High‐fat diet‐induced obesity in myostatin null mice

The objective of this experiment was to examine the resistance to diet‐induced obesity of myostatin (Mstn) null mice and determine if genes involved in thermogenesis were altered in these mice. Four‐week‐old male Mstn null and wild type mice were given ad libitum access to diets with 10 or 60% kcal...

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Bibliographic Details
Published in:The FASEB journal Vol. 24; no. S1; p. 547.10
Main Authors: Dilger, Anna Carol, Gabriel, Savannah R, Kutzler, Louis W, Boler, Dustin D, Killefer, John
Format: Journal Article
Language:English
Published: Federation of American Societies for Experimental Biology 01-04-2010
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Summary:The objective of this experiment was to examine the resistance to diet‐induced obesity of myostatin (Mstn) null mice and determine if genes involved in thermogenesis were altered in these mice. Four‐week‐old male Mstn null and wild type mice were given ad libitum access to diets with 10 or 60% kcal from fat for 12 weeks. Glucose tolerance was determined after 0, 4, 8 and 12 weeks on diet. Body composition, muscle and fat pad weights, as well as other markers of metabolic syndrome were recorded and mRNA expression of several genes was examined in muscle, fat and liver. High‐fat fed mice consumed more calories and deposited weight and calories more efficiently than control mice. After 12 weeks of high‐fat feeding, body weight, body fat, fat pad weight, fasting blood glucose, serum insulin and leptin expression in adipose tissue were increased in both wild type and Mstn null mice. However, for all these parameters, the increase in Mstn null mice was less pronounced than in wild type mice indicating partial resistance to fat gain with excessive caloric consumption. Contrary to previous research, glucose tolerance was not altered in Mstn null mice. Furthermore, expression of some thermogenic genes including UCP‐3 and PGC1β were increased in adipose tissue of Mstn null mice fed high‐fat diets which may account for differences in obesity susceptibility.
ISSN:0892-6638
1530-6860
DOI:10.1096/fasebj.24.1_supplement.547.10