Premium
Fatty liver promotes fibrosis in monkeys consuming high fructose
Author(s) -
Cydylo Michael A.,
Davis Ashley T.,
Kavanagh Kylie
Publication year - 2017
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21720
Subject(s) - nonalcoholic fatty liver disease , fructose , steatosis , fibrosis , fatty liver , medicine , endocrinology , liver fibrosis , physiology , disease , biology , food science
Objective Nonalcoholic fatty liver diseases (NAFLD) are related to development of liver fibrosis which currently has few therapeutic options. Rodent models of NAFLD inadequately model the fibrotic aspects of the disease and fail to demonstrate the spectrum of cardiometabolic diseases without genetic manipulation. This study aimed to document a monkey model of fatty liver and fibrosis, which naturally develop cardiometabolic disease pathophysiologies. Methods Twenty‐seven cynomolgus monkeys ( Macaca fascicularis ) fed diets either low or high in simple carbohydrates, supplied as fructose [control and high‐fructose diet (HRr)], on low‐fat, cholesterol‐free background were studied. The HFr was consumed for up to 7 years, and liver tissue was histologically evaluated for fat and fibrosis extent. Results The HFr diet increased steatosis, and its extent was related to duration of fructose exposure. Lipid droplet size also increased with HFr duration; however, compared with control, the lipid droplets were smaller on average. Fibrosis extent was significantly greater with fructose feeding and was predicted by fructose exposure, extent of fatty liver, and age. Conclusions These data are the first to demonstrate that high‐carbohydrate diets alone can generate both liver fat and fibrosis and thus allow further study of mechanisms and therapeutic options in the translational animal model.