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油酰乙醇胺:对抗肥胖的有力盟友。

Oleoylethanolamide: A fat ally in the fight against obesity.

作者信息

Brown Jacob D, Karimian Azari Elnaz, Ayala Julio E

机构信息

Integrative Metabolism Program, Sanford Burnham Prebys Medical Discovery Institute at Lake Nona, Orlando, FL, United States.

Integrative Metabolism Program, Sanford Burnham Prebys Medical Discovery Institute at Lake Nona, Orlando, FL, United States.

出版信息

Physiol Behav. 2017 Jul 1;176:50-58. doi: 10.1016/j.physbeh.2017.02.034. Epub 2017 Feb 27.

Abstract

Obesity is a pandemic, gateway disease that has thrived in modern, sedentary, high calorie-eating societies. Left unchecked, obesity and obesity-related diseases will continue to plague future generations with heavy burdens on economies, healthcare systems, and the quality of life of billions. There is a significant need to elucidate basic physiological mechanisms and therapies that address this global health care crisis. Oleoylethanolamide (OEA) is an endocannabinoid-like lipid that induces hypophagia and reduces fat mass in rodents. For over a decade, PPAR-α has been the most widely accepted mediator of the hypophagic action of OEA via signaling to homeostatic brain centers. Recent evidence suggests that OEA may also reduce food intake via effects on dopamine and endocannabinoid signaling within hedonic brain centers. Limited study of OEA supplementation in humans has provided some encouraging insight into OEA-based weight loss therapy, but more thorough, controlled investigations are needed. As a potential link between homeostatic and hedonic regulation of food intake, OEA is a prime starting point for the development of more effective obesity therapies.

摘要

肥胖是一种盛行的、引发多种疾病的根源性疾病,在现代久坐不动且高热量饮食的社会中愈发严重。若不加以控制,肥胖及与肥胖相关的疾病将继续困扰后代,给经济、医疗系统以及数十亿人的生活质量带来沉重负担。迫切需要阐明应对这一全球医疗危机的基本生理机制和治疗方法。油酰乙醇胺(OEA)是一种内源性大麻素样脂质,可诱导啮齿动物食欲减退并减少脂肪量。十多年来,PPAR-α一直是OEA通过向稳态脑中枢发出信号而产生食欲减退作用的最广泛接受的介质。最近的证据表明,OEA也可能通过影响享乐脑中枢内的多巴胺和内源性大麻素信号来减少食物摄入量。对人类补充OEA的有限研究为基于OEA的减肥疗法提供了一些令人鼓舞的见解,但仍需要更全面、可控的调查。作为食物摄入稳态调节和享乐调节之间的潜在联系,OEA是开发更有效肥胖疗法的首要切入点。

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