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Published on: May 16, 2021

NO-1886 ameliorates glycogen metabolism in insulin-resistant HepG2 cells by GSK-3β signalling

Zong-Bao Wang1, Huai-Cai Zeng, Han-Song Wei

  • 1Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan, China.

The Journal of Pharmacy and Pharmacology
|January 7, 2012
PubMed
Abstract

Insights

NO-1886, a lipoprotein lipase activator, effectively combats palmitate-induced insulin resistance in HepG2 cells. It enhances glucose consumption and glycogen synthesis, potentially through GSK-3 signaling pathways.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Research

Background:

  • Insulin resistance is a key metabolic disorder.
  • Palmitate exposure in HepG2 cells mimics insulin resistance.
  • Understanding novel therapeutic mechanisms is crucial.

Purpose of the Study:

  • To investigate NO-1886's role in palmitate-induced insulin resistance.
  • To elucidate the molecular mechanisms of NO-1886 action.

Main Methods:

  • HepG2 cells were treated with palmitate to induce insulin resistance.
  • NO-1886's effects on glucose, glycogen, and free fatty acids were analyzed.
  • mRNA and protein levels of key signaling molecules were assessed.

Main Results:

  • Palmitate significantly reduced insulin-induced glucose consumption.
  • NO-1886 (10 µM) stimulated glucose consumption, glycogen synthesis, and FFA absorption.
  • NO-1886 upregulated lipoprotein lipase mRNA and modulated GSK-3β phosphorylation.

Conclusions:

  • NO-1886 ameliorates insulin resistance in HepG2 cells.
  • Glycogen synthesis is enhanced by NO-1886.
  • The mechanism involves GSK-3 signaling pathways.

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