Prolactin improves hepatic steatosis via CD36 pathway

Non-alcoholic fatty liver disease (NAFLD) is a common public health problem affecting up to 25% of the adults around the world [1]. It is associated with a series of metabolic comorbidities. NAFLD is initially caused by an imbalance between lipid demand and supply; however, the pathogenesis of the disease also involves crosstalk between liver and extra-hepatic organs, including adipose tissue and central nervous system (CNS) [2]. By sensing and integration of the peripheral signals (such as leptin), hypothalamic arcuate nucleus (ARC) neurons in CNS can induce hepatic fatty acid oxidation [3].

Source: Journal of Hepatology - February 13, 2018 Category: Gastroenterology Authors: Pengzi Zhang, Zhijuan Ge, Hongdong Wang, Wenhuan Feng, Xitai Sun, Xuehui Chu, Can Jiang, Yan Wang, Dalong Zhu, Yan Bi Source Type: research