Feeding and neuroendocrine responses after recurrent insulin-induced hypoglycemia.
Feeding and neuroendocrine responses after recurrent insulin-induced hypoglycemia.
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反复胰岛素引起的低血糖后的进食和神经内分泌反应。
DOI：
10.1016/j.physbeh.2006.01.007
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发表时间：
2006
影响因子：
2.9
通讯作者：
Levin,BarryE
中科院分区：
文献类型：
--
作者：
Sanders,NicoleM;Figlewicz,DianneP;TaborskyJr,GJ;Wilkinson,CharlesW;Daumen,Wendi;Levin,BarryE
在随后的低血糖期间，先前的低血糖暴露会损害神经内分泌逆向调节反应(CRR)。CRR缺陷导致低血糖是临床综合征低血糖相关自主神经衰竭(HAAF)的一个组成部分。低血糖还能有效地刺激食物摄入量，这是一种重要的行为CRR。因为对低血糖的摄食反应增加是行为性的，而不是荷尔蒙的，我们假设它可能随着反复发生的低血糖而受到不同的调节。为了验证这一假设，我们同时评估了经历一次或三次胰岛素诱导低血糖的大鼠的神经内分泌CRR和食物摄入量。正如预期的那样，反复低血糖显著降低了神经内分泌低血糖CRR。反复低血糖大鼠注射胰岛素120min后，肾上腺素(E)、去甲肾上腺素(NE)和胰高血糖素反应较首次低血糖大鼠显著降低。尽管有这些神经内分泌损伤，但无论是经历第一次低血糖(3.4±0.4克比生理盐水：0.94±0.3克，P<；0.05)还是第三次低血糖发作(低血糖：3.8±0.3克比生理盐水：1.2±0.3克，P<；0.05)，大鼠的摄食量都显著高于基线盐水摄入量。这些发现表明，因低血糖而引起的食物摄入量不会因为反复低血糖而受损。因此，神经内分泌和行为(食物摄入刺激)CRR受反复低血糖经历的不同调节。
Prior exposure to hypoglycemia impairs neuroendocrine counterregulatory responses (CRR) during subsequent hypoglycemia. Defective CRR to hypoglycemia is a component of the clinical syndrome hypoglycemia-associated autonomic failure (HAAF). Hypoglycemia also potently stimulates food intake, an important behavioral CRR. Because the increased feeding response to hypoglycemia is behavioral and not hormonal, we hypothesized that it may be regulated differently with recurrent bouts of hypoglycemia. To test this hypothesis, we simultaneously evaluated neuroendocrine CRR and food intake in rats experiencing one or three episodes of insulin-induced hypoglycemia. As expected, recurrent hypoglycemia significantly reduced neuroendocrine hypoglycemic CRR. Epinephrine (E), norepinephrine (NE) and glucagon responses 120 min after insulin injection were significantly reduced in recurrent hypoglycemic rats, relative to rats experiencing hypoglycemia for the first time. Despite these neuroendocrine impairments, food intake was significantly elevated above baseline saline intake whether rats were experiencing a first (hypoglycemia: 3.4±0.4 g vs. saline: 0.94±0.3 g, P<0.05) or third hypoglycemic episode (hypoglycemia: 3.8±0.3 g vs. saline: 1.2±0.3 g, P<0.05). These findings demonstrate that food intake elicited in response to hypoglycemia is not impaired as a result of recurrent hypoglycemia. Thus, neuroendocrine and behavioral (stimulation of food intake) CRR are differentially regulated by recurrent hypoglycemia experience.