Department of General Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Department of General Surgery, Huashan Hospital, Fudan University, Shanghai, 201907, China.
Sci Rep. 2017 Apr 7;7(1):734. doi: 10.1038/s41598-017-00821-5.
Fatty liver (FL) is one of the risk factors for acute pancreatitis and is also indicative of a worse prognosis as compared to acute pancreatitis without fatty liver (AP). The aim of the present study was to analyze, at the hepatic level, the differentially expressed genes (DEGs) between acute pancreatitis with fatty liver (APFL) rats and AP rats. GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analyses of these DEGs indicated that PPARα signalling pathway and fatty acid degradation pathway may be involved in the pathological process of APFL, which indicated that fatty liver may aggravate pancreatitis through these pathways. Moreover, the excessive activation of JAK/STAT signaling pathway and toll-like receptor signaling pathway was also found in APFL group as shown in heat map. In conclusion, the inhibition of PPARα signaling pathway and the fatty acid degradation pathway may lead to the further disorder of lipid metabolism, which can aggravate pancreatitis.
脂肪肝(FL)是急性胰腺炎的危险因素之一,与无脂肪肝的急性胰腺炎(AP)相比,预后更差。本研究旨在分析脂肪肝性急性胰腺炎(APFL)大鼠与 AP 大鼠肝组织中差异表达基因(DEGs)。这些 DEGs 的 GO(基因本体论)和 KEGG(京都基因与基因组百科全书)通路分析表明,PPARα 信号通路和脂肪酸降解通路可能参与 APFL 的病理过程,这表明脂肪肝可能通过这些通路加重胰腺炎。此外,如图所示,在 APFL 组还发现 JAK/STAT 信号通路和 Toll 样受体信号通路的过度激活。总之,抑制 PPARα 信号通路和脂肪酸降解通路可能导致脂质代谢进一步紊乱,从而加重胰腺炎。