Role of vitamin D in adipose tissue in obese rats programmed by early weaning and post diet calcium

Abstract

We propose that in obese rat adipocytes, 1,25(OH)2 D down-regulates VDR, resulting in vitamin D resistance, characterized by higher Cyp27b1/1α-Hydroxylase and adipogenesis. Calcium therapy appears to be an outstanding strategy for weight loss and improving endocrine metabolic disorders that are obesity associated.

Calcium reduces vitamin D and glucocorticoid receptors in the visceral fat of obese male rats

“…Our findings suggest a vitamin D resistance in adipocytes at PN120 that may be associated with the fat accumulation in SL rats. In another obesity model, we also found, in adult rats, higher Cyp27b1 and lower Vdr in the VAT, with higher C/EBPβ and PPARγ expression in the adipose tissue, which could be a key factor in obesogenesis (Nobre et al 2016).…”

“…Two mechanisms may help to explain the reduction of fat depots in our study: (1) calcium supplementation increases fecal fat excretion (Denke et al 1993, Shahkhalili et al 2001, Jacobsen et al 2005; (2) calcium supplementation decreased CEBP/β and PPARγ expression, 230:2 two proadipogenic and lipogenic biomarkers, in the VAT of early-weaned rats (Nobre et al 2016). Gonzalez and coworkers (2015) have shown that calcium supplementation in humans reduces postprandial appetite sensation.…”

“…Previous data from our group have demonstrated that a calcium-supplemented diet is able to decrease visceral adiposity and 25(OH)D levels in two obesity models (early weaning and postnatal nicotine exposure), which can be associated (Nobre et al 2012(Nobre et al , 2016 or not (Nobre et al 2011) with reduction in food intake. These data lend support to the notion that dietary calcium supplementation can have beneficial effects on adipose tissue through changes in GC and vitamin D metabolism and receptors function.…”

“…This suggests a leptin resistance at the adipocyte level. However, we did not evaluate the leptin signaling pathway in the adipocyte, but we have shown, in a different obesity model, that the adipose tissue had leptin resistance (with lower Ob-R expression) and higher CYP27B1 (Nobre et al 2016). In fact, normal 25(OH)D with increased 1,25(OH)2D levels in obese rats have already been reported in a diet-induced obesity (DIO) model by Park and coworkers (2015).…”

“…This finding was associated with higher CYP27B1 in the visceral adipocyte (the enzyme that activates 25(OH)D to 1,25(OH) 2 D) and with lower vitamin D receptor (VDR) content, which could indicate a vitamin D resistance in the adipocyte level (Nobre et al 2012(Nobre et al , 2016. In addition, Malloy & Feldman (2013) showed that VDR, in the absence of the ligand, inhibits UCP1 expression in human brown adipocytes, suggesting a reduced thermogenic capacity in vitamin D deficiency.…”