The small intestine shields the liver from fructose-induced steatosis.

ABSTRACT: Per capita fructose consumption has increased 100-fold over the last century¹. Epidemiological studies suggest that excessive fructose consumption, and especially consumption of sweet drinks, is associated with hyperlipidaemia, non-alcoholic fatty liver disease, obesity and diabetes^2-7. Fructose metabolism begins with its phosphorylation by the enzyme ketohexokinase (KHK), which exists in two alternatively spliced forms⁸. The more active isozyme, KHK-C, is expressed most strongly in the liver, but also substantially in the small intestine^9,10 where it drives dietary fructose absorption and conversion into other metabolites before fructose reaches the liver^11-13. It is unclear whether intestinal fructose metabolism prevents or contribut

SUBMITTER: Jang C 

PROVIDER: S-EPMC8020332 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature