Prolactin improves hepatic steatosis via CD36 pathway
Prolactin improves hepatic steatosis via CD36 pathway
复制标题
催乳素通过 CD36 途径改善肝脏脂肪变性。
DOI：
10.1016/j.jhep.2018.01.035
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发表时间：
2018-06-01
影响因子：
25.7
通讯作者：
Bi, Yan
中科院分区：
文献类型：
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作者：
Zhang, Pengzi;Ge, Zhijuan;Bi, Yan
背景和目标：催乳素（PRL）是一种多功能的代谢多肽，但其对肝脂肪变性和脂质代谢的影响尚不清楚。在此，我们旨在评估PRL在非酒精性脂肪性肝病（NAFLD）发展中的作用。方法：对456例NAFLD患者、403例经超声诊断为非NAFLD的对照组和85例代谢手术期间获得肝脏组织学检查的个体（44例女性和30例男性NAFLD患者以及11例年龄匹配的非NAFLD女性个体）的血清PRL水平进行了评估。在人肝脏和HepG 2细胞中评价了编码催乳素受体（PRLR）和参与肝脏脂质代谢的信号分子的基因的表达。在游离脂肪酸（FFA）处理的HepG 2细胞中检测PRLR或脂肪酸转位酶（FAT）ICD 36过表达或PRLR敲低对肝脏脂质代谢的影响。（男性：7.9 [范围，5.9-10.3] μ g/L;女性：8.7 [范围，6.1-12.4] μ g/L）比非NAFLD患者（男性：9.1 [范围，6.8-13.0] μ g/L，p = 0.002;女性：11.6 [范围，8.2-16.1] μ g/L，p
Background & Aims: Prolactin (PRL) is a multifunctional polypeptide with effects on metabolism, however, little is known about its effect on hepatic steatosis and lipid metabolism. Herein, we aimed to assess the role of PRL in the development of non-alcoholic fatty liver disease (NAFLD).Methods: The serum PRL levels of 456 patients with NAFLD, 403 controls without NAFLD diagnosed by ultrasound, and 85 individuals with liver histology obtained during metabolic surgery (44 female and 30 male patients with NAFLD and 11 age-matched non-NAFLD female individuals) were evaluated. The expression of the gene encoding the prolactin receptor (PRLR) and signalling molecules involved in hepatic lipid metabolism were evaluated in human liver and HepG2 cells. The effects of overexpression of PRLR or fatty acid translocase (FAT)ICD36 or knockdown of PRLR on hepatic lipid metabolism were tested in free fatty acid (FFA)-treated HepG2 cells.Results: Circulating PRL levels were lower in individuals with ultrasound-diagnosed NAFLD (men: 7.9 [range, 5.9-10.3] mu g/L; women: 8.7 [range, 6.1-12.4]mu g/L) than those with non-NAFLD (men: 9.1 [range, 6.8-13.0] mu g/L, p = 0.002; women: 11.6 [range, 8.2-16.1] mu g/L, p