Capsaicin in Metabolic Syndrome

Nutrients. 2018 May 17;10(5):630. doi: 10.3390/nu10050630.


Capsaicin, the major active constituent of chilli, is an agonist on transient receptor potential vanilloid channel 1 (TRPV1). TRPV1 is present on many metabolically active tissues, making it a potentially relevant target for metabolic interventions. Insulin resistance and obesity, being the major components of metabolic syndrome, increase the risk for the development of cardiovascular disease, type 2 diabetes, and non-alcoholic fatty liver disease. In vitro and pre-clinical studies have established the effectiveness of low-dose dietary capsaicin in attenuating metabolic disorders. These responses of capsaicin are mediated through activation of TRPV1, which can then modulate processes such as browning of adipocytes, and activation of metabolic modulators including AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor α (PPARα), uncoupling protein 1 (UCP1), and glucagon-like peptide 1 (GLP-1). Modulation of these pathways by capsaicin can increase fat oxidation, improve insulin sensitivity, decrease body fat, and improve heart and liver function. Identifying suitable ways of administering capsaicin at an effective dose would warrant its clinical use through the activation of TRPV1. This review highlights the mechanistic options to improve metabolic syndrome with capsaicin.

Keywords: TRPV1; capsaicin; diabetes; insulin resistance; metabolic syndrome; non-alcoholic fatty liver disease; obesity; transient receptor potential vanilloid channel 1.

Publication types

  • Review

MeSH terms

  • AMP-Activated Protein Kinases / drug effects
  • AMP-Activated Protein Kinases / metabolism
  • Adipocytes / drug effects
  • Adipose Tissue / drug effects
  • Animals
  • Capsaicin* / administration & dosage
  • Capsaicin* / chemistry
  • Capsaicin* / pharmacology
  • Diabetes Mellitus, Type 2
  • Diet
  • Glucagon-Like Peptide 1 / drug effects
  • Glucagon-Like Peptide 1 / metabolism
  • Humans
  • Insulin Resistance
  • Metabolic Syndrome* / prevention & control
  • Non-alcoholic Fatty Liver Disease
  • Obesity
  • Oxidation-Reduction
  • PPAR alpha / drug effects
  • PPAR alpha / metabolism
  • TRPV Cation Channels / agonists
  • TRPV Cation Channels / drug effects
  • TRPV Cation Channels / physiology
  • Uncoupling Protein 1 / drug effects
  • Uncoupling Protein 1 / metabolism


  • PPAR alpha
  • TRPV Cation Channels
  • TRPV1 protein, human
  • Uncoupling Protein 1
  • Glucagon-Like Peptide 1
  • AMP-Activated Protein Kinases
  • Capsaicin