近日，来自哥德堡大学的研究者表示，用钝尾毒蜥的唾液制成的药物可有效降低糖尿病患者对食物的渴望度。研究者在用这种药物处理小鼠，发现小鼠终止了对普通食物和巧克力的渴望。
相关研究成果刊登在了近日的国际杂志Journal of Neuroscience上。日益增加的II型糖尿病患者使用药物制剂-艾塞那肽，可以有效控制他们的机体血糖水平，艾塞那肽是由天然物质艾塞那肽-4合成的，这种物质来源于北美大蜥蜴（钝尾毒蜥，Heloderma suspectum）的唾液中。
意想不到的效果
哥德堡大学的研究者发现了这种物质的潜在且意想不到的效果。
降低食物的需求度
在文章中，研究者用小鼠进行研究，发现艾塞那肽-4可以有效降低其对食物的需求度，研究者Karolina Skibicka表示，这是一个未知且不可思议的效果，我们认为这和大脑的机制有关，大脑可以控制小鼠的成瘾行为，而且艾塞那肽-4可影响大脑的奖励和激励区域。
有意思的发现
研究者Suzanne Dickson表示，无数次的节食失败是因为我们被吃的欲望缠绕着，尤其是诱惑性的食物比如糖。随着艾塞那肽-4抑制对食物的渴求欲，这可以帮助肥胖人群控制饮食，进而控制其体重。
进食障碍的治疗
艾塞那肽-4的研究给我们一些建议去治疗那些和饮食障碍相关的疾病，比如强迫性暴食；另外，研究者揭示艾塞那肽-4可以减少酒精的欲求，大脑中涉及饮食冲动和酒精冲动的区域是一样的，因此测定艾塞那肽-4是否可以降低人类对于酒精的需求也显得尤为意思，研究者Skibicka表示。（生物谷：T.Shen编译）
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.
