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MOTS-c eases fatty liver in diabetic mice via hepatic ACE2

Protective effects disappeared in ACE2-knockout mice, pointing to an AMPK-dependent pathway behind exercise-induced MOTS-c secretion.

PR
By Priya Raman · Science Reporter
Oct 21 19:27 ETSource: Nature

The wire

  1. 01In diabetic MASLD mice, skeletal muscle MOTS-c expression was reduced but restored by aerobic exercise; both MOTS-c and exercise improved hepatic steatosis by suppressing lipid synthesis and inflammation.
  2. 02MOTS-c is tracked closely by longevity-peptide users, and this work ties its metabolic effect to a specific hepatic ACE2 and AMPK mechanism rather than a general claim.
  3. 03Findings rest on mice and HepG2 cells, with AMPK inhibitor Compound C blocking ACE2 upregulation in vitro; no human data, dose or safety information is presented.

From the source

Aerobic exercise induced skeletal muscle MOTS-c secretion: A novel therapy for MASLD via hepatic ACE2 regulation

Aerobic exercise is pivotal for managing metabolic dysfunction-associated steatotic liver disease (MASLD), but its mechanisms remain unclear. This study investigates the anti-MASLD effects of MOTS-c, a mitochondrial peptide secreted during aerobic exercise, in diabetic MASLD mice and HepG2 cells. Our study found MOTS-c expression in skeletal muscle was reduced in the MASLD mice but restored by aer

Read at nature.com
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