人們總是認為，吃得越多越容易發(fā)胖,，事實上可能并非如此,。美國科學家近日研究發(fā)現(xiàn)，增加進食并不一定會導致脂肪的增長,。這一發(fā)現(xiàn)為找到控制體重的新藥靶開啟了可能性,。相關論文發(fā)表在6月4日的《細胞—代謝》（Cell Metabolism）雜志上。
美國加州大學舊金山分校的Kaveh Ashrafi等人以秀麗隱桿線蟲（Caenorhabditis elegans）為實驗材料,，利用RNA干擾技術研究了250多種基因，以分析神經(jīng)遞質(zhì)serotonin對進食和脂肪的影響機制,。
結(jié)果發(fā)現(xiàn),，serotonin對食欲和脂肪堆積的控制是通過兩個獨立的信號通路來實現(xiàn)的。一組信號調(diào)控進食，另一組獨立信號調(diào)控脂肪代謝,。這些信號路徑由一連串分子事件組成,，由腦部神經(jīng)元觸發(fā)，并最終“指示”機體燃燒或貯存脂肪,。
Ashrafi表示,，如果這種獨立通道的機制也存在于人體中，那么就可以開發(fā)新的減肥藥作用于脂肪堆積通道,，而不是作用于饑餓抑制路徑（此方法目前收效甚微）,。
他說：“這并不是說進食不重要，但是serotonin對脂肪的控制與進食是截然不同的,。僅僅聚焦于進食的減肥策略已經(jīng)走到頭了,，這也許就是節(jié)食失敗的原因之一。”
研究人員總結(jié)說：“肥胖與苗條并不僅僅由進食行為決定,。更確切地說,，進食行為和脂肪代謝是神經(jīng)系統(tǒng)感知營養(yǎng)獲取時并列而又獨立的反應。（科學網(wǎng) 梅進/編譯）
生物谷推薦原始出處：
Cell Metabolism, Vol 7, 533-544, 04 June 2008
Article
Serotonin Regulates C. elegans Fat and Feeding through Independent Molecular Mechanisms
Supriya Srinivasan,1 Leila Sadegh,1 Ida C. Elle,2 Anne G.L. Christensen,2 Nils J. Faergeman,2 and Kaveh Ashrafi1,
1 Department of Physiology and UCSF Diabetes Center, University of California, San Francisco, San Francisco, CA 94158-2517, USA
2 Department of Biochemistry and Molecular Biology, University of Southern Denmark, DK-5230 Odense M, Denmark
Corresponding author
Kaveh Ashrafi
[email protected]
Summary
We investigated serotonin signaling in C. elegans as a paradigm for neural regulation of energy balance and found that serotonergic regulation of fat is molecularly distinct from feeding regulation. Serotonergic feeding regulation is mediated by receptors whose functions are not required for fat regulation. Serotonergic fat regulation is dependent on a neurally expressed channel and a G protein-coupled receptor that initiate signaling cascades that ultimately promote lipid breakdown at peripheral sites of fat storage. In turn, intermediates of lipid metabolism generated in the periphery modulate feeding behavior. These findings suggest that, as in mammals, C. elegans feeding behavior is regulated by extrinsic and intrinsic cues. Moreover, obesity and thinness are not solely determined by feeding behavior. Rather, feeding behavior and fat metabolism are coordinated but independent responses of the nervous system to the perception of nutrient availability.
