ArticlePDF AvailableLiterature Review

Vitamin D Deficiency, Obesity and Diabetes

Authors:
  • Guangxi Academy of Medical Sciences, the People's Hospital of Guangxi Zhuang Autonomous Region

Abstract

Obesity and type 2 diabetes mellitus (T2DM) are main chronic diseases harming human health. Although the association between obesity and T2DM is well established, the molecular mechanism is still unclear. Accumulating evidence suggests vitamin D plays a role in the development of these diseases. Vitamin D is a necessary nutrient for humans. People usually do not pay attention to supplementing vitamin D, since vitamin D can be produced when their skin is exposed to the sunlight. Nevertheless, even in highly sunny regions, vitamin D deficiency exists, suggesting vitamin D deficiency is a global problem. Vitamin D deficiency has previously been considered only to influence bone metabolism. Accumulating evidence counters this opinion. In vivo studies have revealed that vitamin D deficiency reduces insulin secretion capacity of the islet beta cells in pancreas. Moreover, epidemiological studies have demonstrated that vitamin D deficiency is closely related to obesity and increased risk of T2DM. This review introduces the current work on vitamin D, obesity and diabetes.
35
Copyright © 2015. All rights reserved.
Vitamin D Deciency, Obesity and Diabetes
Y. Li1,2 and L. Zhou1,2
1 College of Animal Science and Technology, Guangxi University, Guangxi, China
2 Guangxi Experiment Centre of Science and Technology, Guangxi University, Guangxi, China
Corresponding author: : Prof. Lei Zhou, College of Animal Science and Technology, Guangxi University, Nanning city, Guangxi Zhuang Auto-
nomous Region, P.R.China, 530004. E-mail: zhoulei@gxu.edu.cn
Abstract
Obesity and type 2 diabetes mellitus (T2DM) are main chronic diseases harming human health. Although the association between obesity and T2DM is well esta-
blished, the molecular mechanism is still unclear. Accumulating evidence suggests vitamin D plays a role in the development of these diseases. Vitamin D is a
necessary nutrient for humans. People usually do not pay attention to supplementing vitamin D, since vitamin D can be produced when their skin is exposed to the
sunlight. Nevertheless, even in highly sunny regions, vitamin D deciency exists, suggesting vitamin D deciency is a global problem. Vitamin D deciency has
previously been considered only to inuence bone metabolism. Accumulating evidence counters this opinion. In vivo studies have revealed that vitamin D deciency
reduces insulin secretion capacity of the islet beta cells in pancreas. Moreover, epidemiological studies have demonstrated that vitamin D deciency is closely related
to obesity and increased risk of T2DM. This review introduces the current work on vitamin D, obesity and diabetes.
Key words: Adipocyte, Insulin resistance, Insulin secretion, Vitamin D, T2DM.
Cellular & Molecular Biology
Cell. Mol. Biol. 2015; 61 (3): 35-38
Published online June 10, 2015 (http://www.cellmolbiol.com)
Received on May 18, 2015, Accepted on June 8, 2015.
doi : 10.14715/cmb/2015.61.3.8
Introduction
Obesity and type 2 diabetes mellitus (T2DM) have
become main chronic diseases that harm human health
not only in developed countries but also in developing
countries. With improvement of living standards and
lifestyle changes, the number of diabetic patients is
increasing dramatically. It is estimated that by the year
2020 there will be approximately 300 million people
affected by T2DM, most of which will occur in deve-
loping countries (1). In China, the number of people
affected by T2DM is 92.4 million, which was estimated
by a recent study using the Oral Glucose Tolerance Test
(OGTT) in 46,239 adults from 14 provinces (2). A large
patient base will adversely inuence both the medical
insurance system and people’s social life. Therefore,
obesity and diabetes are not only a health problem but
also a social problem worldwide.
Control and treatment of obesity and diabetes must
be based on the understanding of their development
mechanisms, which remain unclear. However, over
the past few decades, research has revealed a number
of factors closely correlated with obesity and diabetes.
Among them, the role of vitamin D is gaining more and
more attention.
Source and metabolism of vitamin D
Vitamin D is a necessary nutrient for human health.
Previously, vitamin D supplementation was only used to
prevent rickets. Hence, vitamin D was considered only
to participate in the formation and development of bone.
However, recent studies have revealed that vitamin D
also plays a crucial role in nerve, reproduction, immu-
nity and the endocrine system (3). Vitamin D comprises
two categories: vitamin D2 and vitamin D3. Vitamin D3
is the main form in humans (4) and activates vitamin D
receptor (VDR) which is a nuclear receptor expressed
nearly ubiquitously.
