Dietary Glycotoxins Impair Hepatic Lipidemic Profile in Diet-Induced Obese Rats Causing Hepatic Oxidative Stress and Insulin Resistance

Figure 5

The consumption of a high-fat diet increased glucose intolerance (a), but MG supplementation further increased glucose intolerance and increased plasma insulin levels and HOMA (b). Plasma free fatty acid levels were significantly elevated in HFDMG rats (c). As well, glycation also prevented the hyperadiponectinemia observed in HFD rats (d). In the liver, the high-fat diet caused a decrease in insulin receptor activation (e), which was further increased by glycation, as well as a compensatory increase in GLUT2 (f), which was prevented by glycation. HFD rats had inhibition of key enzymes of de novo lipogenesis as ACC, AceCS, and FAS and upregulation of the desaturation enzyme SCD-1, which was not observed in HFDMG rats (g, h, i). Decreased AMPK activation was also observed in HFDMG rats (j). Intensity was calculated as percentage of Ct; representative WB are shown in the right panel. Ct: Wistar 12 m; MG: Wistar + MG supplementation; HFD: HF diet-fed Wistar; HFDMG: HF diet-fed Wistar + MG supplementation. Bars represent . vs. Ct; # vs. MG; $ vs. HFD. 1 symbol ; 2 symbols ; 3 symbols .