Welle S L, Feldman J
University of Rochester, School of Medicine and Dentistry, Department of Medicine, New York.
J Neural Transm. 1987;70(1-2):63-70. doi: 10.1007/BF01252509.
To examine whether insulin enhances norepinephrine (NE) turnover, an index of sympathetic nerve activity, the effects of excess insulin and streptozotocin (STZ) induced insulin deficiency were examined in Sprague-Dawley rats. Exogenous insulin caused hyperphagia and elevated (approximately 300%) urinary epinephrine excretion, but did not alter cardiac NE content or turnover. STZ-induced insulin deficiency caused hyperglycemia and hyperphagia, but also did not alter cardiac NE content or turnover. Insulin deficiency reduced hepatic NE content 18%, but did not affect NE turnover or content of kidney or spleen. These data do not support the hypothesis that insulin influences cardiac sympathetic nerve activity in rats.
为了研究胰岛素是否会增强去甲肾上腺素(NE)的周转率(一种交感神经活动指标),我们在Sprague-Dawley大鼠中检测了过量胰岛素和链脲佐菌素(STZ)诱导的胰岛素缺乏的影响。外源性胰岛素导致食欲亢进,并使尿中肾上腺素排泄量升高(约300%),但并未改变心脏NE含量或周转率。STZ诱导的胰岛素缺乏导致高血糖和食欲亢进,但同样未改变心脏NE含量或周转率。胰岛素缺乏使肝脏NE含量降低了18%,但不影响NE周转率或肾脏及脾脏中的NE含量。这些数据不支持胰岛素影响大鼠心脏交感神经活动这一假说。