Humans get vitamin D via the sun and through
their diet. When people are exposed to sunlight, solar
ultraviolet B radiation penetrates the skin and converts
7-dehydrocholesterol to previtamin D3, which is rapidly
converted to vitamin D3 that enters the circulation. Most
vitamin D3 is transported in the blood by binding to vita-
min D binding protein (DBP) (85%-88%) or albumin
(12%-15%). In the diet, vitamin D mainly comes from
animal derived food, such as salmon and cod liver oil.
Vitamin D via sun-exposed skin and from the diet
has no biological activity and must be transported to
the liver, where it is metabolized by 25-hydroxylase to
25-hydroxyvitamin D (25-(OH)D3), which is the major
circulating metabolite and a determinant of a patient’s
vitamin D status. However, 25-(OH)D3 has little biolo-
gical activity and needs to be transported to the kidney
for further hydroxylation to its active form, 1,25-dihy-
droxyvitamin D (1,25-(OH)2D3).
Vitamin D and obesity
Obesity is a major risk factor for T2DM (5). Abun-
dant studies have revealed that adipocyte dysfunction
plays a key role in the development of obesity. Interes-
tingly, researchers discovered that vitamin D is stored
in adipocytes, which regulate its levels by storing and
releasing vitamin D. And vitamin D level is signicant
inversely related to BMI (6), indicating vitamin D de-
ciency is related to increased body fat (7). These studies
support that lower vitamin D level increases the risk
of obesity. Another groups also conrmed this conclu-
sion, nding an inverse association between vitamin D
levels and excess weight (8, 9). Moreover, Wortsman et
al. discovered that not only the vitamin D level but the
bioavailability of vitamin D also decreased in obesity
36
Copyright © 2015. All rights reserved.
Y. Li and L. Zhou / VD, Obesity & Diabetes.
(10). Conversely, high vitamin D intake reduces diet-in-
duced obesity (11). Although the specic mechanism of
how vitamin D inuences lipogenesis is still not clear,
some groups have discovered a few clues: Duque et al.
reported 1,25-(OH)2D3 directly suppresses the expres-
sion of peroxisome proliferator-activated receptor γ2
(PPARγ2), which promotes lipogenesis and differen-
tiation of 3T3-L1 preadipocytes (12). In addition, Lee
et al. identied a novel 1,25-(OH)2D3 response element
in the promoter region of insulin-induced gene-2 (In-
sig-2), showing 1,25-(OH)2D3 stimulates the expression
of Insig-2, which inhibits lipogenesis and blocks diffe-
rentiation of preadipocytes (13). These ndings suggest
1,25-(OH)2D3 may also control fat deposits via these
key factors.
Vitamin D and diabetes
In addition to being risk factors for obesity, abnor-
mal insulin secretion and insulin resistance are closely
correlated with the development of diabetes. Some stu-
dies have also revealed a relationship between vitamin
D and these factors.
Vitamin D and insulin secretion
Accumulating evidence demonstrated vitamin D sti-
mulates the islet β cells to secrete insulin through its
active form 1,25-(OH)2D3 (14). It is believed that vita-
min D might regulate insulin signal transduction and
glucose-induced insulin secretion by this pathway. Stu-
dies on ob/ob mice indicated that vitamin D deciency
reduces insulin secretion and that supplementing with
vitamin D increases insulin levels (15). Previous work
conrmed the presence of vitamin D receptor (VDR)
in pancreatic islet β cells and showed impaired insulin
secretion in mice lacking functional VDR (16). These
data suggest vitamin D regulates insulin secretion via
VDR. Moreover, Bland et al. found pancreatic islets
express 1α-hydroxylase, which catalyzes 25-(OH)D3
to 1,25-(OH)2D3, suggesting the local production of
1,25-(OH)2D3 is an important autocrine link between vi-
tamin D status and insulin secretion (17). Furthermore,
an epidemiological study showed vitamin D deciency
increases the risk of metabolic syndrome (18). All these
data support vitamin D is involved in the regulation of
insulin secretion.
Vitamin D and insulin resistance
Insulin resistance is also a major risk factor for
T2DM. Some groups have reported that vitamin D
levels are inversely related to glycated hemoglobin
(HbA1c) (19) and insulin resistance (20, 21). Moreo-
ver, OGTT data from non-diabetic patients revealed an
inverse association between vitamin D and insulin resis-
tance, implying vitamin D deciency increases the risk
of insulin resistance (22). Currently, India has the largest
number of diabetic patients in the world. Although India
has enough sunshine, Indians tend to have low vitamin
D levels, which has been suggested to lead to high risk
for insulin resistance and obesity in Indians (23).
