The mitochondrial-derived peptide MOTS-c is a regulator of plasma metabolites and enhances insulin sensitivity

Physiol Rep. 2019 Jul;7(13):e14171. doi: 10.14814/phy2.14171.

Abstract

MOTS-c is an exercise mimetic and improves insulin sensitivity in aged and diet-induced obese mice. Although plasma markers are good markers for the metabolic condition, whether MOTS-c changes plasma markers in diet-induced obese mice has not been examined. Here, we used an unbiased metabolomics approach to examine the effect of MOTS-c on plasma markers of metabolic dysfunction. We found that three pathways - sphingolipid metabolism, monoacylglycerol metabolism, and dicarboxylate metabolism - were reduced in MOTS-c-injected mice. Interestingly, these pathways are upregulated in obese and T2D models. MOTS-c improves insulin sensitivity and increases beta-oxidation to prevent fat accumulation in DIO mice through these pathways. These results provide us a better understanding of the mechanism of how MOTS-c improves insulin sensitivity and reduces the body weight and fatty liver and opens a new venue for further study.

Keywords: High-fat diet; MOTS-c; insulin resistance; metabolomics.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiposity / drug effects
  • Animals
  • Injections, Intraperitoneal
  • Insulin / blood
  • Insulin Resistance*
  • Lipid Metabolism / drug effects*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitochondrial Proteins / administration & dosage
  • Mitochondrial Proteins / pharmacology*
  • Monoglycerides / blood*
  • Sphingolipids / blood*

Substances

  • Insulin
  • MOTS-c peptide, human
  • Mitochondrial Proteins
  • Monoglycerides
  • Sphingolipids