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大鼠注射2-脱氧-D-葡萄糖后食物摄入量与血浆β-内啡肽的实验性分离

Experimental dissociation of food intake and plasma beta-endorphin following 2-deoxy-D-glucose in rats.

作者信息

Lowy M T, Davis J M, Lamb D R, Malven P V, Yim G K

出版信息

Peptides. 1985 May-Jun;6(3):569-73. doi: 10.1016/0196-9781(85)90123-8.

Abstract

The present studies were undertaken to further assess the role of plasma beta-endorphin (beta-EP) in the hyperphagia induced by the glucose antimetabolite, 2-deoxy-D-glucose (2-DG). Plasma concentrations of immunoreactive beta-EP (ir-beta-EP) were measured at the end of the first hour of feeding in all animals treated with 400 mg/kg 2-DG. Previous studies had shown a consistent, positive association between 2-DG hyperphagia and plasma ir-beta-EP concentrations, but the present data revealed dissociations between hyperphagia and plasma ir-beta-EP. Dexamethasone administration blocked the 2-DG-induced rise in plasma ir-beta-EP, but had no effect on the 2-DG hyperphagia measured at 1 hour. Forced drinking of a 2% NaCl solution decreased 2-DG hyperphagia, but not the 2-DG induced rise in plasma ir-beta-EP. Thus, elevations in plasma ir-beta-EP are not necessary for the full expression of 2-DG-induced hyperphagia in dexamethasone-treated rats. Furthermore, decreased feeding responses to 2-DG could coexist with increased levels of plasma ir-beta-EP in NaCl-treated normal rats. Elevations in plasma ir-beta-EP do not appear to be the critical opiate link in 2-DG induced hyperphagia.

摘要

本研究旨在进一步评估血浆β-内啡肽(β-EP)在葡萄糖抗代谢物2-脱氧-D-葡萄糖(2-DG)诱导的摄食过量中的作用。在所有接受400mg/kg 2-DG治疗的动物进食第一小时结束时,测量血浆免疫反应性β-EP(ir-β-EP)浓度。先前的研究表明,2-DG诱导的摄食过量与血浆ir-β-EP浓度之间存在一致的正相关,但目前的数据显示摄食过量与血浆ir-β-EP之间存在分离。地塞米松给药可阻断2-DG诱导的血浆ir-β-EP升高,但对1小时时测量的2-DG诱导的摄食过量没有影响。强迫饮用2%NaCl溶液可降低2-DG诱导的摄食过量,但不影响2-DG诱导的血浆ir-β-EP升高。因此,血浆ir-β-EP升高对于地塞米松处理的大鼠中2-DG诱导的摄食过量的充分表达并非必要。此外,在NaCl处理的正常大鼠中,对2-DG的摄食反应降低可能与血浆ir-β-EP水平升高同时存在。血浆ir-β-EP升高似乎不是2-DG诱导的摄食过量中的关键阿片类联系。

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