Morishita S, Sato E F, Takahashi K, Manabe M, Inoue M
Department of Biochemistry, Osaka City University Medical School, Japan.
Diabetes Res Clin Pract. 1998 Apr;40(1):1-7. doi: 10.1016/s0168-8227(98)00013-8.
Although various types of stress induce thymus atrophy and suppress immune functions, the mechanisms involved are unknown. To test the hypothesis that thymocyte apoptosis plays a role in stress-induced atrophy of the thymus, we studied the effects of starvation and hypoglycemia on the thymus in the rat. Administration of insulin caused marked hypoglycemia, increased the plasma corticosterone level, and induced fragmentation of thymocyte DNA in fasted but not in fed rats. Administration of either glucose or RU486, a glucocorticoid receptor antagonist, inhibited the apoptosis of thymocytes elicited by insulin. Available evidence suggest that insulin-induced hypoglycemia causes thymocyte apoptosis by promoting glucocorticoid secretion from the adrenal gland.
尽管多种应激会导致胸腺萎缩并抑制免疫功能，但其涉及的机制尚不清楚。为了验证胸腺细胞凋亡在应激诱导的胸腺萎缩中起作用这一假说，我们研究了饥饿和低血糖对大鼠胸腺的影响。注射胰岛素会导致明显的低血糖，提高血浆皮质酮水平，并在禁食大鼠而非进食大鼠中诱导胸腺细胞DNA片段化。注射葡萄糖或糖皮质激素受体拮抗剂RU486可抑制胰岛素引发的胸腺细胞凋亡。现有证据表明，胰岛素诱导的低血糖通过促进肾上腺分泌糖皮质激素而导致胸腺细胞凋亡。
