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

Figure 1 Novel 33 wk high fructose, high cholesterol dietary model induced changes of non-alcoholic steatohepatitis. A: Haematoxylin and eosin stained sections showing ballooning after high fructose, high cholesterol (HFHC) diets (examples of ballooning circled). At right, ballooning scores determined morphometrically; B: Oxidative stress revealed by the immunohistochemical localisation of 4-hydroxynonenal; C: Steatosis grade (grade 0, no fat; grade 1, steatosis occupying less than 33% of the hepatic parenchyma; grade 2, 34%-66% of the hepatic parenchyma; grade 3, more than 66% of the hepatic parenchyma); D: Plasma levels of alanine transaminase (ALT) in the different treatment groups; and E: Lobular inflammation (grade 0:none; grade 1, 1-2 foci/field; grade 2, 3-4 foci/field; grade 3, more than 4 foci/field). Ballooning and oxidative stress were significantly increased by raising the AGE content of the HFHC diet. These changes were attenuated when dietary AGE content was reduced by acetic acid premarination. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001.