Written by Marcia J.Egles, MD. Capsaicin (component of hot peppers) use improved glucose levels in a test with 12 mice by 29% and reduced weight by 10%.
Capsaicin is the spicy component of hot peppers. Beyond its culinary value, capsaicin may also be useful for reducing some of the metabolic problems associated with diabetes and obesity. A laboratory study done with obese mice, whose high-fat diets were supplemented with capsaicin, showed improvements in several measures of diabetes and obesity associated impairments.
In the experiment, twelve young male mice were fattened-up by a high-fat (45 per cent of the calories from lard and soybean oil) diet for ten weeks. These obese mice were then divided into two groups. For the next ten weeks, both groups continued to receive the same diet in equal amounts, but one group’s food was supplemented with capsaicin. The capsaicin comprised 0.015% of the food total, reflective of the amount of capsaicin found in the daily diet of Korea where the study was conducted (1).
The most important finding of the study was that capsaicin was markedly protective against obesity-induced glucose intolerance. Eight weeks into the capsaicin supplementation, the mice underwent glucose tolerance tests. The glucose tolerance test measures how high blood glucose levels climb after the subject eats a set amount of glucose. The control mice were significantly (p less than 0.05) less glucose tolerant than the capsaicin supplemented mice. The glucose level of the control mice reached 312 mg/dl on average at 60 minutes compared to 220mg/dl in the capsaicin mice. At the conclusion of the study’s twenty weeks, control mice were significantly more obese than the capsaicin mice. The average weight of a control mouse was 41 grams compared with 37 grams in the supplemented mice.
In mice as in humans, obesity causes inflammation (2) which contributes to metabolic disorders such as glucose intolerance, type II diabetes, fatty liver disease, and cardiac disease. Comparisons of the microscopic appearance of tissues between the two groups showed more pronounced inflammatory changes in the control mice.
Fatty droplets indicative of fatty liver were numerous in the liver cells of the controls but absent in those of the capsaicin mice.
The insulin resistance of obesity is characterized by increases in levels of free fatty acids and leptin and decreases in levels of the adiponectin (3).( Leptin and adiponectin are proteins.) Plasma levels of free fatty acids and leptin were found to be significantly lower in the capsaicin mice compared to control mice. Conversely, levels of adiponectin, an insulin sensitizer, increased with capsaicin supplementation.
The mechanism of capsaicin’s activity was pursued through evaluation of specific gene and protein activity important to glucose regulation and to inflammatory processes. Capsaicin appears to reduce obesity-induced glucose intolerance not only by suppressing inflammatory responses, but also by enhancing fatty acid processing in adipose tissue and in the liver.
The overall conclusion of the study in mice suggests that capsaicin may be useful in reducing not only obesity-induced inflammation, but also obesity related metabolic disorders such as insulin resistance and fatty liver disease. To date, there is a lack of human clinical studies evaluating capsaicin.
Source: Kang, Ji‐Hye, et al. “Dietary capsaicin reduces obesity‐induced insulin resistance and hepatic steatosis in obese mice fed a high‐fat diet.” Obesity 18.4 (2010): 780-787.
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Posted February 11, 2013.
Marcia Egles, MD, graduated from Vanderbilt University School of Medicine in 1986. She completed her residency in Internal Medicine a St. Louis University Hospital. Dr. Egles is certified in Internal Medicine and is a member of the American College of Physicians. She resides in Avon, IN with her husband and two sons.
References:
- Ji-Hye Kang et al. in Dietary Capsaicin Reduces Obesity-induced Insulin Resistance and Hepatic Steatosis in Obese Mice Fed a High-fat Diet in Obesity (2010) 18,780-787, doi:10.1038/oby.2009.301 (1)
- Xu H, Barnes GT, Yang Q et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest2003;112:1821–1830.
- Lewis GF, Carpentier A, Adeli K, Giacca A. Disordered fat storage and mobilization in the pathogenesis of insulin resistance and type 2 diabetes. Endocr Rev 2002;23:201–229.
