Chitooligosaccharide ameliorates diet-induced obesity in mice and affects adipose gene expression involved in adipogenesis and inflammation

Abstract Chitooligosaccharide (CO) has been reported to have potential antiobestic effects in a few studies, but the antiobesity properties of CO and its related mechanisms in models of dietary obesity remain unclear. We investigated the effect of CO on body weight gain, size of adipocytes, adipokin...

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Bibliographic Details
Published in:Nutrition research (New York, N.Y.) N.Y.), 2012-03, Vol.32 (3), p.218-228
Main Authors: Choi, Eun Hye, Yang, Hyun Pil, Chun, Hyang Sook
Format: Article
Language:English
Subjects:
Adipocytes - drug effects
Adipocytes - metabolism
Adipocytes - pathology
Adipogenesis
Adipogenesis - drug effects
Adipogenesis - genetics
Animals
Anti-Obesity Agents - pharmacology
Anti-Obesity Agents - therapeutic use
Biological and medical sciences
Chitooligosaccharide
Chitosan - pharmacology
Chitosan - therapeutic use
Cytokines - genetics
Cytokines - metabolism
Diet, High-Fat - adverse effects
Dietary Fats - adverse effects
Dietary Supplements
Energy Intake - drug effects
Feeding. Feeding behavior
Fundamental and applied biological sciences. Psychology
Gastroenterology and Hepatology
Gene expression
Gene Expression - drug effects
High-fat diet
Inflammation
Inflammation - drug therapy
Inflammation - genetics
Inflammation - metabolism
Lipid Metabolism - drug effects
Lipid Metabolism - genetics
Lipids - blood
Liver - metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Obese
Microarray Analysis
Obesity
Obesity - drug therapy
Obesity - genetics
Obesity - metabolism
Oligosaccharides - pharmacology
Oligosaccharides - therapeutic use
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Weight Gain - drug effects
Weight Gain - genetics
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Summary:Abstract Chitooligosaccharide (CO) has been reported to have potential antiobestic effects in a few studies, but the antiobesity properties of CO and its related mechanisms in models of dietary obesity remain unclear. We investigated the effect of CO on body weight gain, size of adipocytes, adipokines, and lipid profiles in high-fat (HF) diet-induced obese mice and on the gene expression in adipose tissue using a complementary DNA microarray approach to test the hypothesis that CO supplementation would alleviate HF diet-induced obesity by the alteration of adipose tissue-specific gene expression. Male C57BL/6N mice were fed a normal diet (control), HF diet, or CO-supplemented HF diet (1% or 3%) for 5 months. Compared with the HF diet mice, mice fed the 3% CO-supplemented diet gained 15% less weight but did not display any change in food and energy intake. Chitooligosaccharide supplementation markedly improved serum and hepatic lipid profiles. Histologic examination showed that epididymal adipocyte size was smaller in mice fed the HF + 3% CO. Microarray analysis showed that dietary CO supplementation modulated adipogenesis-related genes such as matrix metallopeptidases 3 , 12 , 13 , and 14 ; tissue inhibitor of metalloproteinase 1 ; and cathepsin k in the adipose tissues. Twenty-five percent of the CO-responsive genes identified are involved in immune responses including the inflammatory response and cytokine production. These results suggest that CO supplementation may help ameliorate HF diet-induced weight gain and improve serum and liver lipid profile abnormalities, which are associated, at least in part, with altered adipose tissue gene expression involved in adipogenesis and inflammation.
ISSN:0271-5317
1879-0739
DOI:10.1016/j.nutres.2012.02.004