來自英國的一組科學(xué)家最近通過研究發(fā)現(xiàn)：一種主要負(fù)責(zé)調(diào)節(jié)食欲的激素在人體內(nèi)通過大腦的兩個(gè)不同區(qū)域發(fā)揮其作用,。
倫敦大學(xué)的科學(xué)家分別分析了大腦視丘下部和前額葉皮質(zhì)的活性，并且通過測(cè)量功能核磁共振獲得的圖像成功預(yù)測(cè)了參與到實(shí)驗(yàn)中的八位體重正常的男性進(jìn)食量的多少。
參與測(cè)試的男性在14小時(shí)內(nèi)沒有進(jìn)食，然后科學(xué)家們?yōu)樗麄?a href="http://hnhlg.com/sell/list-781.html" target="_blank">靜脈注射了被稱為YY多肽的激素，或是安慰劑,，注射后再對(duì)參與者的大腦進(jìn)行掃描。接著小組測(cè)量了這些男性進(jìn)食量的多少,。
結(jié)果發(fā)現(xiàn),，每一位參與者在接受了YY多肽的注射之后進(jìn)食量都變少了，但是對(duì)于那些注射了安慰劑的參與者,，其大腦中視丘下部的活躍性能預(yù)測(cè)出這些男性進(jìn)食量的多少,。與此相比,，注射了YY多肽的參與者，其大腦中前額葉皮質(zhì)的活躍程度也能起到同樣的預(yù)測(cè)作用,。
研究項(xiàng)目負(fù)責(zé)人,，來自UCL英國醫(yī)學(xué)研究理事會(huì)的臨床科學(xué)家Rachel Batterham表示,，這些發(fā)現(xiàn)將有助于肥胖的治療，她說：“肥胖是目前西方社會(huì)所面臨的最大健康問題之一,。”以上研究結(jié)果發(fā)表在《自然》（Nature）上,。（ 教育部科技發(fā)展中心）
原文鏈接：http://www.physorg.com/news111943211.html
原始出處:
Nature advance online publication 14 October 2007 | doi:10.1038/nature06212; Received 31 May 2007; Accepted 31 August 2007; Published online 14 October 2007
PYY modulation of cortical and hypothalamic brain areas predicts feeding behaviour in humans
Rachel L. Batterham1, Dominic H. ffytche2, J. Miranda Rosenthal1, Fernando O. Zelaya2, Gareth J. Barker2, Dominic J. Withers1 & Steven C. R. Williams2
Centre for Diabetes and Endocrinology, Department of Medicine, University College London, London WC1E 6JJ, UK
Centre for Neuroimaging Sciences, King's College London, Institute of Psychiatry, De Crespigny Park, Denmark Hill, London SE5 8AF, UK
Correspondence to: Rachel L. Batterham1 Correspondence and requests for materials should be addressed to R.L.B. (Email: [email protected]).
The ability to maintain adequate nutrient intake is critical for survival. Complex interrelated neuronal circuits have developed in the mammalian brain to regulate many aspects of feeding behaviour, from food-seeking to meal termination. The hypothalamus and brainstem are thought to be the principal homeostatic brain areas responsible for regulating body weight1, 2. However, in the current 'obesogenic' human environment food intake is largely determined by non-homeostatic factors including cognition, emotion and reward, which are primarily processed in corticolimbic and higher cortical brain regions3. Although the pleasure of eating is modulated by satiety and food deprivation increases the reward value of food, there is currently no adequate neurobiological account of this interaction between homeostatic and higher centres in the regulation of food intake in humans1, 4, 5. Here we show, using functional magnetic resonance imaging, that peptide YY3–36 (PYY), a physiological gut-derived satiety signal, modulates neural activity within both corticolimbic and higher-cortical areas as well as homeostatic brain regions. Under conditions of high plasma PYY concentrations, mimicking the fed state, changes in neural activity within the caudolateral orbital frontal cortex predict feeding behaviour independently of meal-related sensory experiences. In contrast, in conditions of low levels of PYY, hypothalamic activation predicts food intake. Thus, the presence of a postprandial satiety factor switches food intake regulation from a homeostatic to a hedonic, corticolimbic area. Our studies give insights into the neural networks in humans that respond to a specific satiety signal to regulate food intake. An increased understanding of how such homeostatic and higher brain functions are integrated may pave the way for the development of new treatment strategies for obesity.
