Debons A F, Siclari E, Das K C, Fuhr B
Endocrinology. 1982 Jun;110(6):2024-9. doi: 10.1210/endo-110-6-2024.
Previous studies from our laboratory suggested that adrenal hormones may participate, directly or indirectly, in the hypothalamic mechanism involved in the regulation of food intake. In the present studies, the effect of adrenalectomy on the development of gold thioglucose (GTG)-induced hyperphagia and obesity in mice was investigated. As expected, damage to the ventromedial hypothalamus by GTG was followed by hyperphagia and obesity. Ablation of the adrenal glands after the administration of GTG prevented the onset and development of hyperphagia and obesity. The administration of cortisone completely restored the hyperphagia and weight gain of GTG-treated adrenalectomized mice. The administration of desoxycorticosterone not only failed to restore the hyperphagia and obesity in these mice but, rather, led to a suppression of food intake, weight loss, and death. It is concluded that 1) GTG-induced hypothalamic hyperphagia and obesity are dependent on adrenal glucocorticoids, and 2) the ability of adrenal glucocorticoids to restore hyperphagia and obesity in hypothalamic lesioned adrenalectomized mice indicates that adrenal glucocorticoids can act on compounds outside of the ventromedial hypothalamus involved in the control of food intake.
我们实验室之前的研究表明，肾上腺激素可能直接或间接地参与下丘脑调节食物摄入的机制。在本研究中，研究了肾上腺切除术对小鼠金硫葡萄糖（GTG）诱导的食欲亢进和肥胖发生发展的影响。正如预期的那样，GTG对腹内侧下丘脑造成损伤后，出现了食欲亢进和肥胖。在给予GTG后切除肾上腺可预防食欲亢进和肥胖的发生及发展。给予可的松可完全恢复接受GTG治疗的肾上腺切除小鼠的食欲亢进和体重增加。给予脱氧皮质酮不仅未能恢复这些小鼠的食欲亢进和肥胖，反而导致食物摄入量减少、体重减轻和死亡。得出的结论是：1）GTG诱导的下丘脑性食欲亢进和肥胖依赖于肾上腺糖皮质激素；2）肾上腺糖皮质激素恢复下丘脑损伤的肾上腺切除小鼠食欲亢进和肥胖的能力表明，肾上腺糖皮质激素可作用于腹内侧下丘脑以外参与食物摄入控制的化合物。
