King B M
Department of Psychology, University of New Orleans, LA 70148.
Neurosci Biobehav Rev. 1988 Spring;12(1):29-37. doi: 10.1016/s0149-7634(88)80071-x.
Recent studies have demonstrated a role for adrenal glucocorticoid hormones in the hyperphagia and obesity which follow lesions of the ventromedial hypothalamus (VMH). Although VMH lesions elevate morning plasma corticosterone levels, it is concluded that this contributes little to the development of obesity. More importantly, animals with VMH lesions appear to be hyperresponsive to very low levels of circulating glucocorticoids. The overeating and obesity are both prevented and reversed by either complete adrenalectomy or complete hypophysectomy (i.e., resulting in plasma corticosterone levels of less than 1.0 microgram/dl) and restored by dosages of glucocorticoids that have no effect on feeding behavior and weight gain in nonlesioned adrenalectomized animals. Mineralocorticoid hormones have no effect on hypothalamic obesity. Judging by the time course of effects on feeding behavior in VMH-damaged mice of a single intracerebroventricular injection of a low dose of glucocorticoid, which has no effect when administered intraperitoneally, it is concluded that glucocorticoids exert their effect centrally in a permissive, rather than a regulatory, manner. Stimulation of the neighboring paraventricular nuclei (PVN) with norepinephrine or neuropeptide Y produces a rapid feeding response which is also abolished by adrenalectomy and restored with administration of glucocorticoids. However, it is unlikely that the PVN is the site at which glucocorticoids exert their effect in animals with VMH lesions, for PVN lesions or knife-cuts, or combination VMH-PVN lesions, also result in hyperphagia and obesity. It is concluded that adrenal glucocorticoid hormones exert their permissive effects on feeding behavior at brain sites other than the medial hypothalamus. The septo-hippocampal complex is suggested as a possible site.
最近的研究表明，肾上腺糖皮质激素在腹内侧下丘脑（VMH）损伤后的食欲亢进和肥胖中起作用。尽管VMH损伤会提高早晨血浆皮质酮水平，但得出的结论是，这对肥胖的发展贡献不大。更重要的是，VMH损伤的动物似乎对循环糖皮质激素的极低水平反应过度。通过完全肾上腺切除术或完全垂体切除术（即导致血浆皮质酮水平低于1.0微克/分升）可预防和逆转暴饮暴食和肥胖，而给予对未损伤的肾上腺切除动物的摄食行为和体重增加无影响的糖皮质激素剂量可使其恢复。盐皮质激素对下丘脑性肥胖没有影响。根据单次脑室内注射低剂量糖皮质激素对VMH损伤小鼠摄食行为的影响时间进程判断（腹腔注射时无影响），得出结论：糖皮质激素以一种允许而非调节的方式在中枢发挥作用。用去甲肾上腺素或神经肽Y刺激邻近的室旁核（PVN）会产生快速的摄食反应，肾上腺切除术也可消除这种反应，给予糖皮质激素可使其恢复。然而，PVN不太可能是糖皮质激素在VMH损伤动物中发挥作用的部位，因为PVN损伤或刀切，或VMH - PVN联合损伤也会导致食欲亢进和肥胖。得出的结论是，肾上腺糖皮质激素在脑内侧下丘脑以外的部位对摄食行为发挥其允许作用。海马隔复合体被认为是一个可能的部位。
