The kielin/chordin-like protein KCP attenuates nonalcoholic fatty liver disease in mice.

ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease and is increasing with the rising rate of obesity in the developed world. Signaling pathways known to influence the rate of lipid deposition in liver, known as hepatic steatosis, include the transforming growth factor (TGF) superfamily, which function through the SMAD second messengers. The kielin/chordin-like protein (KCP) is a large secreted protein that can enhance bone morphogenetic protein signaling while suppressing TGF-β signaling in cells and in genetically modified mice. In this report, we show that aging KCP mutant (Kcp^-/-) mice are increasingly susceptible to developing hepatic steatosis and liver fibrosis. When young mice are put on a high-fat diet, Kcp^-/- mice are also mor

SUBMITTER: Soofi A 

PROVIDER: S-EPMC5142198 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature