Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease

Figure 2 Elevation in profibrotic and proinflammatory cytokine expression in the liver. A: Picrosirius red staining of collagen showing centrilobular sinusoidal fibrosis induced by the 33 wk high fructose, high cholesterol (HFHC) dietary model (c). In animals receiving the HFHC diet, fibrosis was further increased by raising the advanced glycation end products (AGEs) content of the diet (d) and attenuated when dietary AGE content was reduced by acetic acid premarination prior to baking (e). However increasing the AGE content of normal chow did not cause increased fibrosis (compare a, b). Hepatic gene expression of COL1A (B) and αSMA (C) were also significantly increased by raising the AGE content of the diet. Expression of RAGE, a key receptor for AGEs, was elevated in the HFHC model but this was not affected by varying the AGE content of the diet, ^aP < 0.05, ^bP < 0.01 (D).