Skeletal muscle and liver are key metabolic tissues
and have a close relationship with insulin sensitivity
and glucose tolerance. Consequently, skeletal muscle
and hepatic insulin resistance are also presumed to be
chiey responsible for the development of T2DM. It is
worth noting that both these tissues express VDR, mea-
ning vitamin D plays a role in them (24, 25). However,
the specic mechanism by which vitamin D inuences
insulin sensitivity is complicated. Maestro et al. identi-
ed a vitamin D response element in the insulin recep-
tor gene promoter, discovering that 1,25-(OH)2D3 sti-
mulates its transcription and enhances insulin response
(26). These ndings demonstrate vitamin D directly
regulates insulin signaling. On the other hand, accumu-
lating evidence indicates obesity and diabetes actually
are conditions associated with chronic low level inam-
mation. Since NF-κB is able to stimulate many pro-in-
ammatory cytokines, its activation aggravates insulin
resistance. Researchers have discovered 1,25-(OH)2D3
downregulates activation of NF-κB and vitamin D de-
ciency is associated with increased inammation, sug-
gesting vitamin D also has its effects through anti-in-
ammatory actions (21, 27).
Vitamin D status and type 2 diabetes
Researchers are paying more and more attention
to the role of vitamin D in T2DM. Many studies have
demonstrated there is an association between plasma
25-(OH)D3 levels and T2DM (28). Data from the Third
National Health and Nutrition Examination Survey
(USA) indicates lower 25-(OH)D3 increases the risk of
T2DM (29). Analysis of the blood glucose and vitamin
D levels of diabetic patients showed an inverse associa-
tion between 25-(OH)D3 and T2DM (30). Interestingly,
there is a seasonal difference in the effect of vitamin D
on blood glucose. This may be partly attributed to the
lower vitamin D levels in winter (31). Moreover, vita-
min D levels in the diabetic population are signicantly
lower than in the non-diabetic population. Therefore,
researchers have proposed vitamin D levels should be
monitored in diabetic patients (32).
Other studies have investigated the prediction of
T2DM based on vitamin D levels. After a follow-up pe-
riod of 17 years, Mattila et al. found people with higher
vitamin D levels had a 40% lower risk of T2DM com-
pared to those with lower vitamin D levels (33). Ano-
ther study after a follow-up period of 22 years indicated
women have lower serum vitamin D levels than men
and the incidence of T2DM in men is 72% less than
women (34). These data suggest higher vitamin D levels
prevent incidence of T2DM.
Conclusions
Because humans can synthesize vitamin D when ex-
posed to sunlight, it had been previously thought vita-
min D deciency would be unlikely. However, even in
the sunniest regions of the world, vitamin D deciency
is common. In Qatar, which is highly sunny, researchers
demonstrated 68.8% of children had vitamin D decien-
cy (35). Moreover, studies in other countries also shown
30 to 50% of the population have lower than normal
vitamin D levels (36-39). These data reveal vitamin D
deciency has become a global health problem. Due to
the differences of diet, Asians tend to get less vitamin D
from food compared to westerners. Therefore, Asians
may be at especially high risk of vitamin D deciency
than westerners. Undoubtedly, this situation is more
37
Copyright © 2015. All rights reserved.
Y. Li and L. Zhou / VD, Obesity & Diabetes.
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serious in diabetic patients (40). We consider the work
introduced here is just the beginning in this eld. More
work remains to be done to clarify the role of vitamin D
in the development of obesity and T2DM.
Acknowledgements
This work was supported by the grants from National Na-
tural Science Foundation of China (31301947), the Fok
Ying Tong Education Foundation (141025), Guangxi
Natural Science Foundation (2014GXNSFDA118014),
Guangxi Experiment Centre of Science and Technology
(YXKT2014006), and the Scientic Research Founda-
tion of Guangxi University (XTZ130719).
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... Poor vitamin D status has become one of the most prevalent health problem in all phases of life in almost every region of the world (Li & Zhou, 2015;Ly et al., 2012). There is an ever-increasing body of evidence that vitamin D deficiency is not only pertinent to decrease intestinal calcium resorption, but also it underlines the etiology of several metabolic disorders (Avastano, Barrea, Savanelli, 2017). ...
... The most discussed mechanism is that in obese people, vitamin D is distributed into greater fat volume rather than normal weight people (Pourshahidi, 2015). On the other hand, it has been proposed that differentiation of adipocytes is halted by both 1,25 (OH) 2 D and VDR (Li & Zhou, 2015;Marcotorchino et al., 2014). Moreover, an association between adiposity phenotypes and vitamin D receptor (VDR) gene polymorphisms has been implied in numerous studies (Sollid et al., 2016).Therefore, vitamin D deficiency could result in fat augmentation which deteriorated clinical status of obesity (Walsh et al., 2017). ...
... It has been reported that 1,25(OH) 2 D suppresses lipogenesis and blocks preadipocyte differentiation by stimulating insulin-dependent gene-2 (In-sig-2) expression. With these key factors, 1,25(OH) 2 D can control adipose storage [24]. Vitamin D can affect obesity through cell signaling mechanism [25]. ...
