The yellow agouti mutation alters some but not all responses to diet and exercise

被引:17
作者
Chiu, S
Fisler, JS
Espinal, GM
Havel, PJ
Stern, JS
Warden, CH [1 ]
机构
[1] Univ Calif Davis, Rowe Program Genet, Davis, CA 95616 USA
[2] Univ Calif Davis, Dept Nutr, Davis, CA 95616 USA
[3] Univ Calif Davis, Dept Pediat, Davis, CA 95616 USA
[4] Univ Calif Davis, Div Clin Nutr Endocrinol & Vasc Biol, Davis, CA 95616 USA
[5] Univ Calif Davis, Sect Neurobiol Physiol & Behav, Davis, CA 95616 USA
来源
OBESITY RESEARCH | 2004年 / 12卷 / 08期
关键词
agouti; epididymal adipose tissue; subcutaneous; adipose tissue; quantitative PCR; cholesterol;
D O I
10.1038/oby.2004.158
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: Effects of ectopic expression of the agouti signaling protein were studied on responses to diet restriction and exercise in C57BL/6J (B6) mice and obese B6 mice congenic for the yellow agouti mutation [B6.Cg-A(y) (A(y))]. Research Methods and Procedures: Adult male A(y) mice were either kept sedentary or exercised on a running wheel and fed ad libitum or diet restricted until weight matched to ad libitum-fed B6 control mice. Body composition, plasma lipids, leptin, and adiponectin were measured. mRNA levels for leptin, adiponectin, lipoprotein lipase, and pyruvate dehydrogenase kinase 4 were measured in a visceral (epididymal) and a subcutaneous (femoral) fat depot by real-time polymerase chain reaction. Results: Correlations among traits exhibited one of three patterns: similar lines for B6 and A(y) mice, different slopes for B6 and A(y) mice, and/or different intercepts for B6 and A(y) mice. Correlations involving plasma leptin, mesenteric and epididymal adipose weights, or low-density lipoproteincholesterol were most likely to have different slopes and/or intercepts in B6 and A(y) mice. mRNA levels for leptin, Acrp30, pyruvate dehydrogenase kinase 4, and lipoprotein lipase in epididymal adipose tissue were not correlated with corresponding levels in femoral adipose tissue. Discussion: The agouti protein interferes with leptin signaling at melanocortin receptors in the hypothalamus of A(y) mice. Our results are consistent with the hypothesis that the melanocortin portion of the leptin-signaling pathway mediates effects primarily on certain fat depots and on some, but not all, components of cholesterol homeostasis.
引用
收藏
页码:1243 / 1255
页数:13
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