Mechanism of GLP-1 Receptor Agonists-Mediated Attenuation of Palmitic Acid-Induced Lipotoxicity in L6 Myoblasts.

Object. L6 cells were cultured to explore the possible mechanism underlying the improvement of insulin resistance by Liraglutide (LR). Methods. Cells were divided into 5 groups—control, high-fat, 10 nmol/L LR + 0.6 mmol/L palmitic acid (PA) (10LR), 100 nmol/L LR + 0.6 mmol/L PA (100LR), and 1000 nmo...

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Publicado en:BioMed Research International pp. 1 - 9
Autores principales: Kong, Mo-wei, Gao, Yu, Xie, Yu-yu, Xing, En-hong, Sun, Li-xin, Ma, Hui-juan, Xing, Han-ying
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell 12/28/2022
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 12/28/2022
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1155/2022/6237405
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        atl: Mechanism of GLP-1 Receptor Agonists-Mediated Attenuation of Palmitic Acid-Induced Lipotoxicity in L6 Myoblasts.
      aug:
        au:
          Kong, Mo-wei
          Gao, Yu
          Xie, Yu-yu
          Xing, En-hong
          Sun, Li-xin
          Ma, Hui-juan
          Xing, Han-ying
        affil: Department of Endocrinology, Affiliated Hospital of Chengde Medical University, 36 Nanyingzi Street, Shuangqiao District, Chengde City, Hebei Province, China
      sug:
        subj:
          Glucagon-Like Peptide-1 Receptor Agonists Pharmacodynamics
          Stem Cells Drug Effects
          Muscle, Skeletal Drug Effects
          Cell Line Drug Effects
          Lipids Drug Effects
          Insulin Resistance Drug Therapy
          Diabetes Mellitus Drug Therapy
          Animal Studies
          Rats
          Reverse Transcriptase Polymerase Chain Reaction
          Blotting, Western
          Gene Expression Drug Effects
          RNA, Messenger
          Analysis of Variance
          T-Tests
          Data Analysis Software
          Descriptive Statistics
          Cell Viability Drug Effects
          Triglycerides Drug Effects
          Lipids Metabolism
          Signal Transduction Drug Effects
          Metabolic Networks and Pathways Drug Effects
          Biological Markers Analysis
      ab: Object. L6 cells were cultured to explore the possible mechanism underlying the improvement of insulin resistance by Liraglutide (LR). Methods. Cells were divided into 5 groups—control, high-fat, 10 nmol/L LR + 0.6 mmol/L palmitic acid (PA) (10LR), 100 nmol/L LR + 0.6 mmol/L PA (100LR), and 1000 nmol/L LR + 0.6 mmol/L PA (1000LR). CCK-8 method to detect cell viability, GPO-PAP enzymatic method to detect intracellular triglyceride content, and reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) and western blotting methods to detect fatty acid translocase CD36 (FAT/CD36) and fatty acid binding protein 4 (FABP4) in L6 cells, glucose-regulated protein 78 (GRP78), glucose transporter 4 (GLUT4) expression at the mRNA and protein levels, respectively, were performed. Results. We found that after PA intervention for 24 h, the cell viability decreased significantly; the cell viability of the LR group was higher than that of the high-fat group (P < 0.01). After PA intervention, compared with those in the high-fat group, GRP-78, FAT/CD36, FABP4 mRNA ((4.36 ± 0.32 vs. 8.15 ± 0.35); (1.00 ± 0.04 vs. 2.46 ± 0.08); (2.88 ± 0.55 vs. 8.29 ± 0.52), P < 0.01) and protein ((3338.13 ± 333.15 vs. 4963.98 ± 277.29); (1978.85 ± 124.24 vs. 2676.07 ± 100.64); (3372.00 ± 219.84 vs. 6083.20 ± 284.70), both P < 0.01) expression decreased in the LR group. The expression levels of GLUT4 mRNA ((0.75 ± 0.04 vs. 0.34 ± 0.03), P < 0.01) and protein ((3443.71 ± 191.89 vs. 2137.79 ± 118.75), P < 0.01) increased. Conclusion. Therefore, we conclude that LR can reverse PA-induced cell inactivation and lipid deposition, which may be related to the change in GRP-78, FAT/CD36, FABP4, GLUT4, and other factors.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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