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Catalpol ameliorates hepatic insulin resistance in type 2 diabetes through acting on AMPK/NOX4/PI3K/AKT pathway

Jiting Yan1, Changyuan Wang1, Yue Jin1

  • 1Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, China.

Pharmacological Research
|December 29, 2017
PubMed

Insights

Catalpol, a natural compound, effectively combats hepatic insulin resistance in type 2 diabetes by regulating gluconeogenesis and glycogen synthesis. It works by modulating the AMPK/NOX4/PI3K/AKT pathway, reducing oxidative stress.

Area of Science:

  • Metabolic Diseases
  • Pharmacology
  • Cellular Biology

Background:

  • Type 2 diabetes is marked by insulin resistance and hyperglycemia.
  • Catalpol, from Rehmannia glutinosa, shows potential anti-diabetic effects.

Purpose of the Study:

  • To investigate catalpol's therapeutic effects on hepatic insulin resistance in type 2 diabetes.
  • To elucidate the underlying cellular mechanisms of catalpol's action.

Main Methods:

  • Type 2 diabetes induced in mice (HFD + STZ) and HepG2 cells (glucosamine).
  • Assessed effects on gluconeogenesis, glycogen synthesis, oxidative stress (NOX4), and signaling pathways (AMPK, PI3K/AKT).
  • Utilized PI3K inhibitor (LY294002) and siRNA for NOX4 and AMPK knockdown.

Main Results:

  • Catalpol decreased hepatic gluconeogenesis and increased glycogen synthesis in vivo and in vitro.
  • Catalpol reduced NOX4-mediated oxidative stress and activated AMPK and PI3K/AKT pathways.
  • Inhibiting PI3K, NOX4, or AMPK blocked catalpol's beneficial effects.

Conclusions:

  • Catalpol ameliorates hepatic insulin resistance in type 2 diabetes.
  • The mechanism involves regulating the AMPK/NOX4/PI3K/AKT pathway.
Keywords:
AMPKCatalpolInsulin resistanceNOX4Type 2 diabetes

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