Amodiaquine improves insulin resistance and lipid metabolism in diabetic model mice

Diabetes Obes Metab. 2018 Jul;20(7):1688-1701. doi: 10.1111/dom.13284. Epub 2018 Apr 14.

Abstract

Aims: Although peroxisome proliferator-activated receptors (PPARs)α/γ dual agonists can be beneficial for treatment of dyslipidemia in patients with type 2 diabetes, their use is limited owing to various side effects, including body weight gain, edema, and heart failure. We aimed to demonstrate that amodiaquine, an antimalarial agent, has potential as a PPARα/γ dual agonist with low risk of adverse effects.

Methods: We screened a Prestwick library (Prestwick Chemical; Illkirch, France) to identify novel PPARα/γ dual agonists and selected amodiaquine (4-[(7-chloroquinolin-4-yl)amino]-2-[(diethylamino)methyl]phenol), which activated both PPAR-α & -γ, for further investigation. We performed both in vitro, including glucose uptake assay and fatty acid oxidation assay, and in vivo studies to elucidate the anti-diabetic and anti-obesity effects of amodiaquine.

Results: Amodiaquine selectively activated the transcriptional activities of PPARα/γ and enhanced both fatty acid oxidation and glucose uptake without altering insulin secretion in vitro. In high-fat diet-induced obese and genetically modified obese/diabetic mice, amodiaquine not only remarkably ameliorated insulin resistance, hyperlipidemia, and fatty liver but also decreased body weight gain.

Conclusion: Our findings suggest that amodiaquine exerts beneficial effects on glucose and lipid metabolism by concurrent activation of PPARα/γ. Furthermore, amodiaquine acts as an alternative insulin-sensitizing agent with a positive influence on lipid metabolism and has potential to prevent and treat type 2 diabetes while reducing the risk of lipid abnormalities.

Keywords: antidiabetic drug; dyslipidaemia; fatty liver; glucose metabolism; glycaemic control; insulin resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Amodiaquine / pharmacology*
  • Animals
  • Antimalarials / pharmacology*
  • Blood Glucose / drug effects*
  • Blood Glucose / metabolism
  • Body Weight
  • Cell Proliferation
  • Diet, High-Fat
  • Disease Models, Animal
  • Fatty Acids / metabolism
  • Fatty Liver
  • Hyperlipidemias
  • In Vitro Techniques
  • Insulin Resistance*
  • Lipid Metabolism / drug effects*
  • Liver / drug effects*
  • Liver / metabolism
  • Mice
  • Mice, Obese
  • Oxidation-Reduction
  • PPAR alpha / agonists*
  • PPAR gamma / agonists*
  • Triglycerides / metabolism

Substances

  • Antimalarials
  • Blood Glucose
  • Fatty Acids
  • PPAR alpha
  • PPAR gamma
  • Triglycerides
  • Amodiaquine