據(jù)英國(guó)媒體9月2日?qǐng)?bào)道,，科學(xué)家的最新研究發(fā)現(xiàn),，并非只有我們的嘴巴能夠享受美味食物，其實(shí)我們的肚子和胃也能嘗出食物的味道,。這項(xiàng)研究的過(guò)程發(fā)表在《美國(guó)國(guó)家科學(xué)院院刊》（PNAS）上,。
這項(xiàng)最新研究表明，存在于舌頭上能夠檢測(cè)甜味的蛋白質(zhì),，也同時(shí)存在于胃腸道,；在這里，它們同樣能嘗出糖果的味道,。這項(xiàng)研究的負(fù)責(zé)人是紐約西奈山醫(yī)學(xué)院神經(jīng)科學(xué)家羅伯特·馬格斯基,，他說(shuō)：“其實(shí),，腸道與舌頭品嘗甜味的方式是一樣的。”
不過(guò),，即便你有意識(shí)地去體驗(yàn)?zāi)c道品嘗甜味的感覺,，也可能毫無(wú)收獲。馬格斯基推測(cè),，腸道對(duì)味道的感覺,，會(huì)以其他形式體現(xiàn)出來(lái)。比如,，人們吃了某種事物后,，會(huì)有特別滿足的感覺，尤其是鮮美多汁,、香甜可口的食物會(huì)讓你產(chǎn)生非常幸福的感覺,。
馬格斯基及其同事研究了人類和老鼠的腸道組織，并在老鼠身上做了一系列試驗(yàn),，才得出了上述結(jié)論,。在研究中，馬格斯基發(fā)現(xiàn),，腸道上的味覺細(xì)胞與舌頭上的非常相似。過(guò)去,，曾有研究表明,，味覺受體T1R3 ，以及一種名為“腸道味導(dǎo)素”(gut-expressed gustducinn)的蛋白質(zhì),，對(duì)甜味覺的形成非常重要,。科學(xué)家推測(cè),，受體可能會(huì)促使腸道釋放激素,。
當(dāng)嘴巴嚼碎食物，食物糜進(jìn)入胃部得到進(jìn)一步消化后,，就會(huì)進(jìn)入人體的小腸,。在這里，食物會(huì)被分解成各種組分,，比如葡萄糖,。糖分子與腸道上的蛋白質(zhì)受體結(jié)合后，就會(huì)促使腸道釋放激素,，調(diào)節(jié)胰島素的生成量和我們的食欲,。
與舌頭上的味覺細(xì)胞一樣，肚子里也有類似的細(xì)胞,。馬格斯基說(shuō)：“在腸道上,，很可能存在會(huì)對(duì)糖分子,、脂肪分子、氨基酸分子甚至‘苦味分子’作出反應(yīng)的細(xì)胞,，這與舌頭對(duì)酸甜苦辣作出反應(yīng)的機(jī)制很相似,。因此，我們的肚子也能品嘗味道,。”
這些發(fā)現(xiàn)將有助于肥胖癥和糖尿病的治療,。同時(shí)發(fā)表在《美國(guó)國(guó)家科學(xué)院院刊》上的另一篇文章指出：腸道上的味覺受體還能調(diào)節(jié)一種化學(xué)物質(zhì)的生成量，而這種化學(xué)物質(zhì)又能決定人體應(yīng)該從食物中汲取多少糖分,。既然富含糖的食物可能引發(fā)糖尿病和肥胖癥,，對(duì)腸道上的味覺受體“下功夫”就可能變成一種新的治療這兩種疾病的方法。另外,，受到味覺受體調(diào)控的激素可以刺激食欲,，那么科學(xué)家也可以利用它來(lái)降低食欲。
原始出處:
Published online before print August 27, 2007
Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0706890104
Medical Sciences
Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1
( enteroendocrine cells | gastrointestinal chemosensation | glucose sensor | incretin )
Hyeung-Jin Jang *, Zaza Kokrashvili , Michael J. Theodorakis *, Olga D. Carlson *, Byung-Joon Kim *, Jie Zhou *, Hyeon Ho Kim *, Xiangru Xu *, Sic L. Chan *, Magdalena Juhaszova *, Michel Bernier *, Bedrich Mosinger , Robert F. Margolskee , and Josephine M. Egan *
*National Institute on Aging/National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224; and Department of Neuroscience, Mount Sinai School of Medicine, 1425 Madison Avenue, Box 1065, New York, NY 10029
Communicated by Linda M. Bartoshuk, University of Florida, Gainesville, FL, July 23, 2007 (received for review May 16, 2007)
Glucagon-like peptide-1 (GLP-1), released from gut endocrine L cells in response to glucose, regulates appetite, insulin secretion, and gut motility. How glucose given orally, but not systemically, induces GLP-1 secretion is unknown. We show that human duodenal L cells express sweet taste receptors, the taste G protein gustducin, and several other taste transduction elements. Mouse intestinal L cells also express -gustducin. Ingestion of glucose by -gustducin null mice revealed deficiencies in secretion of GLP-1 and the regulation of plasma insulin and glucose. Isolated small bowel and intestinal villi from -gustducin null mice showed markedly defective GLP-1 secretion in response to glucose. The human L cell line NCI-H716 expresses -gustducin, taste receptors, and several other taste signaling elements. GLP-1 release from NCI-H716 cells was promoted by sugars and the noncaloric sweetener sucralose, and blocked by the sweet receptor antagonist lactisole or siRNA for -gustducin. We conclude that L cells of the gut "taste" glucose through the same mechanisms used by taste cells of the tongue. Modulating GLP-1 secretion in gut "taste cells" may provide an important treatment for obesity, diabetes and abnormal gut motility.
