Singular effects of PPAR agonists on nonalcoholic fatty liver disease of diet-induced obese mice

• DOI: 10.1016/j.lfs.2015.02.003
• Publication Date: 2015-03-04T05:30:27Z
• Authors: Sandra Barbosa-da...; Vanessa Souza-Mello; D'Angelo Carlo Ma...; Thatiany de Souza...; Marcia Barbosa Ag...; Carlos Alberto Ma...
• Keywords: Bezafibrate; Steatosis; Lipogenesis

To assess the effects of peroxisome proliferator-activated receptor (PPAR) agonists on glucose tolerance and hepatic lipid metabolism in diet-induced obese mice. Male C57BL/6 mice received a standard chow diet (SC, 10% energy as lipids) or high-fat (HF, 50% for 10 weeks, after which treatment was initiated, forming groups: SC group, HF HF-BZ group (HF + bezafibrate, pan-PPAR agonist), HF-WY WY-14643, PPARalpha agonist) HF-GW GW1929, PPARgamma agonist). Treatments lasted four weeks. Insulin resistance liver remodeling were evaluated by biochemical molecular approaches. The overweight. Conversely, presented with body masses equal to those All treatments restored insulin sensitivity blood adiponectin levels. Hepatic steatosis prevented shown elevated mRNA levels Carnitine palmitoyl transferase-1a both groups, favored enhanced beta-oxidation. Marked decreases triacylglycerol confirmed these findings. In contrast, exhibited increased fatty acid translocase/CD136 levels, contributing lipogenesis. WY14643 bezafibrate most effectively improved adverse metabolic caused obesity IR. results reinforce central role PPARalpha, well its contrary relationship regulation homeostasis lipolytic pathways liver.