Myeloid-derived miR-6236 potentiates adipocyte insulin signaling and prevents hyperglycemia during obesity

Nat Commun. 2024 Jun 25;15(1):5394. doi: 10.1038/s41467-024-49632-z.

Abstract

Adipose tissue macrophages (ATMs) influence obesity-associated metabolic dysfunction, but the mechanisms by which they do so are not well understood. We show that miR-6236 is a bona fide miRNA that is secreted by ATMs during obesity. Global or myeloid cell-specific deletion of miR-6236 aggravates obesity-associated adipose tissue insulin resistance, hyperglycemia, hyperinsulinemia, and hyperlipidemia. miR-6236 augments adipocyte insulin sensitivity by inhibiting translation of negative regulators of insulin signaling, including PTEN. The human genome harbors a miR-6236 homolog that is highly expressed in the serum and adipose tissue of obese people. hsa-MIR-6236 expression negatively correlates with hyperglycemia and glucose intolerance, and positively correlates with insulin sensitivity. Together, our findings establish miR-6236 as an ATM-secreted miRNA that potentiates adipocyte insulin signaling and protects against metabolic dysfunction during obesity.

MeSH terms

  • Adipocytes* / metabolism
  • Adipose Tissue / metabolism
  • Animals
  • Humans
  • Hyperglycemia* / genetics
  • Hyperglycemia* / metabolism
  • Hyperinsulinism / genetics
  • Hyperinsulinism / metabolism
  • Insulin Resistance* / genetics
  • Insulin* / metabolism
  • Macrophages / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Myeloid Cells / metabolism
  • Obesity* / genetics
  • Obesity* / metabolism
  • PTEN Phosphohydrolase* / genetics
  • PTEN Phosphohydrolase* / metabolism
  • Signal Transduction*

Substances

  • MicroRNAs
  • Insulin
  • PTEN Phosphohydrolase