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Background Vitamin D is classified as an immunomodulatory hormone that is synthesized because of skin exposure to sunlight. It is known to come into play during the regulation of hormone secretion, immune functions, cell proliferation, and differentiation. Its deficiency can cause many diseases and their associated pleiotropic effects. In addition, in relation to its eminent function as regards adaptive immune response and innate immune response, vitamin D level is associated with immune tolerance. Methods Literature search prior to May 2021 was conducted through selected websites, including the MEDLINE, Embase, Web of Science, Cochrane Central, www.ClinicalTrials.gov , PubMed, Science Direct, Google Scholar, and EFSA. Results Vitamin D is found effective for the regulation of hormone secretion, immune functions, and cell proliferation along with differentiation. Its role as an immune modulator is based on the presence of receptors on many immune cells and the synthesis of its active metabolite from these cells. Vitamin D, an immune system modulator, inhibits cell proliferation and stimulates cell differentiation. A fair number of immune system diseases, encompassing autoimmune disorders alongside infectious diseases, can occur because of low serum vitamin D levels. Supplementation of vitamin D has positive effects in lessening the severity nature of disease activity; there exists no consensus on the dose to be used. Conclusion It is figured out that a higher number of randomized controlled trials are essential to evaluate efficacy pertaining to clinical cases, treatment duration, type, and dose of supplementation and pathophysiology of diseases, immune system functioning, and the effect of vitamin D to be administered.
... 13,14 The recent renewed interest in vitamin D results from a worsening trend of worldwide deficiency as well as novel insights regarding its effects on glucose metabolism. 1,[15][16][17][18][19] Vitamin D deficiency was defined as a serum circulating 25(OH)D levels of <20 ng/mL based on the Endocrine Society Clinical Practice Guidelines. 20 Normal FBG was defined as blood glucose of < 110 mg/dL, 21 and elevated liver enzymes were defined as one or more measurement of AST (>34 U/L), ALT (>41 U/L), 22 and ALP (>115 U/L) in both genders. ...
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Background Vitamin D is a fat-soluble hormone that plays an important role in glycaemic control. In addition, it has a positive effect on improving liver enzyme function. Aim This study was performed to examine the effect of intramuscular injection of vitamin D on serum 25-hydroxyvitamin D [25(OH)D] levels, glycemic control, and liver enzymes in Libyan patients suffering from type 2 diabetes mellitus (T2DM) with vitamin D deficiency. Methods and Materials This cross-sectional study enrolled 100 T2DM (50 males and 50 females). Their serum 25(OH)D, fasting blood glucose (FBG), and liver enzymes were measured at the baseline and 12 weeks after treatment with vitamin D (200,000 IU) injection monthly for 3 months. Data analysis involved the estimation of mean ± standard error (SE) and comparison of means between pre and post-treatment values using paired t-test. Independent t-test was used to compare the means between males and females. The level of significance was set at p < 0.05. Results Females had a lower 25(OH)D blood levels than males at baseline (7.03 ± 0.25 ng/mL versus 7.86 ± 0.26 ng/mL, respectively p < 0.02). 25(OH)D levels in both sexes was increased significantly from 7.45 ± 0.18 ng/mL to 26.69 ± 0.24 ng/mL after 12 weeks of vitamin D injections (p < 0.001), with no significant differences between male and females. FBG levels in both sexes was significantly decreased from 144.68 ± 1.84 mg/dL to 85.96 ± 0.34 mg/dL post treatment (p < 0.001). Alanine aminotransferase (ALT) was increased from 10.24 ± 0.17 U/L at baseline to 20.34 ± 1.15 U/L post treatment (p < 0.001). Similarly, aspartate aminotransferase (AST) was increased from 11.23 ± 0.21 to 20.57 ± 0.22 U/L (p < 0.001), and alkaline phosphatase (ALP) was decreased from 124.95 ± 1.15 U/L to 111.17 ± 1.27 U/L (p < 0.001). There were no significant differences between male and female liver enzymes either pre- or post-vitamin D injections Conclusion Treatment with vitamin D injection showed a significant increase in 25(OH)D accompanied by decreased FBG and ALP levels and increased ALT and AST levels. Vitamin D levels should be monitored and adjusted in diabetic patients.
... Another mechanism involves the pleotropic effect of vitamin D. Vitamin D deficiency could link TNs with IR and obesity. Low vitamin D levels were reported in TNs [15], obesity [42], and IR [43]. Vitamin D had a pleiotropic effect and was reported to have an anti-neoplastic and anti-inflammatory effect which could be involved in thyroid cancer tumorigenesis [44]. ...
... Obesity, particularly visceral obesity, is considered as one of the most well-known risk factors for prevalence of T2DM. The concomitance of vitamin D deficiency and obesity has also been established as a possible link between prevalence of diabetes and obesity [15]. Vitamin D deficiency was related to a lower quality of life and compliance with diabetes treatment [16]. ...
