Several recent studies suggest that adiponectin is protective against various types of liver injuries, steatosis, and fibrosis (43-46). Our group has examined the potential roles of adiponectin in alcoholic and nonalcoholic fatty liver diseases in mice (43). In both ob/ob obese mice and mice fed with a high fat-ethanol diet, chronic treatment with recombinant adiponectin dramatically alleviated hepatomegaly and steatosis (fatty liver), and also significantly attenuated inflammation and the elevated levels of serum alanine aminotransferase (ALT), a marker of liver injury. These protective effects were partly attributed to adiponectin's ability to increase carnitine palmitoyltransferase I activity and enhance hepatic fatty acid oxidation, and to decrease hepatic lipogenesis and TNF-a production (43).
Masaki et al. investigated the effect of adiponectin on liver injury induced by D-galactosamine/LPS (GalN/LPS) in KK-Ay obese mice (44). The authors found that pre-treatment with adiponectin ameliorated the GalN/LPS-induced elevation of serum AST and ALT levels, and also decreased the apoptotic and necrotic changes in hepatocytes, resulting in a marked reduction in lethality. Kamada et al. demonstrated that adiponectin KO mice were more susceptible to liver fibrosis induced by carbon tetrachloride (CCl^), whereas adenovirus-mediated overexpression of adiponectin prevented the development of this disease (45). In cultured rat hepatic stellate cells, adiponectin suppressed cell proliferation and migration and attenuated transforming growth factor (TGF)-^l-induced nuclear translocation of Smad2 (45,46). In addition, adiponectin has been shown to accelerate the apoptosis of activated hepatic stellate cells (46), and protect hepatocytes from TNF-a-induced death (47).
Was this article helpful?