrhea, alcoholism, use of diuretic and/or calcium antagonist drugs, and reduced renal function were exclusion criteria. Homeostasis model assessment for insulin resistance (HOMA-IR) was used as the parameter of insulin sensitivity and glucose and HbA(1c) as parameters of metabolic control. At the end of the study, subjects who received magnesium supplementation showed significant higher serum magnesium concentration (0.74 +/- 0.10 vs. 0.65 +/- 0.07 mmol/l, P = 0.02) and lower HOMA-IR index (3.8 +/- 1.1 vs. 5.0 +/- 1.3, P = 0.005), fasting glucose levels (8.0 +/- 2.4 vs. 10.3 +/- 2.1 mmol/l, P = 0.01), and HbA(1c) (8.0 +/- 2.4 vs. 10.1 +/- 3.3%, P = 0.04) than control subjects. Oral supplementation with MgCl(2) solution restores serum magnesium levels, improving insulin sensitivity and metabolic control in type 2 diabetic patients with decreased serum magnesium levels.
Article
Although hypomagnesemia reduces insulin sensitivity, benefits of magnesium supplementation to non-diabetic insulin resistant subjects has not been established. Our purpose was to determine whether oral magnesium supplementation with magnesium chloride (MgCl2) 2.5 g daily modify insulin sensitivity in non-diabetic subjects. This study was a 3 months randomized double-blind placebo-controlled trial. Apparently healthy subjects were eligible to participate if they had insulin resistance (HOMA-IR index equal or greater than 3.0) and hypomagnesemia (Serum magnesium levels equal or lower than 0.74 mmol/l). Subjects were randomized to receive either, MgCl2 2.5 g daily or placebo by 3-months. At baseline there were not significant anthropometric or laboratory differences between both groups. At ending of the study, magnesium-supplemented subjects significantly increased their serum magnesium levels (0.61 +/- 0.08 to 0.81 +/- 0.08 mmol/l, p<0.0001) and reduced HOMA-IR index (4.6 +/- 2.8 to 2.6 +/- 1.1, p<0.0001), whereas control subjects did not (0.62 +/- 0.08 to 0.61 +/- 0.08 mmol/l, p=0.063 and 5.2 +/- 1.9 to 5.3 +/- 2.9, p=0.087). Oral magnesium supplementation improves insulin sensitivity in hypomagnesemic non-diabetic subjects. Clinical implications of this finding have to be established.
Article
The aim of this review was to elaborate a synthesis about the discussions on magnesium and diabetes mellitus, in the last 14 years. The magnesium deficiency has been associated with chronic diseases, amongst them, diabetes mellitus. Epidemiological studies had shown low levels of magnesium ingestion in the general population, as well as a relation between the ingestion of food rich in magnesium and the reduction of diabetes installation and its complications. Hypomagnesemia is frequently present in diabetic patients, however there is not an exact elucidation of the mechanism of magnesium deficiency in diabetes mellitus. On the other hand, in the presence of this illness, it is observed that inadequate metabolic control can affect the corporal concentrations of magnesium, developing hypomagnesemia, which may be still directly related with some micro and macrovascular complications observed in diabetes, as cardiovascular disease, retinopathy and neuropathy. This way, the chronic complications of diabetes can appear precociously. Based on this, the supplementation with magnesium has been suggested in patients with diabetes mellitus who have proven hypomagnesemia and the presence of its complications.
Aspectos metab olicos e Nutricionais do Magn esio
  • J S Severo
  • Jbs Morais
  • Tmc Freitas
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