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Background: Diabetes mellitus type 2 and vitamin D deficiency are both prevalent in the Saudi Arabia. Vitamin D deficiency treatment with supplements carries a risk of intoxication. Aim: The present study is aimed at elucidating the effect of exercise on modulation of metabolic status and vitamin D level in patients with type 2 diabetes mellitus (T2DM). Methods: A sum of 110 type 2 diabetic patients were voluntarily enrolled for the present investigation by dividing them into two separate groups (55 individuals for each group), the diabetic study group and diabetic control group. The diabetic study group was engaged in the training program using treadmill exercise. Laboratory parameters were monitored before and after the training program. Results: There were significant elevation in the diabetic study group compared to diabetic control group regarding postexercise vitamin D level, high-density lipoprotein (HDL) (p value ≤ 0.001, 0.045; respectively). In addition, triglycerides, low-density lipoprotein (LDL), glycosylated hemoglobin (HbA1C), and homeostatic model assessment-insulin resistance (HOMA-IR) were significantly decreased (p value < 0.001 for all mentioned parameters). Moreover, there were significant higher level in postexercise parameters as compared to preexercise level in the diabetic study group. Conclusion: The exercise training program improved the metabolic control and vitamin D level after three months of intervention.
... Vitamin D3 is a steroid hormone that plays an essential role in skeletal and non-skeletal tissues (5). Due to poor lifestyle choices, diabetes, especially DM II, has skyrocketed in recent years (6). Obesity and diabetes mellitus type II are diseases of human health. ...
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Objectives: Nowadays, vitamin D3 (VitD3) deficiency is among the most common dietary deficiencies around the world. Researchers have paid more attention to VitD3 because it is a vital element of the body and has a plausible relationship with various diseases such as diabetes mellitus type II. This study was conducted to examine the prevalence of vitamin D3 deficiency and its relationship with blood sugar levels in people with diabetes undergoing coronary artery bypass grafting (CABG). Methods: An observational study was conducted in 2017 in Shahid Madani Hospital, Tabriz, Iran, for 8 months. Due to the use of census sampling, only 115 patients with diabetes and open-heart surgery were enrolled in the study. A questionnaire collected information on the participants' demographics, medical history, VitD3 levels and blood glucose levels. Data were analyzed using SPSS ver. 25. Independent t-test was used to compare quantitative data, and chi-square test was used to compare categorical variables. Results: One hundred and fifteen out of 348 patients who had CABG surgery were diabetic. Moreover, 24.7% of patients with diabetes had VitD3 deficiency. The results of the coefficient-correlation test indicated that there was a significant relationship between the mean blood glucose level and VitD3 level (p < 0.05). Conclusions: The results of this study suggest that patients with diabetes can improve their blood glucose control after CABG surgery by taking sufficient VitD3. Therefore, it should be considered as a principle of the hospital operation to prescribe VitD3 prior to surgery for these patients.
... The age-related increase in insulin resistance is associated with adiposity, sarcopenia, and physical inactivity which has also been identified as risk factors for dysglycemia [18]. Furthermore, vitamin D deficiency is one of the factors accelerating insulin resistance, obesity and DM [19][20][21]. The ADA recommends to screen individuals having high BMI with other risk factors and all others aged ≥ 45 years for dysglycemia at a minimum of three-year intervals using one of the screening tools such as FPG, OGTT, or HbA 1C [17]. ...
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Introduction Dysglycemia includes prediabetes and diabetes. We aimed to study the prevalence of dysglycemia, and its associations with age and body mass index (BMI) among community dwelling adults in Sri Lanka. Methods The prevalence of dysglycemic state (FPG > 100 mg/dL) and its associations with age and BMI in males and females were estimated. The association between gender and glycemic status in different BMI ranges and age groups were estimated. The optimal cutoff points of BMI to determine the risk of dysglycemia in both genders were calculated. Results Prevalence of prediabetes and diabetes of females were 25.3% and 16.4% and of males were 26.2% and 17.4% respectively. Dysglycemia showed a significant positive correlation with age in both genders and a significant positive correlation with BMI in males (p < 0.05). Aging (OR = 1.05, CI 1.02-1.08, p < 0.001) and increasing BMI (OR = 1.10, CI 1.05-1.15, p < 0.001) of males and aging (OR = 1.04, CI 1.02-1.06, p < 0.001) of females are significantly associated with dysglycemia. The optimal cutoff point of BMI for males was 22.86 kg/m 2 (sensitivity 76.6%, specificity 53.9%) to determine the risk of dysglycemia. Conclusions Four out of ten adults in the screened population were dysglycemic. An increase in BMI is significantly associated with dysglycemic status in males compared to females. The recommended cutoff value of BMI as 23 kg/m 2 for South Asian population to categorize overweight individuals has an adequate sensitivity to recognize dysglycemic adult males but not the females in this community.
