Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomized controlled trial

Belenchia, Anthony; Tosh, Aneesh K.; Hillman, Laura S.; Peterson, Carol A.

doi:10.3945/ajcn.112.050013

Cited by 282 publications

(280 citation statements)

References 46 publications

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“…Korean girls with low VD levels could be at increased risk for metabolic disorders. The study supports the favorable effects of vitamin D supplementation on reducing insulin resistance [34][35][36]. A lower VD level could be a risk factor for developing insulin resistance and type 2 diabetes in the obese population.…”

Section: Discussionsupporting

confidence: 55%

Low Vitamin D Serum Levels May Be a Modifiable Risk Factor for Obesity and Cognitive Impairment in Middle-Age Egyptian Women

Kazem¹,

Moaty²,

El-Shebini³

et al. 2014

Open Access Maced J Med Sci

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SUBJECTS AND METHODS:This study included 2 groups, Group-1(cases) consists of 120 obese females and Group-2 (controls) consists of 30 non-obese females. The included females were subjected to full clinical examination, anthropometric measurements and Kendrick Battery for evaluation of cognitive functions (short term memory and attention). Evaluation of serum Vitamin D, Parathyroid hormone, C-peptide and fasting blood glucose were done. The obese group was put on a balanced low caloric diet (900-1000 K Calories/day) for 2 months, where reevaluation was performed. RESULTS:Comparing obese group with non-obese control group revealed significant lower mean level of serum vitamin D associated with significant lower cognitive functions test and higher fasting blood glucose. After 2 months of low caloric diet, a significant increase in the serum level of vitamin D, accompanied with improvement in cognitive functions and decrease in fasting blood glucose and improved insulin resistance was seen. A correlation is found between vitamin D serum level and cognitive functions.CONCLUSION: A lower vitamin D serum level could be a modifiable risk factor for obesity, insulin resistance and cognitive impairment in middle age females.

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Section: Discussionsupporting

confidence: 55%

Low Vitamin D Serum Levels May Be a Modifiable Risk Factor for Obesity and Cognitive Impairment in Middle-Age Egyptian Women

Kazem¹,

Moaty²,

El-Shebini³

et al. 2014

Open Access Maced J Med Sci

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“…Currently, the best available inflammatory biomarker is CRP, an acute phase reactant that is a reliable, independent predictor of the risk of myocardial infarction, stroke and cardiovascular death (111) . Clinical trials of vitamin D supplementation show inconsistent results regarding an effect on CRP concentrations: most report no effect (77,80,97,(112)(113)(114)(115)(116) , whereas some show reductions in CRP concentrations (74,117,118) . Some trials have measured highsensitivity CRP (hsCRP), which can detect low-grade inflammation.…”

Section: Inflammationmentioning

confidence: 99%

Vitamin D and risk of CVD: a review of the evidence

Fry

Sanders

2015

Proc. Nutr. Soc.

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This review summarises evidence for an association between vitamin D status and CVD and the mechanisms involved. Vitamin D 3 is predominantly provided by the action of UVB from sunlight on skin. Average UK diets supply 2-3 μg/d vitamin D but diets containing at least one portion of oily fish per week supply about 7 μg/d. Pharmacological doses of vitamin D 2 (bolus injection of 7500 μg or intakes >50 μg/d) result in a smaller increase in plasma 25 (OH)D than those of D 3 but physiological doses 5-25 μg/d seem equivalent. Plasma 25 (OH)D concentrations are also influenced by clothing, obesity and skin pigmentation. Up to 40 % of the population have plasma 25(OH)D concentrations <25 nmol/l in the winter compared with <10 % in the summer. The relative risk of CVD death is 1·41 (95 % CI 1·18, 1·68) greater in the lowest quintile of plasma 25(OH)D according to meta-analysis of prospective cohort studies. Acute deficiency may inhibit insulin secretion and promote inflammation thus increasing the risk of plaque rupture and arterial thrombosis. Chronic insufficiency may increase arterial stiffness. There is no evidence to support claims of reduced CVD from existing trials with bone-related health outcomes where vitamin D was usually co-administered with calcium. Although several trials with cardiovascular endpoints are in progress, these are using pharmacological doses. In view of the potential toxicity of pharmacological doses, there remains a need for long-term trials of physiological doses of D 2 and D 3 with CVD incidence as the primary outcome. Ergocalciferol: Cholecalciferol: Cardiovascular riskVitamin D deficiency causes rickets in children and osteomalacia in adults and may contribute to the causation of CVD. Cholecalciferol (vitamin D 3 ) is made by the action of UVB light on the skin but is also provided in the diet from foods of animal origin (eggs, oily fish and meat). Ergocalciferol (vitamin D 2 ) is present in fungi that have been exposed to UVB irradiation. Both forms of vitamin D undergo 25-hydroxylation in the liver to form 25(OH) metabolites, most of which circulate in plasma bound to the vitamin D binding protein (VDBP). In the kidney, 25 hydroxyvitamin D (25(OH)D) is converted to the biologically active metabolite 1,25 dihydroxyvitamin D (1,25 (OH) 2 D) by the action of 1α-hydroxylase (Fig. 1). This then binds to the vitamin D receptor, which is a highaffinity nuclear hormone receptor that regulates gene expression (1) . Measurement of serum 25(OH)D to assess vitamin D status has predominantly used immunoassays, which show lower sensitivity (about 30 %) to D 2 metabolites than gold-standard methods such as HPLC/tandem MS. Formerly, a lack of standardisation of methods and appropriate quality control made comparisons between studies difficult (2) . The situation has been remedied by the availability (3) of standard reference serum (SRM 972, National Institute of Standards and Technology) and a quality control programme in the UK organised by the Vitamin D External Quality Assessment Scheme (4) . It has...

