A little orphan runs to fat: the orphan receptor small heterodimer partner as a key player in the regulation of hepatic lipid metabolism.

摘要

Nonalcoholic fatty liver disease (NAFLD) encompasses a disease spectrum ranging from relatively benign "pure" fatty liver to steatohepatitis [nonalcoholic steatohepatitis (NASH)] with inflammation and fibrosis, which can progress to cirrhosis and hepato-cellular cancer. Because it is closely associated with metabolic syndrome and insulin resistance, NAPLD is already the leading cause of elevated liver function tests in Western countries, and we should be prepared to see more of it (including NASH at the more severe end of this spectrum) in the near future. Although considerable progress has been made with the use of insulin sensitizers such as metformin and glitazones, no generally accepted pharmacological treatment of NAFLD/NASH is available. As some of these therapeutic shortcomings have to be attributed to our limited understanding of the pathogenesis of NAFLD, studies such as the present article by Huang et al., which shed more light on the pathogenesis and uncover novel potential therapeutic targets in NAFLD, are very welcome.