Dietary capsaicin reduces obesity-induced insulin resistance and hepatic steatosis in obese mice fed a high-fat diet

Obesity (Silver Spring). 2010 Apr;18(4):780-7. doi: 10.1038/oby.2009.301. Epub 2009 Oct 1.


Obesity-induced inflammation contributes to the development of obesity-related metabolic disorders such as insulin resistance, type 2 diabetes, fatty liver disease, and cardiovascular disease. In this study, we investigated whether dietary capsaicin can reduce obesity-induced inflammation and metabolic disorders such as insulin resistance and hepatic steatosis. Male C57BL/6 obese mice fed a high-fat diet for 10 weeks received a supplement of 0.015% capsaicin for a further 10 weeks and were compared with unsupplemented controls. Glucose intolerance was estimated by glucose tolerance tests. Transcripts of adipocytokine genes and the corresponding proteins were measured by reverse transcription-PCR and enzyme-linked immunosorbent assay, and macrophage numbers were determined by flow cytometric analysis. Transient receptor potential vanilloid type-1 (TRPV-1), peroxisome proliferator-activated receptor (PPAR)-alpha, and PPARgamma coactivator-1alpha (PGC-1alpha) mRNAs were also measured by RT-PCR, and PPARalpha luciferase assays were performed. Dietary capsaicin lowered fasting glucose, insulin, leptin levels, and markedly reduced the impairment of glucose tolerance in obese mice. Levels of tumor necrosis factor-alpha (TNFalpha), monocyte chemoattractant protein-1 (MCP-1), and interleukin (IL)-6 mRNAs and proteins in adipose tissue and liver decreased markedly, as did macrophage infiltration, hepatic triglycerides, and TRPV-1 expression in adipose tissue. At the same time, the mRNA/protein of adiponectin in the adipose tissue and PPARalpha/PGC-1alpha mRNA in the liver increased. Moreover, luciferase assays revealed that capsaicin is capable of binding PPARalpha. Our data suggest that dietary capsaicin may reduce obesity-induced glucose intolerance by not only suppressing inflammatory responses but also enhancing fatty acid oxidation in adipose tissue and/or liver, both of which are important peripheral tissues affecting insulin resistance. The effects of capsaicin in adipose tissue and liver are related to its dual action on PPARalpha and TRPV-1 expression/activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiponectin / genetics
  • Adiponectin / metabolism
  • Adipose Tissue / metabolism
  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Anti-Inflammatory Agents / therapeutic use*
  • Blood Glucose / metabolism
  • Capsaicin / pharmacology
  • Capsaicin / therapeutic use*
  • Dietary Fats / administration & dosage
  • Dietary Fats / metabolism
  • Dietary Supplements
  • Disease Models, Animal
  • Fatty Liver / drug therapy*
  • Fatty Liver / etiology
  • Fatty Liver / metabolism
  • Flow Cytometry
  • Gene Expression
  • Glucose Intolerance / etiology
  • Glucose Intolerance / metabolism
  • Hypoglycemic Agents / pharmacology
  • Hypoglycemic Agents / therapeutic use*
  • Inflammation / genetics
  • Insulin / blood
  • Insulin Resistance*
  • Leptin / blood
  • Lipid Metabolism / drug effects
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • Obesity / complications*
  • Obesity / drug therapy
  • Obesity / metabolism
  • PPAR alpha / chemistry
  • PPAR alpha / genetics
  • PPAR alpha / metabolism
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • TRPV Cation Channels / genetics
  • TRPV Cation Channels / metabolism
  • Triglycerides / metabolism


  • Adiponectin
  • Anti-Inflammatory Agents
  • Blood Glucose
  • Dietary Fats
  • Hypoglycemic Agents
  • Insulin
  • Leptin
  • PPAR alpha
  • RNA, Messenger
  • TRPV Cation Channels
  • TRPV1 protein, human
  • Triglycerides
  • Capsaicin