Abstract
Obesity predisposes to vitamin D deficiency (VDD) and glucose abnormalities. It is currently debated if vitamin D administration may improve glucose homeostasis by interacting with modulators of insulin sensitivity, such as adiponectin and its oligomers. In a 4-week inpatient study on a metabolic rehabilitation program, consisting of individualized caloric restriction and aerobic physical exercise in obese subjects with VDD, we assessed the acute effects of 600,000 IU cholecalciferol given per os VD group, 12 subjects; body mass index (BMI) 42.7 ± 1.3 kg/m2) or placebo per os (PL group, 12 subjects, BMI 39.8 ± 0.9 kg/m2) on high (HWM-A), medium (MMW-A), and low molecular weight adiponectin (LMW-A), as quantified by western immunoblot (WIB) and ELISA. During the 4-week study, dieting promoted a similar magnitude of weight loss in VD and PL groups. Compared to the PL group, cholecalciferol administration increased 25(OH)Vit D levels (p < 0.001) and promoted a significant increase of HMW-A expression analyzed by WIB (p = 0.02). In parallel, a significant decrease of leptin/HMW-A ratio (p < 0.05), a biomarker of metabolic homeostasis, was observed. During the study, changes of MMW-A and LMW-A occurred independently of cholecalciferol administration, and were likely explained by weight loss. At odds with these findings, the ELISA assessment of adiponectin oligomers showed no modifications in the VD group or PL group. Current findings suggest that acute cholecalciferol administration selectively modifies HMW-A and the leptin/HMW-A ratio.
Highlights
Vitamin D is a fat-soluble secosteroid hormone that has an established physiological role in mineral and bone homeostasis
We found no difference in anthropometric variables between the VD group and the PL group at baseline, including body mass index (BMI) and body weight
While it should be noted that the placebo group tended to have slightly milder baseline measures of severe obesity and metabolic dysfunction compared to the vitamin D group, these differences were not statistically significant and, we hypothesize that this divergence played a negligible effect on the main findings of this study
Summary
Vitamin D is a fat-soluble secosteroid hormone that has an established physiological role in mineral and bone homeostasis. The VDR is widely expressed in human tissues, where it likely mediates the pleiotropic functions of vitamin D [1]. Vitamin D deficiency (VDD) affects up to 95% of patients with severe obesity [3], and an associative network relates VDD and obesity to low grade inflammatory state, insulin resistance, metabolic syndrome, and type 2 diabetes mellitus (T2DM) [3,4,5]. The possibility that vitamin D3 supplementation may help to prevent the risk of T2DM has been challenged, and the ability of vitamin D3 supplementation to improve fasting glucose, HbA1c levels, or insulin resistance in patients with impaired glucose tolerance (IGT), gestational diabetes, or T2DM is openly debated [9]
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