Metabolismo e fígado em camundongos alimentados cronicamente com frutose: papel da vitamina D, deficiência e suplementação

Abstract

Fructose added to soft drinks and processed foods, as well as the frequent detection of vitamin D deficiency in the body, are two insults increasingly considered to cause target organ damage. We studied the liver after a chronic high-fructose diet deficient and supplemented with vitamin D. Sixty adult C57Bl/6 male mice were allocated into six groups (n=10) for ten weeks, according to the experimental diet: control (C), vitamin D deficient control (CDD), vitamin D supplemented control (CDS), fructose (F), vitamin D deficient fructose (FDD) and vitamin D supplemented fructose (FDS). Gene expressions of the vitamin D receptor (Vdr) and Cyp27b1 and plasma level of 25-hydroxyvitamin D ensured that diets caused vitamin D deficiency or supplementation. Body mass did not change, but blood pressure (BP) increased in CDD, F and FDD, while BP was controlled in FDS. Insulin, glucose tolerance, and insulin resistance were observed in both vitamin D deficiency and fructose groups but improved with vitamin D supplementation. Liver steatosis and fibrosis were observed in CDD, F, and FDD groups. Furthermore, F and FDD showed activation of hepatic stellate cells. Gene expressions of lipogenesis and inflammation increased in the CDD, F and FDD groups, but decreased with vitamin D supplementation. In conclusion, we demonstrated the adverse effects of vitamin D deficiency on metabolism, hepatic steatosis and, combined with fructose intake, hepatic interstitial fibrosis with hepatic stellate cell activation, and alteration of lipogenesis, beta-oxidation and hepatic inflammation. All these data improved when vitamin D was supplemented in animals.