Endocrine · 2025
PLIN5 regulates lipid metabolism via PGC-1α/Drp1 signaling in islet β-cells.
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Sun Zhenyu, Zhao Jiahao, Fan Siwen, Huang Xingyu, Fu Hao, Liu Haiyan, Sun Wen, Zhou Zihui, Wu Danlian, Zhu Xia
Аннотация
AIMS: This study investigated the protective role of Perilipin 5 (PLIN5) in pancreatic β-cell dysfunction under diabetic conditions, focusing on its regulatory effects on lipid metabolism and mitochondrial dynamics.
MATERIALS AND METHODS: Diabetic db/db mice and pancreatic beta cell line INS-1 were employed to investigate the role of PLIN5 in insulin secretion and lipid metabolism under high glucose (HG) conditions. The phenotypic changes were evaluated by staining and measurement of biochemical indexes. The molecular mechanism was explored by biological techniques such as Western blotting, qPCR, immunofluorescence and lentivirus infection.
RESULTS: PLIN5 was decreased under diabetic conditions which was related to lipid accumulation in the pancreas. The in vitro knockdown of PLIN5 promoted apoptosis in INS-1 cells, leading to a reduction in insulin secretion mediated by lipid accumulation. PLIN5 knockdown also promoted mitochondrial dysfunction in normal-glucose-cultured INS-1 cells mainly through decreasing PGC-1α and increasing Drp1 levels. In contrast, PLIN5 overexpression reversed the damage caused by HG in INS-1 cells, such as increased apoptosis and lipid accumulation, mitochondrial dysfunction and weakened capacity of insulin secretion. PLIN5 overexpression also blunted the inhibitory effects of HG on PGC-1α and Drp1 expressions. The reduced expression of PLIN5 also led to decreased binding of PGC-1α to the promoter region of Drp1.
CONCLUSIONS: Our data indicate that PLIN5 acts as a potent regulator of lipid accumulation in pancreatic β cells treated with HG through the modulation of PGC-1α and Drp1.
MATERIALS AND METHODS: Diabetic db/db mice and pancreatic beta cell line INS-1 were employed to investigate the role of PLIN5 in insulin secretion and lipid metabolism under high glucose (HG) conditions. The phenotypic changes were evaluated by staining and measurement of biochemical indexes. The molecular mechanism was explored by biological techniques such as Western blotting, qPCR, immunofluorescence and lentivirus infection.
RESULTS: PLIN5 was decreased under diabetic conditions which was related to lipid accumulation in the pancreas. The in vitro knockdown of PLIN5 promoted apoptosis in INS-1 cells, leading to a reduction in insulin secretion mediated by lipid accumulation. PLIN5 knockdown also promoted mitochondrial dysfunction in normal-glucose-cultured INS-1 cells mainly through decreasing PGC-1α and increasing Drp1 levels. In contrast, PLIN5 overexpression reversed the damage caused by HG in INS-1 cells, such as increased apoptosis and lipid accumulation, mitochondrial dysfunction and weakened capacity of insulin secretion. PLIN5 overexpression also blunted the inhibitory effects of HG on PGC-1α and Drp1 expressions. The reduced expression of PLIN5 also led to decreased binding of PGC-1α to the promoter region of Drp1.
CONCLUSIONS: Our data indicate that PLIN5 acts as a potent regulator of lipid accumulation in pancreatic β cells treated with HG through the modulation of PGC-1α and Drp1.