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Vitamin D Deficiency in Obese Children and Its Relationship to Insulin Resistance and Adipokines  [PDF]
Christian L. Roth,Clinton Elfers,Mario Kratz,Andrew N. Hoofnagle
Journal of Obesity , 2011, DOI: 10.1155/2011/495101
Abstract: Low-serum concentrations of 25-hydroxyvitamin D [25(OH)D] are associated with insulin resistance in adults. Less data are available in pediatric populations. Serum 25(OH)D serum concentrations were assessed in 125 obese and 31 nonobese children (age ?y, range 6–16?y, 49% male) living in Bonn, Germany. The relationship between 25(OH)D, measured by liquid chromatography-tandem mass spectrometry, and measures of insulin sensitivity and adipokines adiponectin and resistin were analyzed. Seventy-six % of subjects were 25(OH)D deficient (<20?ng/mL). Higher insulin, homeostasis model assessment-insulin resistance (HOMA-IR , ), and hemoglobin A1c ( ) as well as lower quantitative insulin-sensitivity check index (QUICKI , ) values were found in obese children with lower 25(OH)D concentrations even after adjustment for gender, age, and body mass index. Furthermore, 25(OH)D correlated significantly with adiponectin, but not with resistin. Our results suggest that hypovitaminosis D is a risk factor for developing insulin resistance independent of adiposity. 1. Introduction Obesity is the primary risk factor for the development of impaired glucose tolerance, type 2 diabetes mellitus, and the metabolic syndrome. The prevalence of type 2 diabetes among children and adolescents has increased at an alarming rate during the last two decades, with the highest prevalence among African American adolescents [1]. Studies have shown that lifestyle factors contribute to this development. As obese children are usually sedentary and therefore less likely to play outdoors, their exposure to sunlight may be limited [2]. In addition, unhealthy high caloric food might be low in mineral and vitamin content [3, 4]. Both represent risk factors for developing vitamin D deficiency. Additionally, bioavailability of vitamin D in obese subjects might be low because of its deposition in a fat tissue [5] and higher body fat mass might be associated with a higher risk of vitamin D deficiency [6]. Vitamin D plays a central role in skeletal health. Additionally, vitamin D might also provide protection against major health problems such as autoimmune disease, cardiometabolic disease, and cancer [7, 8]. In a recent population study, subjects with cardiovascular disease had a greater frequency of vitamin D deficiency (defined as 25-hydroxyvitamin D [25(OH)D] levels <20?ng/mL) than those without [9]. Beta-cell function improves after the administration of vitamin D to animals [10–12] and humans [13] with vitamin D deficiency. In adult humans, low-serum 25(OH)D levels have been correlated with
The effect of vitamin D on insulin resistance in patients with type 2 diabetes  [cached]
Talaei Afsaneh,Mohamadi Mahnaz,Adgi Zahra
Diabetology & Metabolic Syndrome , 2013, DOI: 10.1186/1758-5996-5-8
Abstract: Introduction Over the past decade, numerous non-skeletal diseases have been reported to be associated with vitamin D deficiency including type2 diabetes mellitus (T2DM). Different studies provide evidence that vitamin D may play a functional role in glucose tolerance through its effects on insulin secretion and insulin sensitivity. This study evaluates the effects of vitamin D supplementation on insulin resistance in T2DM. Method Through a before-after study, 100 patients with T2DM, 30–70 years old, were recruited from an Arak diabetes clinic as consecutive attenders. Participants were assessed for clinical and biochemistry. Serum insulin and, 25(OH)D concentration, and HOMA-IR was calculated. All measurements were performed at the beginning and the end of the study. Patients received 50,000 unit of vitamin D3 orally per week for eight weeks, Statistical analysis was made using SPSS17. The results were analyzed by descriptive tests, and a comparison between variables were made using paired T-tests or Wilcoxon tests, as appropriate. Results 100 participants including 70 women (70%) and 30 men (30%) took part in the study. All results were presented as Mean±SD, or medians of non-normally distributed. 24% of the participants were Vitamin D deficient {serum 25(OH)D ≤ 20 ng/ml(50 nmol/l)}. Mean serum 25 (OH) D concentration was 43.03± 19.28 ng/ml (107.5±48.2 nmol/l). The results at baseline and at the end, for FPG were 138.48±36.74 and 131.02±39 mg/dl (P=0.05), for insulin, 10.76±9.46 and 8.6±8.25 μIu/ml (P=0.028) and for HOMA-IR, 3.57±3.18 and 2.89±3.28 (P=0.008) respectively. Conclusion Our data showed significant improvements in serum FPG, insulin and in HOMA-IR after treatment with vitamin D, suggested that vitamin D supplementation could reduce insulin resistance in T2DM.
