Perilipin5 protects against lipotoxicity and alleviates endoplasmic reticulum stress in pancreatic β-cells.

Background: Chronic exposure of pancreatic β-cells to excess free fatty acids is thought to contribute to type 2 diabetes pathogenesis in obesity by impairing β-cell function and even leading to apoptosis. In β-cells, lipid droplet-associated protein perilipin 5 (PLIN5) has been shown to enhance ins...

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Publicado en:Nutrition & Metabolism Vol. 16; no. 1
Autores principales: Zhu, Yunxia, Zhang, Xiaoyan, Zhang, Li, Zhang, Mingliang, Li, Ling, Luo, Deng, Zhong, Yuan
Formato: research tables/charts Journal Article
Publicado: BioMed Central 7/30/2019
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 7/30/2019
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      pub: BioMed Central
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        10.1186/s12986-019-0375-2
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        atl: Perilipin5 protects against lipotoxicity and alleviates endoplasmic reticulum stress in pancreatic β-cells.
      aug:
        au:
          Zhu, Yunxia
          Zhang, Xiaoyan
          Zhang, Li
          Zhang, Mingliang
          Li, Ling
          Luo, Deng
          Zhong, Yuan
        affil: Department of Geriatrics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, No.600, Yishan Road, 200233, Shanghai, China
      sug:
        subj:
          Carrier Proteins Metabolism
          Fatty Acids Metabolism
          Oxidation-Reduction
          Endoplasmic Reticulum
          Stress, Physiological
          Islets of Langerhans Metabolism
          Animal Studies
          Mice
          Apoptosis
          Diabetes Mellitus, Type 2
          Insulin
          Cell Viability
          Biological Assay
          Analysis of Variance
          T-Tests
      ab: Background: Chronic exposure of pancreatic β-cells to excess free fatty acids is thought to contribute to type 2 diabetes pathogenesis in obesity by impairing β-cell function and even leading to apoptosis. In β-cells, lipid droplet-associated protein perilipin 5 (PLIN5) has been shown to enhance insulin secretion by regulating intracellular lipid metabolism; the roles of PLIN5 in response to lipotoxicity remain poorly understood. Methods: INS-1 β-cells were transfected with PLIN5-overexpression adenovirus (Ad-PLIN5) and treated with palmitate. C57BL/6 J male mice were fed with high fat diet and tail intravenous injected with adeno-associated virus overexpressing PLIN5 (AAV-PLIN5) in β-cells. Results: Our data showed that palmitate and PPAR agonists including WY14643 (PPARα), GW501516 (PPARβ/δ), rosiglitazone (PPARγ) in vitro all induced PLIN5 expression in INS-1 cells. Under palmitate overload, although upregulating PLIN5 promoted lipid droplet storage, it alleviated lipotoxicity in INS-1 β-cells with improved cell viability, cell apoptosis and β-cell function. The protection role of PLIN5 in β-cell function observed in cell experiments were further verified in in vivo study indicated by mitigated glucose intolerance in high fat diet fed mice with β-cell-specific overexpression of PLIN5. Mechanistic experiments revealed that enhanced FAO induced by elevation of PLIN5, followed by decreased ER stress may be a major mechanism responsible for alleviation of lipotoxicity observed in the present study. Conclusions: Our finding substantiated the important role of PLIN5 in protection against lipotoxicity in β-cells.
      pubtype: Academic Journal
      doctype:
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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