Welch C C, Kim E M, Grace M K, Billington C J, Levine A S
Department of Medicine, VA Medical Center, Minneapolis, MN 55417, USA.
Brain Res. 1996 May 20;721(1-2):126-31. doi: 10.1016/0006-8993(96)00151-5.
Opioid involvement in regulating the intake of highly palatable diets was studied by examining the effect of feeding either a cornstarch-based diet (CHO) or a high fat diet containing sucrose (Fat/Sucrose) on hypothalamic opioid levels. Rats received either CHO ad libitum, Fat/Sucrose ad libitum, Fat/Sucrose pair-fed to the caloric intake of CHO, or Fat/Sucrose at 60% of ad libitum Fat/Sucrose intake. Animals receiving Fat/Sucrose ad libitum consumed more calories and gained more weight than animals receiving CHO (P < 0.001). Relative to CHO, ad libitum intake of Fat/Sucrose elevated proDynorphin mRNA levels in the arcuate and Dynorphin A1-17 levels in the paraventricular nucleus (PVN) (P < 0.05), but did not affect arcuate mRNA levels of proEnkephalin or proOpiomelanocortin (POMC), or PVN levels of Met-Enkephalin or beta-Endorphin. Pair-feeding the Fat/Sucrose diet to the level of intake of the CHO diet resulted in levels of proDynorphin and Dynorphin A1-17 that were similar in the two diet groups. Pair-feeding Fat/Sucrose reduced mRNA levels of proDynorpin, proEnkephalin and POMC, and Dynorphin A1-17 levels, relative to ad libitum feeding of Fat/Sucrose. Met-Enkephalin and beta-Endorphin were not affected by dietary treatment. Feeding Fat/Sucrose at 60% of ad libitum intake resulted in mRNA levels of proDynorphin, proEnkephalin and POMC, and Dynorphin A1-17 levels that were similar to those observed in CHO group. Hypothalamic Dynorphin A1-17 and proDynorphin mRNA levels are stimulated by feeding a highly palatable diet rich in fat and sucrose. The increased synthesis may be due in part to a palatability-induced overconsumption of calories. Caloric restriction of the same diet decreases mRNA levels of proDynorphin, proEnkephalin and POMC, as well as levels of Dynorphin A1-17.
通过研究给予基于玉米淀粉的饮食（CHO）或含蔗糖的高脂肪饮食（脂肪/蔗糖）对下丘脑阿片类物质水平的影响，来探讨阿片类物质在调节高适口性饮食摄入中的作用。大鼠自由摄取CHO、自由摄取脂肪/蔗糖、将脂肪/蔗糖的摄入量配对控制为与CHO的热量摄入量相同，或将脂肪/蔗糖的摄入量控制为自由摄取量的60%。自由摄取脂肪/蔗糖的动物比摄取CHO的动物消耗更多热量且体重增加更多（P < 0.001）。相对于CHO，自由摄取脂肪/蔗糖会使弓状核中前强啡肽原mRNA水平和室旁核（PVN）中强啡肽A1-17水平升高（P < 0.05），但不影响弓状核中脑啡肽原或阿黑皮素原（POMC）的mRNA水平，也不影响PVN中甲硫脑啡肽或β-内啡肽的水平。将脂肪/蔗糖饮食的摄入量配对控制为与CHO饮食的摄入量相同，导致两个饮食组中前强啡肽原和强啡肽A1-17的水平相似。与自由摄取脂肪/蔗糖相比，配对控制脂肪/蔗糖的摄入量会降低前强啡肽原、脑啡肽原和POMC的mRNA水平以及强啡肽A1-17的水平。饮食处理对甲硫脑啡肽和β-内啡肽没有影响。将脂肪/蔗糖的摄入量控制为自由摄取量的60%，导致前强啡肽原、脑啡肽原和POMC的mRNA水平以及强啡肽A1-17的水平与CHO组中观察到的水平相似。喂食富含脂肪和蔗糖的高适口性饮食会刺激下丘脑强啡肽A1-17和前强啡肽原mRNA水平。合成增加可能部分归因于适口性诱导的热量过度消耗。对相同饮食进行热量限制会降低前强啡肽原、脑啡肽原和POMC的mRNA水平以及强啡肽A1-17的水平。