The Effect of Puberty on Interaction between Vitamin D Status and Insulin Resistance in Obese Asian-Indian Children  [PDF]
Rajesh Khadgawat,Tushanth Thomas,Monita Gahlot,Nikhil Tandon,Vin Tangpricha,Deepak Khandelwal,Nandita Gupta
International Journal of Endocrinology , 2012, DOI: 10.1155/2012/173581
Abstract: To study the effect of puberty on the relationship between serum 25-hydroxyvitamin D (25(OH)D) and parameters of insulin kinetics in obese Asian-Indian children. Material and Methods. The study population included 62 obese Asian-Indian children and adolescents in the age group of 6–17 years. Blood glucose, serum insulin, and serum 25(OH)D were measured. Total body fat was measured by dual energy X-ray absorptiometry. Indices of insulin resistance (HOMA-IR, AUC for insulin) and sensitivity (WBISI) were calculated after oral glucose tolerance test. Result. A total of 62 subjects (35 boys; mean age = 13.0 ± 3 years; BMI = 29.3 ± 4.8?kg/sq?M; 19 subjects in Tanner stage 1, 11 in stage 2, 6 in stage 3, 3 in stage 4, and 23 subjects in Tanner stage 5) were studied. All study subjects were vitamin D deficient with a mean serum 25(OH)D of 8.5 ± 4.2?ng/mL. No significant relationship was observed between serum 25(OH)D and parameters of insulin kinetics in prepubertal children. However, a significant inverse correlation was seen between serum 25(OH)D and HOMAIR ( , ) in postpubertal subjects. Conclusion. The relationship between vitamin D status and parameters of insulin kinetics are affected by puberty. 1. Introduction Vitamin D deficiency was once thought to exclusively affect bone metabolism, but now there is ample evidence of its role in many other conditions including metabolic syndrome, autoimmune diseases, and cancer [1]. Vitamin D receptors are recognized to be in numerous extraskeletal tissues, such as pancreas and muscle [2]. A systematic review by Pittas and colleagues [3] reported that vitamin D may have a beneficial effect on the action of insulin, either directly or indirectly. Several observational studies in adults, including the Framingham Heart Study [4], have reported an inverse association between vitamin D status and insulin resistance. However, data from children and adolescents do not consistently report this inverse relationship [5–10]. Even in studies reporting this association in adolescents and children, the strength of association has been found to be very modest [6]. Further, none of the studies in adolescents have studied the effect of puberty on this association. A fall in insulin sensitivity with compensatory increase in insulin secretion has been reported in puberty [11, 12]. High prevalence of cardiometabolic risk factors, including insulin resistance (64.8% of normal weight children had at least one cardiometabolic abnormality), even in healthy young children of normal weight, has been reported in Indian children and adolescents
Role of Vitamin D in Insulin Secretion and Insulin Sensitivity for Glucose Homeostasis  [PDF]
Jessica A. Alvarez,Ambika Ashraf
International Journal of Endocrinology , 2010, DOI: 10.1155/2010/351385
Abstract: Vitamin D functions are not limited to skeletal health benefits and may extend to preservation of insulin secretion and insulin sensitivity. This review summarizes the literature related to potential vitamin D influences on glucose homeostasis and insulin sensitivity. Cross-sectional data provide some evidence that circulating 25-hydroxyvitamin D (25(OH)D) is inversely associated with insulin resistance, although direct measurements of insulin sensitivity are required for confirmation. Reported associations with insulin secretion, however, are contradictory. Available prospective studies support a protective influence of high 25(OH)D concentrations on type 2 diabetes mellitus risk. There is a general lack of consistency in vitamin D intervention outcomes on