Butyrate Improves Insulin Sensitivity and Increases Energy Expenditure in Mice
Butyrate Improves Insulin Sensitivity and Increases Energy Expenditure in Mice Zhanguo Gao 1 , Jun Yin 1 , Jin Zhang 1 , Robert E. Ward 2 , Roy J. Martin 1 , Michael Lefevre 2 , William T. Cefalu 1 and Jianping Ye 1 1 Antioxidant and Gene Regulation Laboratory, Pennington Biomedical Research Center,...
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Published in | Diabetes (New York, N.Y.) Vol. 58; no. 7; pp. 1509 - 1517 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Alexandria, VA
American Diabetes Association
01.07.2009
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Subjects | |
Online Access | Get full text |
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Summary: | Butyrate Improves Insulin Sensitivity and Increases Energy Expenditure in Mice
Zhanguo Gao 1 ,
Jun Yin 1 ,
Jin Zhang 1 ,
Robert E. Ward 2 ,
Roy J. Martin 1 ,
Michael Lefevre 2 ,
William T. Cefalu 1 and
Jianping Ye 1
1 Antioxidant and Gene Regulation Laboratory, Pennington Biomedical Research Center, Louisiana State University System, Baton
Rouge, Louisiana;
2 Nutrition and Food Sciences, Utah State University, Logan, Utah.
Corresponding author: Jianping Ye, yej{at}pbrc.edu .
Abstract
OBJECTIVE We examined the role of butyric acid, a short-chain fatty acid formed by fermentation in the large intestine, in the regulation
of insulin sensitivity in mice fed a high-fat diet.
RESEARCH DESIGN AND METHODS In dietary-obese C57BL/6J mice, sodium butyrate was administrated through diet supplementation at 5% wt/wt in the high-fat
diet. Insulin sensitivity was examined with insulin tolerance testing and homeostasis model assessment for insulin resistance.
Energy metabolism was monitored in a metabolic chamber. Mitochondrial function was investigated in brown adipocytes and skeletal
muscle in the mice.
RESULTS On the high-fat diet, supplementation of butyrate prevented development of insulin resistance and obesity in C57BL/6 mice.
Fasting blood glucose, fasting insulin, and insulin tolerance were all preserved in the treated mice. Body fat content was
maintained at 10% without a reduction in food intake. Adaptive thermogenesis and fatty acid oxidation were enhanced. An increase
in mitochondrial function and biogenesis was observed in skeletal muscle and brown fat. The type I fiber was enriched in skeletal
muscle. Peroxisome proliferator–activated receptor-γ coactivator-1α expression was elevated at mRNA and protein levels. AMP
kinase and p38 activities were elevated. In the obese mice, supplementation of butyrate led to an increase in insulin sensitivity
and a reduction in adiposity.
CONCLUSIONS Dietary supplementation of butyrate can prevent and treat diet-induced insulin resistance in mouse. The mechanism of butyrate
action is related to promotion of energy expenditure and induction of mitochondria function.
Footnotes
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received November 24, 2008.
Accepted March 24, 2009.
Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work
is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
© 2009 by the American Diabetes Association. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0012-1797 1939-327X |
DOI: | 10.2337/db08-1637 |