Branco L G
Departamento de Fisiologia, Faculdade de Odontologia de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brazil.
Am J Physiol. 1997 Jan;272(1 Pt 2):R1-5. doi: 10.1152/ajpregu.1997.272.1.R1.
The present study was designed to test the hypothesis that hypoglycemia induces hypothermia in ectotherms and to elucidate the mechanisms responsible for behavioral hypothermia. Behavioral hypothermia is a stress response that occurs in organisms ranging from protozoans to mammals, but very little is known about the cellular mechanisms involved. Toads equipped with a temperature probe were tested in a thermal gradient (10-40 degrees C). Insulin was used to reduce plasma glucose levels, and an inhibitor of glucose utilization, 2-deoxy-D-glucose (2-DG), was used to cause intracellular glucopenia. Insulin injections into the dorsal lymph sac caused significant reductions of both plasma glucose levels and body temperature. To determine if the response was mediated by extracellular glucose receptors or an intracellular mechanism. 2-DG was also injected into the lymph sac. 2-DG caused a similar drop in body temperature and a marked increase in plasma glucose. To assess the role of central thermoregulatory mechanisms, a smaller dose of 2-DG was injected into the fourth cerebral ventricle or the lymph sac. Intracerebroventricular injection of 2-DG caused a decrease in body temperature despite elevated circulating glucose levels, whereas injection into the lymph sac caused no significant change. The data indicate that exclusion of glucose from central rather than peripheral sites plays a major role in the hypoglycemia-induced behavioral hypothermia and that intracellular mechanisms rather than extracellular glucose receptors are involved in this response. Hypothermia may be a beneficial response to hypoglycemia in toads because it dampens cellular oxidative demands during glucose deprivation.
本研究旨在验证低血糖会导致变温动物体温过低这一假说,并阐明行为性体温过低的相关机制。行为性体温过低是一种应激反应,在从原生动物到哺乳动物的各类生物体中都会出现,但对于其中涉及的细胞机制却知之甚少。给蟾蜍安装温度探头后,在热梯度环境(10 - 40摄氏度)中进行测试。使用胰岛素降低血浆葡萄糖水平,并使用葡萄糖利用抑制剂2-脱氧-D-葡萄糖(2-DG)引发细胞内葡萄糖缺乏。向蟾蜍背部淋巴囊注射胰岛素会导致血浆葡萄糖水平和体温显著降低。为了确定该反应是由细胞外葡萄糖受体还是细胞内机制介导的,也将2-DG注射到淋巴囊中。2-DG导致体温出现类似下降,同时血浆葡萄糖显著升高。为了评估中枢体温调节机制的作用,将较小剂量的2-DG注射到第四脑室或淋巴囊中。脑室内注射2-DG尽管循环葡萄糖水平升高,但仍导致体温下降,而注射到淋巴囊中则未引起显著变化。数据表明,低血糖诱导的行为性体温过低主要是由于中枢而非外周部位的葡萄糖缺失所致,并且该反应涉及细胞内机制而非细胞外葡萄糖受体。体温过低可能是蟾蜍对低血糖的一种有益反应,因为它在葡萄糖缺乏期间可降低细胞氧化需求。