insulin secretion and sensitivity, likely due to differences in subject populations, length of interventions, and forms of vitamin D supplementation. Vitamin D receptor gene polymorphisms and vitamin D interactions with the insulin like growth factor system may further influence glucose homeostasis. The ambiguity of optimal vitamin D dosing regimens and optimal therapeutic concentrations of serum 25(OH)D limit available intervention studies. Future studies, including cross-sectional and prospective, should be performed in populations at high risk for both vitamin D deficiency and type 2 diabetes mellitus. Well-designed, placebo-controlled, randomized intervention studies are required to establish a true protective influence of vitamin D on glucose homeostasis. 1. Introduction Over the last decade, numerous nonskeletal disease associations have been reported with vitamin D deficiency, including type 2 diabetes mellitus (T2DM). Circulating 25-hydroxyvitamin D (25(OH)D) concentrations are considered an indicator of vitamin D status [1, 2]. Compared to healthy controls, subjects with T2DM have been observed to have significantly lower circulating 25(OH)D concentrations [3–5]. Perhaps not coincidently, both vitamin D deficiency and T2DM share the same risk factors, including African-American, Asian, or Hispanic ethnicity, increased adiposity, age, and physical inactivity (which may translate to decreased time spent outdoors or reduced sun exposure) [6, 7]. Seasonal variations in glucose and insulin concentrations have been reported [8], which may correlate with seasonal variations in 25(OH)D concentrations [9]. Although not within the scope of this review, vitamin D has likewise been implicated in the development of type 1 diabetes mellitus due to its modulation of the immune system [10]. T2DM is
Effect of vitamin D on insulin resistance and anthropometric parameters in Type 2 diabetes; a randomized double-blind clinical trial
Ramin Heshmat, Ozra Tabatabaei-Malazy, Shabnam Abbaszadeh-Ahranjani, Samimeh Shahbazi, Ghazal Khooshehchin, Fathemeh Bandarian, Bagher Larijani
DARU Journal of Pharmaceutical Sciences , 2012, DOI: 10.1186/2008-2231-20-10
Abstract: This randomized double-blind clinical trial was conducted with 42 diabetic patients in two groups; intervention group with single intramuscular injection of 300,000 International Unit (IU) of vitamin D3 and the placebo group. After recording demographic and anthropometric factors (waist circumference, blood pressure and body mass index), fasting blood samples was taken for measurement of blood glucose, 25-hydroxyvitamin D3 (25-OHD3), insulin, glycosylated hemoglobin A1c (HbA1c) and estimation of Homeostasis Model Assessment Index (HOMA) in two times; before study and after three months.Two groups had similar baseline characteristics (each group?=?21 subjects). Three months after vitamin D injection, HbA1c, anthropometric factors and HOMA index in intervention group stayed constant, however, serum 25- OHD3 was significantly increased (p?=?0.007).The present data is not convincing and further studies with large sample sizes are needed to show the definite effect of injection of vitamin D on control of diabetes and its risk.Prevalence of type 2 diabetes mellitus (T2DM) is increasing worldwide. Nowadays over 360 million people are suffering from diabetes and it is expected that its prevalence reach a staggering 552 million by 2030 [1]. T2DM is defined by impaired glucose tolerance, chronic hyperglycemia, altered insulin secretion, and complications that come from induction of oxidative stress [2]. One of novel strategy toward prevention and control of T2DM is vitamin D supplementation. Besides the role of vitamin D in calcium homeostasis and bone metabolism, other effects also have been proposed for this mineral. Vitamin D is essential for normal insulin secretion in response to glucose and also for maintenance of glucose tolerance [3-6]. In a study performed on 126 healthy adults with normal blood glucose, an association between vitamin D deficiency with beta cell dysfunction and insulin resistance was observed [7]. Such an association has also been established in type
