Endocrine Abstracts

Introduction: 25-hydroxyvitamin D (25(OH)D3) deficiency has been associated with diabetes and obesity. However, the mechanisms underlying these relationships are not completely understood. Vitamin D receptor (VDR) is expressed in adipose tissue; it has been reported a higher expression in obese patients than in lean subjects, suggesting a differential vitamin D dynamics in adipose tissue according to the obesity degree. In addition, 1, 25-dihydroxyvitamin D3 (1,25(OH)2D3) is able to modify VDR gene expression in mice 3T3-L1 preadipocytes.

Objective: To analyse plasma 25(OH)D3 and VDR gene expression in adipose tissue according to BMI and glycemic status. To evaluate the influence of 1,25(OH)2D3 and VDR gene expression in human adipose tissue cultures.

Materials and methods: We recruited and classified 119 subjects according to their BMI (lean, overweight, obese, and morbidly obese subjects) and to their glycemic status: normoglycemic (NG) and prediabetic/diabetic (P/D) patients. We measure plasma 25(OH)D3 and parathyroid hormone (PTH) levels as well as VDR gene expression in visceral adipose tissue. Adipose tissue from morbidly obese (ATMO) and lean (ATL) donors were cultured and treated with a range of 1,25(OH)2D3 concentrations.

Results: Plasma 25(OH)D3 were lower in P/D patients compared to NG subjects in the four BMI groups (P<0.05). Plasma 25(OH)D3 levels correlated negatively with HOMA-IR (P<0.01) and glucose (P<0.05). No differences were found in plasma 25(OH)D3 levels according to the BMI. There was a higher VDR gene expression levels in morbidly obese patients (P<0.05) compared to groups with lower BMI. 1,25(OH)2D3 increased VDR gene expression in ATMO, but not in ATL (P<0.05).

Conclusion: Plasma 25(OH)D3 are diminished in P/D patients compared to NG subjects independently of BMI and are closely related with glucose metabolism variables, suggesting that vitamin D deficiency is associated more with carbohydrate metabolism than with obesity. Adipose tissue VDR gene expression was significantly higher in morbidly obese patients than in the other BMI groups and its regulation by 1,25(OH)2D3 was only demostrated in morbidly obese subjects.