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題 名 | 胰島素及瘦素對於下視丘的體重控制與食物攝取所扮演的角色=Role of Insulin and Leptin in Hypothalamic Control of Body Weight and Food Intake |
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作 者 | 許青雲; 陳思萍; | 書刊名 | 長庚科技學刊 |
卷 期 | 1 2002.09[民91.09] |
頁 次 | 頁135-144 |
分類號 | 418.27 |
關鍵詞 | 胰島素; 瘦素; 視經胜冴Y; 食物攝取; 體重; 肥胖; Insulin; Leptin; Neuropeptide Y; Food intake; Body weight; Obesity; |
語 文 | 中文(Chinese) |
中文摘要 | 中樞(主要是下視丘)以及周邊(特別是脂肪組織)經由一套複雜的交互作用以維持體重恆定。促進攝食之神經胜肽(例如神經胜肽Y,orexin等)具有增加進食,減少能量消耗及加速脂肪儲存,厭食神經胜肽(例如胰島素,瘦素等)則降低食慾,增加能量消耗及減少體脂肪儲存,兩者在正常生理下,保持動態平衡。從胰島(細胞分泌的胰島素,其增加瘦素合成及分泌,並且進入下視丘的神經元,抑制神經胜肽Y的作用而減少食物攝取。近來動物實驗的研究顯示,如果老鼠的下視丘缺乏且胰島素受體(NIRKO小鼠),將導致增加食量及儲存過多體脂肪,伴隨飲食引起的肥胖。因此,胰島素及瘦素為腦部長期調節食量與體重的肥胖訊息(Adiposity signals)。雖然,引起肥胖的原因有很多,色含基因調控失常、暴飲暴食等。我們藉由歸納近年來的相關研究報告以釐清下視丘的胰島索及瘦素調節攝食與控制體重所扮演的角色。 |
英文摘要 | Body weight homeostasis is maintained via a series of complex interactions that occur between central (dominant the hypothalamus) and the periphery (particular the adipose tissues). Under normal conditions, a dynamic equilibrium exists between orexigenic peptides (e.g. neuropeptide Y, orexin, ect.), which favor food intake, decrease energy expenditure, and facilitate fat storage, and anorexigenic peptides (e.g. insu1in, leptin, ect.), which decrease food intake, increase energy expenditure, and lose fat store. Insu1in is secreted by pancreatic beta cel1s. It stimulates leptin synthesis and release and also act on the hypothalamic nucleus where they may decrease food intake by decreasing the effects of neuropeptide Y. Recent animal research showing that neuron-specific in insulin receptors knockout mice (NIRKO mice) have increased food intake and developed diet-sensitive obesity with excessive body fat storage. Leptin and insulin serve as adiposity signals to the brain for the long-term regulation of food intake and body weight. Although there are multiple factors involving obesity, including genetic dysregulation and hyperphagia. This articles seeks to minireview the current literatures and illustrate the role of insulin and leptin in hypothalamic control of food intake and body weight. |
本系統中英文摘要資訊取自各篇刊載內容。