Lipoprotein lipase links vitamin D, insulin resistance, and type 2 diabetes: a cross-sectional epidemiological study
Yifan Huang, Xiaoxia Li, Maoqing Wang, Hua Ning, Lima A, Ying Li, Changhao Sun
Cardiovascular Diabetology , 2013, DOI: 10.1186/1475-2840-12-17
Abstract: The study cohort consisted of 2708 subjects (1326 males, 1382 females; mean age 48.5 ± 12.6?years) in main communities of Harbin, China. Serum 25(OH)D, LPL, free fatty acids (FFAs), fasting glucose (FG), fasting insulin, lipid profile, apoA and apoB concentrations were measured.Serum 25(OH)D concentration was positively associated with LPL (β = 0.168, P < 0.001). LPL was inversely associated with IR and T2D. Subjects in the lowest quartile of LPL had the highest risk of IR [odds ratio (OR) = 1.85, 95% CI = 1.22-2.68] and T2D (OR = 1.65, 95% CI = 1.14-2.38). Serum 25(OH)D was also inversely associated with IR and T2D. Vitamin D deficiency [25(OH)D < 20?ng/ml] was associated with an increasing risk of IR (OR = 1.91, 95% CI = 1.23-2.76) and T2D (OR = 2.06, 95% CI = 1.37-3.24). The associations of 25(OH)D with IR and T2D were attenuated by further adjustment for LPL.LPL is associated with serum 25(OH)D, IR and T2D in the Chinese population. These results suggest a potential mediating role of LPL in the associations of 25(OH)D with IR and T2D.Lipoprotein lipase (LPL) is a member of the so-called lipase superfamily which includes hepatic lipase, pancreatic lipase and LPL itself [1]. Although it is mainly synthesized by the parenchymal cells in adipose, skeletal and cardiac muscle, LPL has its physiological site of action at the capillary endothelial cell surface where the enzyme catalyzes the lipolysis of triglyceride (TG) to provide free fatty acids (FFAs) and 2-monoacylglycerol for tissue utilization [2,3]. Therefore, LPL plays a central role in lipid metabolism and is widely distributed in various tissues. In addition to its effect on the lipid metabolism, LPL is also directly or indirectly implicated in some pathophysiological conditions such as insulin resistance (IR) and type 2 diabetes (T2D). Reduction of LPL is observed in patients with T2D and individuals with IR [4-6]. Low LPL activity accompanied by high TG was observed in diabetic dyslipidemia [7].In addition
Vitamin D Deficiency in Obese Children and Its Relationship to Insulin Resistance and Adipokines  [PDF]
Christian L. Roth,Clinton Elfers,Mario Kratz,Andrew N. Hoofnagle
Journal of Obesity , 2011, DOI: 10.1155/2011/495101
Abstract: Low-serum concentrations of 25-hydroxyvitamin D [25(OH)D] are associated with insulin resistance in adults. Less data are available in pediatric populations. Serum 25(OH)D serum concentrations were assessed in 125 obese and 31 nonobese children (age 11.9±2.7 y, range 6–16 y, 49% male) living in Bonn, Germany. The relationship between 25(OH)D, measured by liquid chromatography-tandem mass spectrometry, and measures of insulin sensitivity and adipokines adiponectin and resistin were analyzed. Seventy-six % of subjects were 25(OH)D deficient (<20 ng/mL). Higher insulin, homeostasis model assessment-insulin resistance (HOMA-IR =?0.269, =0.023), and hemoglobin A1c (HbA1c) as well as lower quantitative insulin-sensitivity check index (QUICKI =0.264, =0.030) values were found in obese children with lower 25(OH)D concentrations even after adjustment for gender, age, and body mass index. Furthermore, 25(OH)D correlated significantly with adiponectin, but not with resistin. Our results suggest that hypovitaminosis D is a risk factor for developing insulin resistance independent of adiposity.
