Abstract
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.
Highlights
CapsaicinCapsaicin was first isolated in 1876 [1], its structure was determined in 1919 [2], and it was chemically synthesized in 1930 [3]
transient receptor potential vanilloid channel 1 (TRPV1) has been identified on pancreatic β-cells, and channel channel activation has been associated with improved insulin secretion [37]
Insulin resistance was considered as the major component in the development of metabolic syndrome, and it was called insulin resistance syndrome [51]. This hypothesis was supported by an animal study, which provided evidence that insulin resistance developed before other components of metabolic syndrome [52]
Summary
Capsaicin was first isolated in 1876 [1], its structure was determined in 1919 [2], and it was chemically synthesized in 1930 [3]. TRPV1 was identified on GLP-1-expressing intestinal cells, which upon activation stimulated. TRPV1 was identified on GLP-1-expressing intestinal cells, which upon activation stimulated GLP-1. GLP-1 is an incretin hormone that induces expansion of insulin-secreting β-cell release [34]. GLP-1 is an incretin hormone that induces expansion of insulin-secreting β-cell mass; mass; this change augments glucose-stimulated insulin secretion [35]. TRPV1 has been identified on pancreatic β-cells, and channel channel activation has been associated with improved insulin secretion [37]. Capsaicin induces pain by sensitization of TRPV1, sensitization of TRPV1, leading to inflammation producing pain [28,40]. Exposure to high or repeated doses of or repeated doses of capsaicin leads to desensitization of TRPV1, producing analgesia [40].
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