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Amelioration of obesity-induced diabetes by a novel autophagy enhancer

Hyejin Lim1, Myung-Shik Lee1

  • 1Severance Biomedical Science Institute and Dept. of Medicine, Yonsei University College of Medicine, Seoul, Korea.

Cell Stress
|June 22, 2019
PubMed

Insights

A novel small molecule, MSL, enhances autophagy by activating Tfeb. This improves lipid clearance and mitochondrial function, benefiting metabolic health in obese mice.

Area of Science:

  • Metabolic research
  • Cellular biology
  • Pharmacology

Background:

  • Autophagy insufficiency is linked to metabolic syndrome and diabetes.
  • Enhancing autophagy may benefit obese individuals' metabolism.
  • Identifying small molecules that boost autophagy is crucial for therapeutic development.

Purpose of the Study:

  • To screen for novel small molecules that enhance autophagy.
  • To investigate the metabolic effects of identified autophagy enhancers.
  • To explore the therapeutic potential of autophagy enhancement in metabolic diseases.

Main Methods:

  • Screened over 7000 chemical substances using a Renilla-LC3-based luciferase assay.
  • Identified and characterized a novel autophagy enhancer, MSL (4-(4-fluorophenyl)sulfonyl-5-methylthio-2-phenyloxazole).
  • Assessed MSL's effects on Tfeb activation, lipid clearance (lipophagy), inflammasome activation, mitochondrial function, and metabolic profiles in vitro and in vivo.

Main Results:

  • MSL was identified as a potent autophagy enhancer via Tfeb activation.
  • MSL treatment expedited lipid clearance, likely through lipophagy.
  • MSL ameliorated mitochondrial dysfunction, reducing inflammasome activation and improving metabolic profiles in obese mice.

Conclusions:

  • MSL demonstrates significant potential as a therapeutic agent for metabolic disorders.
  • Autophagy enhancement through small molecules like MSL offers a promising strategy for treating obesity and related conditions.
  • Targeting autophagy pathways can improve metabolic health by enhancing lipid metabolism and reducing inflammation.
Keywords:
Ca2+Tfebcalcineurinlysosomephosphatase

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