The vitamin D receptor polymorphism in the translation initiation codon is a risk factor for insulin resistance in glucose tolerant Caucasians
Ken C Chiu, Lee-Ming Chuang, Carol Yoon
BMC Medical Genetics , 2001, DOI: 10.1186/1471-2350-2-2
Abstract: There were 18 FF, 21 Ff, and 10 ff subjects. Since only 10 ff subjects were identified, they were pooled with the Ff subjects during analyses. The FF and Ff/ff groups had similar glucose levels at each time point before and after a glucose challenge. The Ff/ff group had higher insulin levels than the FF group at fasting (P=0.006), 30 minutes (P=0.009), 60 minutes (P=0.049), and 90 minutes (P=0.042). Furthermore, the Ff/ff group also had a larger insulin area under the curve than the FF group (P=0.009). While no difference was noted in %B, the Ff/ff group had a lower %S than the FF group (0.53 vs. 0.78, P=0.006). A stepwise regression analysis confirmed that the Fok I polymorphism was an independent determinant for %S, accounting for 29.3% of variation in %S when combined with waist-hip ratio.We report that the Fok I polymorphism at the VDR gene locus is associated with insulin sensitivity, but has no influence on beta cell function in healthy Caucasians. Although this polymorphism has been shown to affect the activation of vitamin D-dependent transcription, the molecular basis of the association between this polymorphism and insulin resistance remains to be determined.Although conflicting findings about bone mineral density (BMD) in patients with type 2 diabetes have been reported, there are substantial data which support the notion that type 2 diabetes is associated with increased BMD [1,2,3]. The Rotterdam Study [2], which involved 5,931 subjects, including 243 men and 355 women with type 2 diabetes, provides the most convincing evidence. They found that diabetic men and women had increased BMD independent of age, obesity, the use of estrogen, thiazide, or loop diuretics, impairment in the ability of daily living, and smoking [2]. Furthermore, hyperinsulinemia has been reported to be associated with an increased BMD in diabetic [4] and non-diabetic subjects [5]. From the Rancho Bernardo Study [5], the level of fasting insulin was significantly and positively assoc
D-Chiro-Inositol – Its Functional Role in Insulin Action and its Deficit in Insulin Resistance  [PDF]
Joseph Larner
Experimental Diabetes Research , 2002, DOI: 10.1080/15604280212528
Abstract: In this review we discuss the biological significance of D-chiro-inositol, originally discovered as a component of a putative mediator of intracellular insulin action, where as a putative mediator, it accelerates the dephosphorylation of glycogen synthase and pyruvate dehydrogenase, rate limiting enzymes of non-oxidative and oxidative glucose disposal.
Evidence to Support a Putative Role for Insulin Resistance in Chronic Kidney Disease
W Shehab-Eldin, A Ragheb, S Gazarin, A Shoker
Arab Journal of Nephrology and Transplantation , 2009,
Abstract: Introduction: The primary cause of morbidity and mortality in the renal patient is a cardiovascular event. Insulin resistance (IR) contributes to this event by increasing cardiovascular disease (CVD) and accelerating rates of decline in kidney function. Here we review the historical background of IR in patients with chronic kidney disease (CKD) and present evidence for a role of IR in accelerating cardiovascular and renal diseases. Review: The high prevalence of IR in CKD patients is well documented. It is suggested that increased IR in the renal patient is caused by uremia as well as by other known factors in the general population. Patients with CKD have an alarmingly high risk for cardiovascular morbidity and mortality. There is overwhelming evidence to support a role for IR in increased CVD morbidity and mortality in the general population, which is likely to extend to CKD patients. Some of the traditional treatment measures for IR, such as metformin, may not be applicable to the renal patient. Other options include weight reduction, exercise, treatment of anemia to improve exercise tolerance, treatment of vitamin D deficiency, thiazolidinediones, and dialysis. IR is estimated by studying the relationship between blood glucose and the concomitant insulin level. Such measurement may help identify patients at increased risk for future cardiovascular events and guide treatment measures. Conclusion: Sufficient evidence supports the increased prevalence of IR in kidney patients. Treating IR may retard the progression of CKD and decrease the incidence of cardiovascular events in this high risk population.
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