Rat 25 Hydroxy Vitamin D3 ELISA Kit

Our previous study showed that feeding mice with vitamin D deficiency diet markedly alleviated high-fat-diet-induced overweight, hyperinsulinemia, and hepatic lipid accumulation. Moreover, vitamin D deficiency up-regulated the expression of uncoupling protein 3 (Ucp3) in white adipose tissue (WAT) and brown adipose tissue (BAT). The present study aimed to further investigate the effects of vitamin D and vitamin D receptor (Vdr) on Ucp1-3 (Ucps) expression in brown adipocyte and the mechanism involved in it. Rat primary brown adipocytes were separated and purified. The effects of the 1,25(OH)(2)D-3 (1,25-dihydroxyvitamin D3; the hormonal form of vitamin D) and Vdr system on Ucps expression in brown adipocytes were investigated in basal condition and activated condition by isoproterenol (ISO) and triiodothyronine (T3). Ucps expression levels were significantly down-regulated by 1,25(OH)(2)D-3 in the activated brown adipocyte. Vdr silencing reversed the down-regulation of Ucps by 1,25(OH)(2)D-3, whereas Vdr overexpression strengthened the down-regulation effects. Hairless protein did express in brown adipocyte and was localized in cell nuclei. 1,25(OH)(2)D-3 increased Hairless protein expression in the cell nuclei. Hairless (Hr) silencing notably elevated Ucps expression in activated condition induced by ISO and T3. Moreover, immunoprecipitation results revealed that Vdr could interact with Hairless, which might contribute to decreasing expression of Vdr target gene Ucps. These data suggest that vitamin D suppresses expression of Ucps in brown adipocyte in a Vdr-dependent manner and the corepressor Hairless protein probably plays a role in the down-regulation.

The present study assessed the prevalence of vitamin D deficiency in an urban south Indian population in individuals with different grades of glucose tolerance. A total of 1500 individuals (900 normal glucose tolerance (NGT), 300 prediabetes and 300 with type 2 diabetes mellitus (T2DM)) who were not on vitamin D supplementation were randomly selected from the Chennai Urban Rural Epidemiological Study follow-up study. Anthropometric, clinical examination and biochemical investigations (25-hydroxyvitamin D (25(OH)D), insulin, glycated Hb (HbA1c) and serum lipids) were measured. Vitamin D deficiency was defined as serum 25(OH)D < 20 center dot 0 ng/ml, insufficiency as 20-29 center dot 9 ng/ml and sufficiency as >= 30 ng/ml. Of the 1500 individuals studied, 45 % were males and the mean age was 46 (sd12) years. Vitamin D levels lowered with increasing degrees of glucose tolerance (NGT: 21 (sd11); prediabetes: 19 (sd10); T2DM: 18 (sd11) ng/ml,P< 0 center dot 001). The overall prevalence of vitamin D deficiency was 55 % and was significantly higher among individuals with T2DM (63 %) followed by prediabetes (58 %) and NGT (51 %) (P-for trend< 0 center dot 001). Women had 1 center dot 6 times the risk of vitamin D deficiency compared with men (unadjusted OR 1 center dot 6 (95 % CI 1 center dot 3, 2 center dot 0) and adjusted OR 1 center dot 6 (95 % CI 1 center dot 2, 1 center dot 9)). However, there was no increasing trend observed with increasing age. The prevalence of abdominal obesity (66v. 49 %), generalised obesity (80v. 64 %), the metabolic syndrome (45v. 37 %) and insulin resistance (38v. 27 %) was significantly higher in those with vitamin D deficiency compared with those without. This study shows that vitamin D deficiency is highly prevalent in this urban south Indian population and was higher among individuals with T2DM and prediabetes compared with those with NGT.