Amir S
Department of Psychology, Concordia University, Montreal, Que., Canada.
Brain Res. 1988 Jul 5;455(1):201-3. doi: 10.1016/0006-8993(88)90135-7.
Thyrotropin-releasing hormone (TRH) prevents the development of drug- or stress-induced hyperglycemia in mice through action at central sites. To study the role of the pituitary in mediating this action, we have evaluated the effect of TRH analogs lacking hypophysiotropic activity, acid-TRH and DN 1417, in blocking glucagon-induced hyperglycemia in mice. In addition, the effect of hypophysectomy on TRH antihyperglycemic action was examined. It was found that central injection of acid-TRH or DN 1417 (0.1-10 micrograms) fully mimics TRH in blocking glucagon (5 micrograms)-stimulated hyperglycemia. Moreover, TRH (1 or 10 micrograms) was fully active in blocking glucagon-induced hyperglycemia in hypophysectomized mice. These results exclude the possibility that pituitary factors play a role in the central antihyperglycemic action of TRH.
促甲状腺激素释放激素(TRH)通过作用于中枢部位来预防小鼠因药物或应激诱导的高血糖症。为了研究垂体在介导这一作用中的角色,我们评估了缺乏促垂体活性的TRH类似物——酸性TRH和DN 1417,对阻断小鼠胰高血糖素诱导的高血糖症的作用。此外,还研究了垂体切除对TRH抗高血糖作用的影响。结果发现,中枢注射酸性TRH或DN 1417(0.1 - 10微克)在阻断胰高血糖素(5微克)刺激的高血糖症方面完全模拟了TRH的作用。此外,TRH(1或10微克)在阻断垂体切除小鼠中胰高血糖素诱导的高血糖症方面也具有完全活性。这些结果排除了垂体因子在TRH中枢抗高血糖作用中发挥作用的可能性。