Chronic, in vivo, PPAR[alpha] activation prevents lipid overload in rat liver induced by high fat feeding

Chronic, in vivo, PPARα activation prevents lipid overload in rat liver induced by high fat feeding Purpose: Peroxisome proliferator-activated receptors (PPAR`s) are lipid sensors and when activated they modify gene expression of proteins regulating fatty acid (FA) metabolism in liver cells. The aim of the present study was to examine the in vivo effects of PPAR α and γ activation combined with high fat diet (HFD) feeding on the lipid content and FA profile in the liver. Material/Methods: We assessed whether in vivo activation of PPARs (α or γ) affects lipid accumulation in the liver induced by HFD feeding. Furthermore, as PPAR activity may be a key factor regulating long chain fatty acids (LCFA) flux and subsequent LCFA utilization in the liver, we prompted to investigate also the FA profile in different lipid fractions in this tissue. Results: PPARα agonist (WY 14,643) treatment reduced the accumulation of liver lipids free fatty acids (FFA:-30%, diacylglycerols DAG: -27% and triacylglycerols TAG: -60%, p