胃饥饿素调节小鼠白色脂肪组织中的肥胖以及棕色脂肪组织中的解偶联蛋白1（UCP1）mRNA表达。
Ghrelin regulates adiposity in white adipose tissue and UCP1 mRNA expression in brown adipose tissue in mice.
作者信息
Tsubone Tetsuo, Masaki Takayuki, Katsuragi Isao, Tanaka Katsuhiro, Kakuma Tetsuya, Yoshimatsu Hironobu
机构信息
Department of Internal Medicine 1, School of Medicine, Faculty of Medicine, Oita Medical University, 1-1 Idaigaoka, Hasama, Oita 879-5593, Japan.
出版信息
Regul Pept. 2005 Aug 15;130(1-2):97-103. doi: 10.1016/j.regpep.2005.04.004.
To examine the involvement of ghrelin in obesity, we investigated the effects of treatment with peripherally administered ghrelin on food intake, adiposity, and expression of uncoupling protein (UCP) mRNA in brown (BAT) and white (WAT) adipose tissue in mice. Acute bolus administration of ghrelin at a dose of 120 nmol/kg increased cumulative food intake over 4 and 24 h as compared to controls (p<0.05 for each), whereas 12 nmol/kg/day ghrelin showed no remarkable effect (p>0.1). Chronic repeated treatment with 12 nmol/kg/day ghrelin for 7 days increased body weight and adiposity assessed by the weight of adipose tissue, triglyceride content in WAT (p<0.05 for each versus control). In addition, the same treatment decreased and increased mRNA expression of BAT UCP1 and WAT UCP2, respectively (p<0.05 for each). In conclusion, ghrelin can regulate body weight, adiposity and UCPs mRNA expression in mice. The present results provide evidence for a new regulatory loop involving ghrelin and UCP, and add novel insights into the regulatory mechanisms of obesity.
为研究胃饥饿素在肥胖中的作用，我们研究了外周给予胃饥饿素对小鼠食物摄入量、肥胖程度以及棕色脂肪组织（BAT）和白色脂肪组织（WAT）中解偶联蛋白（UCP）mRNA表达的影响。与对照组相比，以120 nmol/kg的剂量急性推注胃饥饿素可使4小时和24小时的累积食物摄入量增加（每组p<0.05），而12 nmol/kg/天的胃饥饿素则无显著影响（p>0.1）。以12 nmol/kg/天的胃饥饿素进行7天的慢性重复治疗可增加体重和肥胖程度，通过脂肪组织重量、WAT中的甘油三酯含量评估（每组与对照组相比p<0.05）。此外，相同治疗分别降低和增加了BAT UCP1和WAT UCP2的mRNA表达（每组p<0.05）。总之，胃饥饿素可调节小鼠体重、肥胖程度和UCPs mRNA表达。本研究结果为涉及胃饥饿素和UCP的新调节环路提供了证据，并为肥胖的调节机制增添了新见解。
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