Therapeutic potential of peroxisome proliferators--activated receptor-alpha/gamma dual agonist with alleviation of endoplasmic reticulum stress for the treatment of diabetes

Diabetes. 2008 Mar;57(3):737-45. doi: 10.2337/db07-0972. Epub 2007 Dec 7.

Abstract

Objective: Peroxisome proliferator-activated receptor (PPAR) alpha/gamma dual agonists have the potential to be used as therapeutic agents for the treatment of type 2 diabetes. This study evaluated the function of macelignan, a natural compound isolated from Myristica fragrans, as a dual agonist for PPARalpha/gamma and investigated its antidiabetes effects in animal models.

Research design and methods: GAL4/PPAR chimera transactivation was performed and the expression of PPARalpha/gamma target genes was monitored to examine the ability of macelignan to activate PPARalpha/gamma. Additionally, macelignan was administrated to obese diabetic (db/db) mice to investigate antidiabetes effects and elucidate its molecular mechanisms.

Results: Macelignan reduced serum glucose, insulin, triglycerides, free fatty acid levels, and triglycerides levels in the skeletal muscle and liver of db/db mice. Furthermore, macelignan significantly improved glucose and insulin tolerance in these mice, and without altering food intake, their body weights were slightly reduced while weights of troglitazone-treated mice increased. Macelignan increased adiponectin expression in adipose tissue and serum, whereas the expression and serum levels of tumor necrosis factor-alpha and interleukin-6 decreased. Macelignan downregulated inflammatory gene expression in the liver and increased AMP-activated protein kinase activation in the skeletal muscle of db/db mice. Strikingly, macelignan reduced endoplasmic reticulum (ER) stress and c-Jun NH(2)-terminal kinase activation in the liver and adipose tissue of db/db mice and subsequently increased insulin signaling.

Conclusions: Macelignan enhanced insulin sensitivity and improved lipid metabolic disorders by activating PPARalpha/gamma and attenuating ER stress, suggesting that it has potential as an antidiabetes agent for the treatment of type 2 diabetes.

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism
  • Adipose Tissue, White / drug effects
  • Adipose Tissue, White / metabolism
  • Animals
  • Cell Line
  • Diabetes Mellitus, Type 2 / drug therapy*
  • Endoplasmic Reticulum / drug effects*
  • Insulin Receptor Substrate Proteins
  • Lignans / chemistry
  • Lignans / pharmacology*
  • Lignans / therapeutic use*
  • Liver / drug effects
  • Liver / metabolism
  • Mice
  • Mice, Obese
  • Molecular Structure
  • Myristica / chemistry
  • PPAR alpha / agonists*
  • PPAR gamma / agonists*
  • Stress, Physiological
  • Thapsigargin

Substances

  • Adaptor Proteins, Signal Transducing
  • Insulin Receptor Substrate Proteins
  • Irs1 protein, mouse
  • Lignans
  • PPAR alpha
  • PPAR gamma
  • Thapsigargin
  • macelignan