瘦素通过调节胆汁酸代谢影响胆石症的形成。
Leptin Influence Cholelithiasis Formation by Regulating Bile Acid Metabolism.
机构信息
Department of Hepatobiliary Surgery, the Affiliated Hospital of Southwest Medical University, Luzhou, China.
Department of Hepatobiliary Surgery, Mianyang No.3 People's Hospital, Sichuan, China.
出版信息
Turk J Gastroenterol. 2021 Jan;32(1):97-105. doi: 10.5152/tjg.2020.19594.
BACKGROUND
Bile acid metabolism is a contributing factor that promotes cholelithiasis. Recent studies have suggested novel roles of leptin in the formation of gallbladder stones (GS); however, no evidence confirmed the function of leptin in the formation of primary intrahepatic bile duct stones (PIBDS) . In the current study, the liver tissues of patients with GS and PIBDS were collected to check the mRNA and protein expression levels of BSEP.
METHODS
L02 cells stimulated with leptin were served for the expression of OB-Rb, AMPKα2, and BSEP by quantitative-polymerase chain reaction (q-PCR), Western blot, and immunohistochemistry, respectively.
RESULTS
The results showed that the level of serum leptin was higher in the GS group than in the control and PIBDS groups. Compared with the control group, the expression levels of OB-Rb, p-AMPKa2, and BSEP decreased significantly in the GS and PIBDS groups. In vitro, compared with the control cells, the protein levels of OB-Rb, p-AMPKa2, and BSEP increased in the L02 cells cultured with leptin. However, these enhancements disappeared when the cells were co-cultured with leptin plus Compound C.
CONCLUSION
The present results suggest that cholelithiasis, especially the formation of PIBDS, was connected with leptin, which could regulate bile acid metabolism through the OB-Rb/AMPKa2/BSEP signaling pathway.
背景
胆汁酸代谢是促进胆石形成的一个因素。最近的研究表明瘦素在胆囊结石（GS）形成中有新的作用；然而，没有证据证实瘦素在原发性肝内胆管结石（PIBDS）形成中的作用。在本研究中，收集了 GS 和 PIBDS 患者的肝组织，以检查 BSEP 的 mRNA 和蛋白表达水平。
方法
用瘦素刺激 L02 细胞，通过定量聚合酶链反应（q-PCR）、Western blot 和免疫组织化学分别检测 OB-Rb、AMPKα2 和 BSEP 的表达。
结果
结果表明，GS 组血清瘦素水平高于对照组和 PIBDS 组。与对照组相比，GS 和 PIBDS 组 OB-Rb、p-AMPKa2 和 BSEP 的表达水平显著降低。体外，与对照细胞相比，在瘦素培养的 L02 细胞中，OB-Rb、p-AMPKa2 和 BSEP 的蛋白水平增加。然而，当细胞与瘦素加 Compound C 共培养时，这些增强作用消失了。
结论
本研究结果提示胆石病，特别是 PIBDS 的形成与瘦素有关，瘦素可能通过 OB-Rb/AMPKa2/BSEP 信号通路调节胆汁酸代谢。
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