... The age-related increase in insulin resistance is associated with adiposity, sarcopenia, and physical inactivity which has also been identified as risk factors for dysglycemia [18]. Furthermore, vitamin D deficiency is one of the factors accelerating insulin resistance, obesity and DM [19][20][21]. The ADA recommends to screen individuals having high BMI with other risk factors and all others aged ≥ 45 years for dysglycemia at a minimum of three-year intervals using one of the screening tools such as FPG, OGTT, or HbA 1C [17]. ...
Article
IntroductionDysglycemia includes prediabetes and diabetes. We aimed to study the prevalence of dysglycemia, and its associations with age and body mass index (BMI) among community dwelling adults in Sri Lanka.Methods The prevalence of dysglycemic state (FPG > 100 mg/dL) and its associations with age and BMI in males and females were estimated. The association between gender and glycemic status in different BMI ranges and age groups were estimated. The optimal cut-off points of BMI to determine the risk of dysglycemia in both genders were calculated.ResultsPrevalence of prediabetes and diabetes of females were 25.3% and 16.4% and of males were 26.2% and 17.4% respectively. Dysglycemia showed a significant positive correlation with age in both genders and a significant positive correlation with BMI in males (p < 0.05). Aging (OR = 1.05, CI 1.02–1.08, p < 0.001) and increasing BMI (OR = 1.10, CI 1.05–1.15, p < 0.001) of males and aging (OR = 1.04, CI 1.02–1.06, p < 0.001) of females are significantly associated with dysglycemia. The optimal cut-off point of BMI for males was 22.86 kg/m2 (sensitivity 76.6%, specificity 53.9%) to determine the risk of dysglycemia.Conclusions Four out of ten adults in the screened population were dysglycemic. An increase in BMI is significantly associated with dysglycemic status in males compared to females. The recommended cut-off value of BMI as 23 kg/m2 for South Asian population to categorize overweight individuals has an adequate sensitivity to recognize dysglycemic adult males but not the females in this community.
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Background: The purpose of this study was to find correlation between vitamin D, Physical exercise on glycaemic control in patients of type2DM. Methods: The study was conducted from November 2019 to December 2020 among subjects above 40 years of age at sub-district hospital Sopore, North Kashmir. Total 400 patients diagnosed with diabetes were registered for the study. Questionnaire containing relevant patient information was collected at regular intervals. Statistical analysis were performed. Results: Biochemistry values in the studied subjects with Type2DM compared to healthy controls in the study revealed that fasting glucose level,HbA1c,LDL,triglycerides,uric acid were higher inT2DM group compared to the control group. The results of our study showed that Vitamin D deficiency, lack of physical exercise, family history of T2DM, hypertension and smoking were significant predictors of diabetes. In Type2DM patients, mean vitamin D value was 21.45ng/ml opposed to 40ng/ml in the control group. Also physical activity was found to be higher in control group when compared to cases with p -value less than 0.00001. Also family history of DM was significantly higher in cases when compared to control group with p-value of 0.044.There was also statistically significant difference when parameters like HTN and smoking were compared (both higher in cases as against the control group) between two groups with p value 0.044 and 0.029 respectively. Conclusion: Vit D, physical exercise,family history of diabetes may be contributing factors for the rising burden of diabetes globally and in India.We need to take cognisance of the factors leading to the rising global burden of DM and take appropriate and necessary measures to stop this growing menace.
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Adult women are more likely to be obese than men. Moreover, there is evidence that obesity is a risk factor for increased insulin resistance (IR) and hypovitaminosis D (VITD), conditions related to metabolic and endocrinologic disturbance. We performed a cross-sectional study with 103 women diagnosed with obesity, recruited between 2009 and 2013, in an obesity referral outpatient clinic in Bahia, Brazil. Laboratory and clinical characteristics were compared between the groups according to the degree of obesity (I, II and III), and levels of 25-hydroxyvitamin D [25(OH)D] were used to define the VITD status (insufficiency and no insufficiency). We calculated the homeostatic model assessment-IR (HOMA-IR) index to assess insulin resistance in the groups. Our analyses revealed that HOMA-IR values and VITD levels were inversely correlated. Furthermore, we observed a distinct expression profile of values of laboratory markers according to 25(OH)D levels. Negative correlations were found between HOMA-IR and body mass index (BMI) in VITD insufficient participants but not in those with the sufficiency. Furthermore, multivariate regression demonstrated independent associations between lower levels of 25(OH)D and increased values of HOMA-IR. These findings suggests that lower levels of VITD are strongly associated with the increased IR in obese women. Keywords: vitamin D; obesity; women; insulin resistance; HOMA-IR
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Context: The relationship between 25-hydroxyvitamin D [25(OH)D] and obesity and type 2 diabetes is not completely understood. Vitamin D receptor (VDR) expression in adipose tissue (AT) is related to obesity and might be regulated by 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. Objective: To analyze serum 25(OH)D and VDR gene expression in AT according to body mass index (BMI) and glycemic status and the effect of 1,25(OH)2D3 on AT according to BMI. Design and patients: Two cohorts were studied: 1) 118 subjects classified according to their BMI (lean, overweight, obese, or morbidly obese [MO]) and their glycemic status (normoglycemic [NG] and prediabetic and diabetic [P&D]); and 2) 30 obese subjects (BMI > 30 kg/m(2)) classified as NG and P&D. VDR gene expression was analyzed during preadipocyte differentiation and in vitro stimulation with 1,25(OH)2D3 of AT explants from donors with different BMI values. Setting: University Hospital. Main outcome measures: Serum 25(OH)D, parathyroid hormone (PTH), and AT VDR gene expression. Results: 25(OH)D levels were lower in P&D than NG subjects, significantly so in the lean and MO groups (P < .05). 25(OH)D levels correlated negatively with homeostasis model of assessment for insulin resistance (HOMA-IR) (r = -0.200; P = .032) and glucose (r = -0.295; P = .001), but not with BMI. VDR gene expression was higher in MO than in the other BMI groups (P < .05). 1,25(OH)2D3 increased VDR gene expression in AT from obese patients (P < .05) but not from lean subjects. Conclusions: 25(OH)D levels are diminished in P&D compared to NG subjects, independently of BMI, and are closely related to glucose metabolism variables, suggesting that vitamin D deficiency is associated more with carbohydrate metabolism than with obesity. Moreover, AT has a different response to 1,25(OH)2D3 depending on the degree of obesity.
