Indexed on: 31 May '19Published on: 30 Mar '19Published in: The British journal of nutrition
Reduced plasma vitamin D levels may contribute to excessive white adipose tissue, insulin resistance and dyslipidemia. We evaluated the effect of chronic oral vitamin D supplementation on adiposity and insulin secretion in monosodium glutamate (MSG)-treated rats. During their first five days of life, male neonate rats received subcutaneous injections of MSG (4g/Kg), while the control (CON) group received saline solution. After weaning, groups were randomly distributed into vitamin D-supplemented (12µg/Kg; 3 times/week) and non-supplemented (NS) rats, forming four experimental groups (n=15 rats/group): CON-NS; CON-VD; MSG-NS and MSG-VD. At 76 days of life, rats were submitted to an oral glucose tolerance test (OGTT; 2g/Kg) and, at 86 days, obesity, insulin resistance and plasma metabolic parameters were evaluated. Pancreatic islets were isolated for glucose-induced insulin secretion (GIIS); cholinergic insulinotropic response and muscarinic 3 receptor (M3R), protein kinase C (PKC) and A (PKA) expressions. Pancreas was submitted to histological analyses. Vitamin D supplementation decreased hyperinsulinemia (86%), hypertriglyceridemia (50%) and restored insulin sensibility (89%) in MSG-VD rats, without modifying adiposity, OGTT or GIIS, compared to the MSG-NS group. The cholinergic action was reduced (57%) in islets from MSG-VD rats, without any change in M3R, PKA or PKC expression. In conclusion, chronic oral vitamin D supplementation of MSG-obese rats was able to prevent hyperinsulinemia and insulin resistance, improving triglyceridemia without modifying adiposity. A reduced cholinergic pancreatic effect, in response to vitamin D, could be involved in the normalization of plasma insulin levels, an event that appears to be independent of M3R and its downstream pathways.