Steger R W, Rabe M B
Department of Physiology, Southern Illinois University School of Medicine, Carbondale 62901-6512, USA.
Proc Soc Exp Biol Med. 1997 Jan;214(1):1-11. doi: 10.3181/00379727-214-44064.
The adverse effects of diabetes on the circulatory, visual, renal, and peripheral nervous system are commonly recognized and have been extensively studied. The effects of decreased insulin secretion or resistance to insulin action on endocrine glands have not been as carefully documented. Both clinical and animal research have demonstrated that diabetes mellitus is commonly associated with altered thyroid, adrenal and gonadal function. Some of these changes are reversed with insulin replacement therapy, but endocrine function is not always restored to normal even with rigorous glycemic control. Patients with poorly controlled diabetes exhibit basal and stimulated growth hormone (GH) hypersecretion, while patients with good metabolic control still present with diurnal and exercise-induced GH hypersecretion. In contrast, diabetes suppresses GH secretion in the rat. It is unclear why GH secretion is altered, but clinical and experimental evidence exists for diabetes-associated changes in GH-releasing hormone and somatostatin release as well as for changes in the pituitary response to these hypothalamic hormones. The thyroid hormones, T3 and T4, are usually suppressed in both humans and experimental animals with diabetes. This effect of diabetes appears to involve changes in hypothalamic thyrotropin-releasing hormone (TRH) secretion as well as changes in pituitary thyrotropin (TSH) release and direct effects at the level of the thyroid gland. Adrenal cortical function is often enhanced in diabetes, most likely due to alterations in glucocorticoid feedback responses. There is much conflicting data on adrenal medullary function in diabetes; responses to stress and exercise, however, are often abnormal. Finally, male and female reproductive function is often disrupted in diabetes. Data from animal studies suggest that the major cause is altered hypothalamic LHRH secretion secondary to diabetes-induced changes in hypothalamic neurotransmitter metabolism.
糖尿病对循环系统、视觉系统、肾脏和周围神经系统的不良影响已得到普遍认可，并已进行了广泛研究。胰岛素分泌减少或胰岛素作用抵抗对内分泌腺的影响尚未得到如此详尽的记录。临床和动物研究均表明，糖尿病通常与甲状腺、肾上腺和性腺功能改变有关。其中一些变化可通过胰岛素替代疗法逆转，但即使进行严格的血糖控制，内分泌功能也并非总能恢复正常。糖尿病控制不佳的患者表现出基础和刺激状态下生长激素（GH）分泌过多，而代谢控制良好的患者仍存在昼夜及运动诱导的GH分泌过多。相比之下，糖尿病会抑制大鼠的GH分泌。目前尚不清楚GH分泌为何会改变，但有临床和实验证据表明糖尿病会导致GH释放激素和生长抑素释放发生变化，以及垂体对这些下丘脑激素的反应发生变化。甲状腺激素T3和T4在糖尿病患者和实验动物中通常都会受到抑制。糖尿病的这种影响似乎涉及下丘脑促甲状腺激素释放激素（TRH）分泌的变化、垂体促甲状腺激素（TSH）释放的变化以及甲状腺水平的直接作用。糖尿病患者的肾上腺皮质功能通常会增强，这很可能是由于糖皮质激素反馈反应的改变。关于糖尿病患者肾上腺髓质功能的数据存在很多矛盾之处；然而，其对应激和运动的反应往往异常。最后，糖尿病常导致男性和女性生殖功能紊乱。动物研究数据表明，主要原因是糖尿病引起的下丘脑神经递质代谢变化继发下丘脑促黄体生成素释放激素（LHRH）分泌改变。