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The aim of this study was to investigate the relationship between serum 25-hydroxy vitamin D (25-OHD) and insulin sensitivity and β-cell function in newly diagnosed type 2 diabetes. 395 newly diagnosed type 2 diabetes patients were enrolled in this study. Venous blood samples were collected at 0 min, 30 min, and 120 min of OGTT to measure serum glucose and insulin. Matsuda ISI and HOMA-IR were used to determine insulin sensitivity. The ratio of 0-120 min area under curve of insulin to glucose (insulin release index, INSR) was calculated as surrogate index of β-cell insulin secretion function. The products of insulin secretion indices multiplied by Matsuda insulin sensitivity index were used as disposition indices. Patients were divided into three groups according to tertiles (T1, T2, and T3) of 25-OHD concentration. There was significant difference among three groups for HOMA-IR, Matsuda ISI, and INSR. HOMA-IR, Matsuda ISI, INSR, and DI were undifferentiated among three groups in male patients. But HOMA-IR, Matsuda ISI, and INSR were significantly different among three groups in female patients after being adjusted by confounding factors. In conclusion, serum 25-OHD is associated with insulin sensitivity and β-cell function for female newly diagnosed type 2 diabetes patients, and the association is ambiguous in males.
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Vitamin D deficiency is associated with a range of muscle disorders including myalgia, muscle weakness and falls. In humans, polymorphisms of the vitamin D receptor (VDR) gene are associated with variations in muscle strength and in mice, genetic ablation of VDR results in muscle fiber atrophy and motor deficits. However, mechanisms by which VDR regulates muscle function and morphology remain unclear. A crucial question is whether VDR is expressed in skeletal muscle and directly alters muscle physiology. Using PCR, western blot and immunohistochemistry (VDR-D6 antibody), we detected VDR in murine quadriceps muscle. Detection by western blot was dependent on the use of hyperosmolar lysis buffer. Levels of VDR in muscle were low compared to duodenum and dropped progressively with age. Two in vitro models, C2C12 and primary myotubes, displayed dose- and time-dependent increases in expression of both VDR and its target gene CYP24A1 following 1,25(OH)2D treatment. Primary myotubes also expressed functional CYP27B1 as demonstrated by luciferase reporter studies, supporting an auto-regulatory vitamin D-endocrine system in muscle. Myofibers isolated from mice retained (3)H-25OHD3 and this increased following 3 hrs pre-treatment with 1,25(OH)2D (0.1 nM). No such response was seen in myofibers from VDR-knockout mice. In summary, vitamin D receptor is expressed in skeletal muscle, and vitamin D regulates gene expression and modulates ligand-dependent uptake of 25OHD3 in primary myofibers.
