Nagai K, Nagai N, Sugahara K, Niijima A, Nakagawa H
Division of Protein Metabolism, Osaka University, Japan.
Neurosci Biobehav Rev. 1994 Winter;18(4):579-84. doi: 10.1016/0149-7634(94)90014-0.
The role of the hypothalamic suprachiasmatic nucleus (SCN) was examined in rats and obtained following results: (a) The time-dependent (light > dark) hyperglycemic response to intracranial injection of 2-deoxy-D-glucose (2DG) disappeared in rats with bilateral lesions of the SCN, in rats on weeks 4-6 after surgical blinding, and in congenitally blind (hereditary microphthalmic) rats; (b) The hyperglycemia induced by electrical stimulation of the SCN was not observed in weeks 4-8 after surgical blinding; (c) Change in the blood glucose concentration after insulin injection into the SCN was eliminated by SCN lesions; (d) Alterations in activity of autonomic efferents to peripheral organs on light exposure disappeared after SCN lesions; (e) SCN lesions decreased the blood glucagon level and increased the blood insulin level; (f) SCN lesions decreased protein intake, and glucagon increased it; (g) Increases in the plasma renin activity and vasopressin concentration after water-deprivation were suppressed in hereditary microphthalmic rats with abnormal SCN. These findings suggest that the SCN is involved in the mechanism of blood glucose and body fluid intake as well as that of circadian rhythm.
对大鼠下丘脑视交叉上核(SCN)的作用进行了研究,并得到以下结果:(a)在双侧SCN损伤的大鼠、手术致盲后4 - 6周的大鼠以及先天性失明(遗传性小眼症)大鼠中,对颅内注射2 - 脱氧 - D - 葡萄糖(2DG)产生的随时间变化(光照>黑暗)的高血糖反应消失;(b)手术致盲后4 - 8周未观察到电刺激SCN诱导的高血糖;(c)SCN损伤消除了向SCN注射胰岛素后血糖浓度的变化;(d)SCN损伤后,光照时外周器官自主传出活动的改变消失;(e)SCN损伤降低了血糖素水平,升高了胰岛素水平;(f)SCN损伤减少了蛋白质摄入,而血糖素增加了蛋白质摄入;(g)在SCN异常的遗传性小眼症大鼠中,缺水后血浆肾素活性和血管加压素浓度的升高受到抑制。这些发现表明,SCN参与了血糖和体液摄入机制以及昼夜节律机制。