美國研究者經(jīng)由腦部掃描發(fā)現(xiàn),，面對誘人的高熱量食物，瘦人的大腦可以比胖人調(diào)動出更活躍的沖動控制力。這可能是胖瘦分化明顯的原因之一。
這項(xiàng)由美國耶魯大學(xué)和南加州大學(xué)研究者合作的研究,，以報(bào)告形式刊登在最新一期《臨床研究期刊》月刊。
法新社援引報(bào)告內(nèi)容報(bào)道,，借助核磁共振成像技術(shù),，研究者比對觀察胖人和瘦人在面對高熱量食物時(shí)的大腦反應(yīng)。結(jié)果發(fā)現(xiàn),，面對高熱量食物的圖片時(shí),，瘦人大腦中控制沖動區(qū)域的活躍度增強(qiáng)，而胖人這一區(qū)域活躍程度不明顯,。
在耶魯大學(xué)康涅狄格醫(yī)學(xué)院研究者羅伯特·舍溫看來,，這一比對研究說明，“人們之所以不能完全控制對食物的欲望,，本質(zhì)上出于生理因素”,。
共有9名偏瘦和5名肥胖志愿者參與比對測試。志愿者在進(jìn)食兩小時(shí)后進(jìn)行腦部掃描,，主要觀測大腦中負(fù)責(zé)發(fā)出抑制進(jìn)食信號的大腦前額葉皮質(zhì)區(qū)活躍度,。
比對結(jié)果顯示，飯后兩小時(shí),，面對高熱量食物誘惑,，胖人的前額葉皮質(zhì)區(qū)活躍度不及瘦人，換句話說,，胖人大腦的抑制進(jìn)食能力更差,。
試驗(yàn)同時(shí)測定志愿者血糖值，發(fā)現(xiàn)血糖值差異對前額葉皮質(zhì)區(qū)活躍度確實(shí)產(chǎn)生影響,，但不改變胖人比瘦人抑制進(jìn)食能力更差的總體狀況,。
舍溫在接受路透社電話采訪時(shí)說，盡管這一發(fā)現(xiàn)有待更大規(guī)模研究核實(shí),，但胖瘦群體大腦中抑制進(jìn)食區(qū)域活躍度差異確實(shí)有可能是胖人更愛高熱量食物的原因之一,。
這項(xiàng)研究旨在發(fā)現(xiàn)導(dǎo)致肥胖的生理因素。在美國,，三分之一成年人和將近17%未成年人受肥胖困擾,。（生物谷 Bioon.com）
doi:10.1172/JCI57873
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PMID:
Circulating glucose levels modulate neural control of desire for high-calorie foods in humans
Kathleen A. Page, Dongju Seo, Renata Belfort-DeAguiar, Cheryl Lacadie, James Dzuira, Sarita Naik, Suma Amarnath, R. Todd Constable, Robert S. Sherwin and Rajita Sinha
Obesity is a worldwide epidemic resulting in part from the ubiquity of high-calorie foods and food images. Whether obese and nonobese individuals regulate their desire to consume high-calorie foods differently is not clear. We set out to investigate the hypothesis that circulating levels of glucose, the primary fuel source for the brain, influence brain regions that regulate the motivation to consume high-calorie foods. Using functional MRI (fMRI) combined with a stepped hyperinsulinemic euglycemic-hypoglycemic clamp and behavioral measures of interest in food, we have shown here that mild hypoglycemia preferentially activates limbic-striatal brain regions in response to food cues to produce a greater desire for high-calorie foods. In contrast, euglycemia preferentially activated the medial prefrontal cortex and resulted in less interest in food stimuli. Indeed, higher circulating glucose levels predicted greater medial prefrontal cortex activation, and this response was absent in obese subjects. These findings demonstrate that circulating glucose modulates neural stimulatory and inhibitory control over food motivation and suggest that this glucose-linked restraining influence is lost in obesity. Strategies that temper postprandial reductions in glucose levels might reduce the risk of overeating, particularly in environments inundated with visual cues of high-calorie foods.
