研究者發(fā)現(xiàn),，鈍尾毒蜥的唾液制成的藥物可有效降低糖尿病患者對食物的渴望度,。(Credit: © Rusty Dodson / Fotolia)
近日，來自哥德堡大學的研究者表示,，用鈍尾毒蜥的唾液制成的藥物可有效降低糖尿病患者對食物的渴望度,。研究者在用這種藥物處理小鼠，發(fā)現(xiàn)小鼠終止了對普通食物和巧克力的渴望,。
相關(guān)研究成果刊登在了近日的國際雜志Journal of Neuroscience上,。日益增加的II型糖尿病患者使用藥物制劑-艾塞那肽，可以有效控制他們的機體血糖水平,，艾塞那肽是由天然物質(zhì)艾塞那肽-4合成的,，這種物質(zhì)來源于北美大蜥蜴（鈍尾毒蜥，Heloderma suspectum）的唾液中,。
意想不到的效果
哥德堡大學的研究者發(fā)現(xiàn)了這種物質(zhì)的潛在且意想不到的效果,。
降低食物的需求度
在文章中，研究者用小鼠進行研究,，發(fā)現(xiàn)艾塞那肽-4可以有效降低其對食物的需求度，研究者Karolina Skibicka表示,，這是一個未知且不可思議的效果,，我們認為這和大腦的機制有關(guān)，大腦可以控制小鼠的成癮行為,，而且艾塞那肽-4可影響大腦的獎勵和激勵區(qū)域,。
有意思的發(fā)現(xiàn)
研究者Suzanne Dickson表示，無數(shù)次的節(jié)食失敗是因為我們被吃的欲望纏繞著,，尤其是誘惑性的食物比如糖,。隨著艾塞那肽-4抑制對食物的渴求欲，這可以幫助肥胖人群控制飲食，進而控制其體重,。
進食障礙的治療
艾塞那肽-4的研究給我們一些建議去治療那些和飲食障礙相關(guān)的疾病,，比如強迫性暴食；另外,，研究者揭示艾塞那肽-4可以減少酒精的欲求,，大腦中涉及飲食沖動和酒精沖動的區(qū)域是一樣的，因此測定艾塞那肽-4是否可以降低人類對于酒精的需求也顯得尤為意思,，研究者Skibicka表示,。（生物谷：T.Shen編譯）
doi:10.1523/JNEUROSCI.6326-11.2012
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The Glucagon-Like Peptide 1 (GLP-1) Analogue, Exendin-4, Decreases the Rewarding Value of Food: A New Role for Mesolimbic GLP-1 Receptors
Suzanne L. Dickson1, Rozita H. Shirazi1, Caroline Hansson1, Filip Bergquist2, Hans Nissbrandt2, and Karolina P. Skibicka1
The glucagon-like peptide 1 (GLP-1) system is a recently established target for type 2 diabetes treatment. In addition to regulating glucose homeostasis, GLP-1 also reduces food intake. Previous studies demonstrate that the anorexigenic effects of GLP-1 can be mediated through hypothalamic and brainstem circuits which regulate homeostatic feeding. Here, we demonstrate an entirely novel neurobiological mechanism for GLP-1-induced anorexia in rats, involving direct effects of a GLP-1 agonist, Exendin-4 (EX4) on food reward that are exerted at the level of the mesolimbic reward system. We assessed the impact of peripheral, central, and intramesolimbic EX4 on two models of food reward: conditioned place preference (CPP) and progressive ratio operant-conditioning. Food-reward behavior was reduced in the CPP test by EX4, as rats no longer preferred an environment previously paired to chocolate pellets. EX4 also decreased motivated behavior for sucrose in a progressive ratio operant-conditioning paradigm when administered peripherally. We show that this effect is mediated centrally, via GLP-1 receptors (GLP-1Rs). GLP-1Rs are expressed in several key nodes of the mesolimbic reward system; however, their function remains unexplored. Thus we sought to determine the neurobiological substrates underlying the food-reward effect. We found that the EX4-mediated inhibition of food reward could be driven from two key mesolimbic structures—ventral tegmental area and nucleus accumbens—without inducing concurrent malaise or locomotor impairment. The current findings, that activation of central GLP-1Rs strikingly suppresses food reward/motivation by interacting with the mesolimbic system, indicate an entirely novel mechanism by which the GLP-1R stimulation affects feeding-oriented behavior.
