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巯基乙酸对饥饿大鼠进食的β-肾上腺素能介导的抑制作用

Beta-adrenergic-mediated inhibition of feeding by mercaptoacetate in food-deprived rats.

作者信息

Brandt Karsten, Arnold Myrtha, Geary Nori, Langhans Wolfgang, Leonhardt Monika

机构信息

Institute of Animal Sciences, ETH Zurich, Schorenstrasse 16, 8603 Schwerzenbach, Switzerland.

出版信息

Pharmacol Biochem Behav. 2006 Dec;85(4):722-7. doi: 10.1016/j.pbb.2006.11.002. Epub 2006 Dec 15.

Abstract

This study investigated the effect of intraperitoneal (IP) injections of the fatty acid oxidation (FAO) inhibitor mercaptoacetate (MA, 45.6 mg/kg) on feeding in food-deprived rats. As previously, MA significantly stimulated feeding in ad libitum-fed rats. MA, however, reduced feeding in 18 and 36 h-fasted rats despite apparently antagonizing the fasting-induced increase in hepatic FAO. To test whether this anorectic effect involves beta-adrenergic stimulation, 36 h-fasted rats were IP injected with the nonspecific beta-adrenergic receptor antagonist propranolol (PROP, 0.5 mg/kg) just before MA injection. PROP attenuated MA's feeding-inhibitory effect, suggesting that MA anorexia is at least partially mediated by beta-adrenergic stimulation. Finally, we evaluated the role of subdiaphragmatic vagal afferent fibers in MA's feeding-inhibitory effect by testing the ability of MA to inhibit food intake in fasted rats after subdiaphragmatic vagal deafferentation (SDA). MA inhibited feeding similarly in SDA rats and sham-operated rats. These data demonstrate that subdiaphragmatic vagal afferents are not necessary for the feeding-inhibitory effect of peripheral MA. These results suggest that the FAO inhibitor MA elicits a feeding-inhibitory effect in fasted rats that is mediated by a different mechanism than its feeding-stimulatory effect.

摘要

本研究调查了腹腔注射脂肪酸氧化(FAO)抑制剂巯基乙酸盐(MA,45.6毫克/千克)对饥饿大鼠进食的影响。如前所述,MA显著刺激自由进食大鼠的进食。然而,MA却减少了禁食18小时和36小时大鼠的进食,尽管它明显拮抗了禁食诱导的肝脏FAO增加。为了测试这种厌食作用是否涉及β-肾上腺素能刺激,在注射MA之前,给禁食36小时的大鼠腹腔注射非特异性β-肾上腺素能受体拮抗剂普萘洛尔(PROP,0.5毫克/千克)。PROP减弱了MA的进食抑制作用,表明MA引起的厌食至少部分是由β-肾上腺素能刺激介导的。最后,我们通过测试MA抑制膈下迷走神经去传入(SDA)后禁食大鼠食物摄入的能力,评估膈下迷走神经传入纤维在MA进食抑制作用中的作用。MA对SDA大鼠和假手术大鼠的进食抑制作用相似。这些数据表明,膈下迷走神经传入对于外周MA的进食抑制作用并非必需。这些结果表明,FAO抑制剂MA在禁食大鼠中引发进食抑制作用,其介导机制与其进食刺激作用不同。

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