Thompson D A, Welle S L, Lilavivat U, Pénicaud L, Campbell R G
Life Sci. 1982 Aug 30;31(9):847-52. doi: 10.1016/0024-3205(82)90539-2.
Opioid peptides may act as neuromodulators in the central nervous system to conserve energy stores and water in mammals. To examine this hypothesis in man, the effect of opiate receptor blockade with naloxone on the hunger, thirst, and hypothermic response to 2-deoxy-D-glucose-induced glucoprivic stress was assessed. Opiate receptor blockade decreased stress-induced food intake but did not reduce marked increases in hunger produced by glucoprivation. Naloxone infusions did not change the hypercortisolemic, polydipsic, hypothermic, and thermogenic response to 2-deoxy-D-glucose. While these results do not suggest a major role for a beta-endorphin modulation of stress-induced hunger, hypothermia and water conservation, the reduction of food intake could be due to augmented satiety, perhaps associated with retardation of gastric emptying during opiate receptor blockade.
阿片肽可能作为中枢神经系统中的神经调质,以保存哺乳动物的能量储备和水分。为了在人体中检验这一假设,评估了用纳洛酮阻断阿片受体对饥饿、口渴以及对2-脱氧-D-葡萄糖诱导的糖缺乏应激的低温反应的影响。阿片受体阻断减少了应激诱导的食物摄入量,但并未减轻糖缺乏引起的明显饥饿感增加。输注纳洛酮并未改变对2-脱氧-D-葡萄糖的高皮质醇血症、多饮、低温和产热反应。虽然这些结果并不表明β-内啡肽对应激诱导的饥饿、体温过低和水分保存有主要调节作用,但食物摄入量的减少可能是由于饱腹感增强,这可能与阿片受体阻断期间胃排空延迟有关。