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Adipose tissue macrophage-derived exosomal miR-29a regulates obesity-associated insulin resistance

Ting Liu1, Yu-Chen Sun1, Peng Cheng2

  • 1Department of Endocrinology, Changsha Central Hospital, Changsha, Hunan, 410004, China.

Biochemical and Biophysical Research Communications
|June 3, 2019
PubMed

Insights

Obesity increases exosomal miR-29a from adipose tissue macrophages, impairing insulin sensitivity. Targeting this microRNA offers a potential therapy for obesity-associated type 2 diabetes.

Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Molecular Biology

Background:

  • Obesity-associated insulin resistance precedes type 2 diabetes.
  • Macrophages in adipose tissue regulate insulin sensitivity via exosome-secreted miRNAs.

Purpose of the Study:

  • To investigate the role of exosomal miR-29a derived from obese adipose tissue macrophages (ATMs) in insulin resistance.
  • To identify the mechanism by which miR-29a contributes to insulin resistance.

Main Methods:

  • Quantification of miR-29a in exosomes from obese ATMs.
  • In vitro and in vivo transfer of exosomal miR-29a into target cells.
  • Administration of obese ATMs-Exos to lean mice.
  • Knockdown of miR-29a in obese ATM-Exos.
  • Identification of PPAR-δ as a downstream target.
  • Assessment of insulin sensitivity and effects of PPAR-δ agonist.

Main Results:

  • miR-29a levels are elevated in exosomes derived from obese ATMs.
  • Obese ATMs-Exos transfer miR-29a into adipocytes, myocytes, and hepatocytes, inducing insulin resistance.
  • Administration of obese ATMs-Exos impairs insulin sensitivity in lean mice.
  • Knockdown of miR-29a in obese ATM-Exos mitigates insulin resistance.
  • PPAR-δ is a downstream target of miR-29a, and its agonist partially rescues insulin resistance.

Conclusions:

  • Exosomal miR-29a from obese ATMs contributes to obesity-associated insulin resistance.
  • miR-29a acts via the PPAR-δ pathway.
  • Exosomal miR-29a represents a potential therapeutic target for obesity-related type 2 diabetes.
Keywords:
ATMsExosomesInsulin resistancePPAR-δmiRNAs

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