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“…A limitation of this study is thus the unavailability of measurements for vitamin D-binding protein and IR. Some authors have suggested a possible beneficial effect of vitamin D supplementation on IR or other parameters of glucose metabolism [29,30], although others disagree [31][32][33][34]. It is also possible that other metabolic pathways [35], independent of insulin action, link visceral adipose tissue and lipid profile with 25(OH)vitamin D. Therefore, it has been suggested that the hypertriglyceridemia associated with vitamin D deficiency may be a consequence of a direct effect of vitamin D itself on lipoprotein-lipase activity [7].…”

Section: Discussionmentioning

confidence: 99%

Lipid Accumulation Product and 25-OH-Vitamin D Deficiency in Type 2 Diabetes

et al. 2013

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■ Abstract BACKGROUND:Emerging data suggest a link between vitamin D (25(OH)D) deficiency, type 2 diabetes (T2D), and visceral adiposity. The lipid accumulation product (LAP), strictly correlated with abdominal fat depots, is proposed as marker of dysfunctional adiposity. AIM: To verify the association between 25(OH)D levels and LAP in T2D. METH-ODS: Body mass index (BMI), waist circumference (WC), glucose, HbA1c, lipids, and 25(OH)D were assessed in 420 T2D outpatients and in 150 non-diabetic obese with similar anthropometric characteristics. LAP was computed as the product of sex-specific enlarged WC and triglycerides (TG). RESULTS: In T2D patients, 63.0% showed 25(OH)D deficiency (<20 ng/ml) vs. 71.3% in the obese control group. Overweight males showed a higher prevalence of 25(OH)D deficiency (60.3%) than women (48.8%, p < 0.001), while in obese patients this prevalence was not significant. In both genders, 25(OH)D was not significantly associated with HbA1c and fasting glucose. Age-adjusted 25(OH)D levels were inversely correlated with BMI (p < 0.001), WC (p < 0.001), and LAP (p < 0.001) in both genders. Metabolic syndrome presented an odds ratio (OR) for 25(OH)D deficiency of 1.6 (1.1-2.5, p = 0.048) in females and 1.7 (1.2-2.7, p = 0.016) in males, while the highest quartile of LAP showed an OR of 2.1 (1.2-3.6, p = 0.019) in females and 3.2 (1.6-6.5, p = 0.02) in males. A similar trend was observed in the obese control group. CONCLUSIONS: In the presence of excess weight, subjects with and without T2D frequently feature low 25(OH)D levels. Subjects with higher LAP exhibit a high risk of 25(OH)D deficiency, suggesting that dysfunctional adiposity is a worsening factor for vitamin D hypovitaminosis.

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Correcting vitamin D insufficiency improves insulin sensitivity in obese adolescents: a randomized controlled trial

Abstract: The correction of poor vitamin D status through dietary supplementation may be an effective addition to the standard treatment of obesity and its associated insulin resistance. This trial was registered at clinicaltrials.gov as NCT00994396.

Cited by 282 publications

References 46 publications

Low Vitamin D Serum Levels May Be a Modifiable Risk Factor for Obesity and Cognitive Impairment in Middle-Age Egyptian Women

Low Vitamin D Serum Levels May Be a Modifiable Risk Factor for Obesity and Cognitive Impairment in Middle-Age Egyptian Women

Vitamin D and risk of CVD: a review of the evidence

Lipid Accumulation Product and 25-OH-Vitamin D Deficiency in Type 2 Diabetes

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