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口服油酰乙醇胺会抑制食物摄入。

Food intake is inhibited by oral oleoylethanolamide.

作者信息

Nielsen Mie Julin, Petersen Gitte, Astrup Arne, Hansen Harald S

机构信息

Department of Pharmacology, The Danish University of Pharmaceutical Sciences, Copenhagen, Denmark.

出版信息

J Lipid Res. 2004 Jun;45(6):1027-9. doi: 10.1194/jlr.C300008-JLR200. Epub 2004 Apr 1.

Abstract

Oleoylethanolamide (OEA) may be an endogenous regulator of food intake, and intraperitoneal injection of this compound decreases food intake in 24 h-starved rats. It is generally believed that this kind of lipid amide is rapidly catabolized in the gastrointestinal tract, thereby preventing its use as an oral antiobesity compound. We now show that oral OEA inhibits food intake dose dependently at 90 min after food presentation to starved rats. Food intake was reduced by 15.5% (P < 0.01) by administration of 10 mg/kg OEA. [(3)H]OEA was used to assess the degree of catabolism in the gastrointestinal tract. The endogenous level of this acylethanolamide was increased 11 times in the intestinal tissue (to 3.91 +/- 0.98 nmol/g tissue, mean +/- SEM) at 90 min after food presentation, based on the finding of 0.48% of the dose as intact OEA. These findings reveal unexpected properties of orally administered OEA, which may have potential as a cheap and safe antiobesity drug.

摘要

油酰乙醇胺(OEA)可能是食物摄入的内源性调节剂,腹腔注射该化合物可减少饥饿24小时大鼠的食物摄入量。一般认为,这种脂酰胺在胃肠道中会迅速分解代谢,因此无法用作口服抗肥胖化合物。我们现在表明,口服OEA在给饥饿大鼠喂食后90分钟时剂量依赖性地抑制食物摄入。给予10mg/kg OEA可使食物摄入量减少15.5%(P<0.01)。[³H]OEA用于评估胃肠道中的分解代谢程度。根据完整OEA占剂量0.48%的结果,在喂食后90分钟时,这种酰基乙醇胺在肠道组织中的内源性水平增加了11倍(达到3.91±0.98nmol/g组织,平均值±标准误)。这些发现揭示了口服OEA出人意料的特性,它可能具有作为廉价且安全的抗肥胖药物的潜力。

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