miR-129-5p Inhibits Adipogenesis through Autophagy and May Be a Potential Biomarker for Obesity

Xue Fu1, Lina Jin1, Luyu Han1

  • 1Department of Endocrinology and Metabolism, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Abstract

Insights

MicroRNA-129-5p (miR-129-5p) inhibits adipocyte differentiation and browning by targeting ATG7. Elevated serum miR-129-5p levels in obese patients suggest its potential as a biomarker and therapeutic target for obesity.

Area of Science:

  • Molecular Biology
  • Endocrinology
  • Metabolic Diseases

Background:

  • Obesity pathogenesis is complex, with microRNAs (miRNAs) potentially regulating adipocyte differentiation.
  • This study investigates the role of miR-129-5p in adipogenesis and its link to human obesity.

Purpose of the Study:

  • To elucidate the function of miR-129-5p in adipocyte differentiation and browning.
  • To identify the molecular targets of miR-129-5p in adipogenesis.
  • To explore the potential of serum miR-129-5p as a biomarker for obesity.

Main Methods:

  • Detection of miR-129-5p expression in obese mouse models.
  • In vitro studies on adipocyte differentiation and marker analysis.
  • Bioinformatics and dual-luciferase reporter assays to identify miR-129-5p targets.
  • Analysis of serum miR-129-5p levels in human obesity patients.

Main Results:

  • miR-129-5p expression is elevated in adipose tissue of obese mice.
  • miR-129-5p inhibits adipocyte differentiation and browning, downregulating FABP4, UCP1, and PPARγ.
  • miR-129-5p directly targets ATG7.
  • Serum miR-129-5p levels are significantly higher in obese patients and correlate with BMI and fat percentage.

Conclusions:

  • miR-129-5p regulates adipogenesis via the ATG7-autophagy pathway.
  • Serum miR-129-5p shows promise as a potential biomarker and therapeutic target for obesity.

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