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An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
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Exenatide increases CTRP3 gene expression in adipose cells by inhibiting adipogenesis and induces apoptosis

Meliha Koldemir Gündüz1, Güllü Kaymak2, Ertan Kanbur3

  • 1Kutahya Health Sciences University, Faculty of Engineering and Natural Sciences, Department of Basic Sciences of Engineering, Kütahya, Turkey.

Toxicology in Vitro : an International Journal Published in Association with BIBRA
|September 24, 2022
PubMed

Insights

Exenatide, a Glucagon-Like Peptide-1 Receptor Agonist (GLP-1RA), shows promise for obesity treatment by altering adipogenesis gene expression and increasing apoptosis in 3T3-L1 adipocytes. This weight control drug candidate elevates CTRP3 and reduces PPAR-γ, suggesting therapeutic potential.

Area of Science:

  • Biochemistry and Molecular Biology
  • Pharmacology
  • Cell Biology

Background:

  • The global obesity epidemic necessitates novel weight control pharmacotherapies.
  • Incretin-based therapies, particularly Glucagon-Like Peptide-1 Receptor Agonists (GLP-1RAs), are emerging as potential treatments for obesity.
  • Exenatide is a GLP-1RA with potential applications in weight management.

Purpose of the Study:

  • To evaluate the cytotoxicity of exenatide on 3T3-L1 adipocytes.
  • To investigate the effects of exenatide on adipogenesis-related gene expression, intracellular insulin and glucose levels, and apoptosis.
  • To assess exenatide's potential as a pharmacotherapeutic agent for obesity.

Main Methods:

  • Cytotoxicity was assessed using the MTT assay.
  • Gene expression levels of adipogenesis markers were quantified via qPCR.
  • Apoptosis was analyzed using the Muse Cell Analyzer.
  • Intracellular insulin and glucose levels were measured in treated adipocytes.

Main Results:

  • Exenatide treatment significantly increased C1q/TNF-related protein-3 (CTRP3) expression (p < 0.001).
  • PPAR-γ gene expression was significantly downregulated in exenatide-treated adipocytes (p < 0.001).
  • Intracellular insulin and glucose levels increased, and total apoptosis rose approximately 1.5-fold with exenatide administration.

Conclusions:

  • Exenatide modulates adipogenesis and lipogenesis by altering CTRP3 and PPAR-γ expression.
  • The induction of apoptosis and regulation of key adipogenic genes suggest exenatide's therapeutic potential for obesity.
  • Exenatide represents a promising pharmacotherapeutic candidate for obesity management, warranting further investigation.
Keywords:
3T3-L1 cell lineAdipogenesisCTRP3 geneExenatideObesity

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