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Unlabelled: Evidence suggests an association between low serum 25-hydroxy-vitamin D(3) [25(OH)D(3) ] levels and the presence and prognosis of liver disease. Vitamin D receptor (VDR) has been widely detected in the liver, but its expression in the course of liver disease has never been investigated. We evaluated the hepatic expression of VDR along with that of vitamin D 25-hydroxylases in patients with nonalcoholic steatohepatitis (NASH) or chronic hepatitis C (CHC) and its relationship with hepatic histological features and serum 25(OH)D(3) levels. We evaluated 61 patients (25 NASH and 36 CHC) who had undergone liver biopsy for clinical purposes and 20 subjects without liver disease. Serum 25(OH)D(3) was measured via colorimetric assay. Expression of VDR, CYP2R1, and CYP27A1 was evaluated via immunohistochemistry in hepatocytes, cholangiocytes, and liver inflammatory cells. Parenchymal and inflammatory cells from liver biopsies of patients with NASH and CHC expressed VDR, CYP2R1, and CYP27A1. In NASH patients, VDR expression on cholangiocytes was inversely correlated with steatosis severity (P < 0.02), lobular inflammation (P < 0.01), and nonalcoholic fatty liver disease score (P < 0.03). Moreover, expression of CYP2R1 in hepatocytes correlated strongly with VDR positivity on liver inflammatory cells. In CHC subjects, fibrosis stage was associated with low hepatic CYP27A1 expression, whereas portal inflammation was significantly higher in patients with VDR-negative inflammatory cells (P < 0.009) and low VDR expression in hepatocytes (P < 0.03). Conclusion: VDR is widely expressed in the liver and inflammatory cells of chronic liver disease patients and its expression is negatively associated with the severity of liver histology in both NASH and CHC patients. These data suggest that vitamin D/VDR system may play a role in the progression of metabolic and viral chronic liver damage. (HEPATOLOGY 2012;56:2180-2187).
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Aims/hypothesis We aimed to investigate the impact of maternal vitamin D deficiency during pregnancy on insulin resistance in male offspring and examine its mechanism. Methods Pregnant Sprague–Dawley rats were maintained on a vitamin-D-free diet with ultraviolet-free light during pregnancy (early-VDD group). Insulin resistance in the male offspring was assessed by HOMA-IR, OGTT and euglycaemic clamp. NEFA, oxidative stress and inflammation levels were estimated as risk factors for insulin resistance. DNA methylation was examined by bisulfate sequencing PCR analysis. Luciferase reporter assay was performed to validate the effect of DNA methylation. Results The offspring in the early-VDD group had significantly higher fasting insulin and HOMA-IR levels, markedly reduced glucose tolerance and significantly lower tissue sensitivity to exogenous insulin at 16 weeks (all p
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Previous studies have yielded conflicting findings on the relationship between low vitamin D (25-OH-D) and impaired glucose homeostasis. In this context, we hypothesized that combined assessment of 25-OH-D with its regulator parathyroid hormone (PTH) may be required for optimal evaluation of the impact of vitamin D status on glucose metabolism. Thus, we evaluated the prospective associations of 25-OH-D and PTH at 3-months postpartum with beta-cell function (Insulin Secretion-Sensitivity Index-2 (ISSI-2)), insulin sensitivity (Matsuda index) and glycemia at 12-months postpartum in 494 women undergoing serial metabolic characterization. Notably, 32% of those with pre-diabetes/diabetes at 12-months postpartum had both vitamin D deficiency and PTH in the highest tertile at 3-months postpartum. On multiple-adjusted linear regression analyses, vitamin D deficiency/insufficiency with PTH in the highest tertile at 3-months independently predicted poorer beta-cell function (P=0.03) and insulin sensitivity (P=0.01), and increased fasting (P=0.03) and 2-hour glucose (P=0.002) at 12-months postpartum. In contrast, vitamin D deficiency/insufficiency with lower PTH did not predict these outcomes. In conclusion, only vitamin D deficiency/insufficiency with increased PTH is an independent predictor of beta-cell dysfunction, insulin resistance and glycemia, highlighting the need for consideration of the PTH/25-OH-D axis when studying the impact of vitamin D status on glucose homeostasis.
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Modulation of apoptosis is emerging as a promising antiobesity strategy because removal of adipocytes through this process will result in reducing body fat. Effects of vitamin D on apoptosis are mediated via multiple signaling pathways that involve common regulators and effectors converging on cellular Ca(2+) . We have previously shown that 1,25-dihydroxyvitamin D3 induces the Ca(2+) signal associated with activation of Ca(2+) -dependent apoptotic proteases in mature adipocytes. In this study, a diet-induced obesity (DIO) mouse model was used to evaluate the role of vitamin D and calcium in adiposity. DIO mice fed high vitamin D3 , high Ca, and high D3 plus high Ca diets demonstrated a decreased body and fat weight gain, improved markers of adiposity and vitamin D status (plasma concentrations of glucose, insulin, adiponectin, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, parathyroid hormone (PTH)), but an increased plasma Ca(2+) . High D3 and Ca intakes were associated with induction of apoptosis and activation of Ca(2+) -dependent apoptotic proteases, calpain and caspase-12, in adipose tissue of DIO mice. The combination of D3 plus Ca was more effective than D3 or Ca alone in decreasing adiposity. The results imply that high vitamin D and Ca intakes activate the Ca(2+) -mediated apoptotic pathway in adipose tissue. Targeting this pathway with vitamin D and Ca supplementation could contribute to the prevention and treatment of obesity. However, this potentially effective and affordable approach needs to be evaluated from a safety point of view.