Figure 3 ER stress and hepatic steatosis: a vicious cycle

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Figure 3 ER stress and hepatic steatosis: a vicious cycle Figure 3 | ER stress and hepatic steatosis: a vicious cycle. In obesity or during continuous fatty acid overload, modification of the lipid composition of the endoplasmic reticulum (ER) membrane increases the phosphatidylcholine (PC) to phosphatidylethanolamine (PE) ratio, which will trigger ER stress, notably by the perturbation of Ca2+ homeostasis. ER stress responses such as the ER-mediated degradation and the unfolded protein response (UPR) counteract ER stress but instead promote hepatocyte lipid accumulation. The reinforcement of hepatic steatosis by ER stress is directly mediated via the induction of de novo lipogenesis, the alteration of the mitochondrial activity and a decreased secretion of VLDL. The UPR cannot resolve the initial stimulus as it is external to the regulated system, and, therefore, a chronic UPR develops. This response in turn contributes to the 'second hit' by inducing oxidative stress, inflammation and apoptosis leading to the development of nonalcoholic steatohepatitis (NASH). Baiceanu, A. et al. (2016) Endoplasmic reticulum proteostasis in hepatic steatosis Nat. Rev. Endocrinol. doi:10.1038/nrendo.2016.124