Carbohydrate intake and nonalcoholic fatty liver disease

Carbohydrate consumption has been implicated in the metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). Reviewed here is basis for this relationship and the recent additional evidence that excessive dietary carbohydrate consumption, especially excessive fructose or sucrose consumption, is playing a role in the epidemic of NAFLD.

A recent cross-sectional epidemiological study has linked fructose consumption to the severity of fibrosis in patients with NAFLD. Clinical trials have shown that consumption of fructose-containing beverages, either has fructose or sucrose, contribute to the development of NAFLD compared to isocaloric alternatives, and that genetic polymorphisms that increase the entry of glucose into lipogenic pathways are associated with fatty liver disease. New animal studies provide additional evidence on the role of carbohydrate-induced de-novo lipogenesis and the gut microbiome in fructose-induced NAFLD. Data also suggest that fructose-induced uric acid production in the liver also plays a role in NAFLD independent of the role of fructose as a substrate for lipogenesis.

Epidemiological studies, clinical trials, and animal studies continue to point to excess dietary carbohydrate, and especially fructose, in contributing to the risk factors for NAFLD.