It is demonstrated that pre-obese Zucker rats, studied before weaning (17 days of age), at a time when they were indistinguishable from lean controls, do hypersecrete insulin in response to glucose or arginine administration when compared to their lean littermates in spite of normal basal insulin levels. When arginine is used as the stimulus, it is shown that pre-obese pups hypersecrete glucagon as well as insulin, the net result of insulin and glucagon oversecretion being probably the observed normoglycemia of these animals. Furthermore, these early substrate-induced increases in pancreatic hormonal secretion could be reduced toward normal values by acute pre-treatment of the pre-obese rats with the cholinergic inhibitor, atropine. It is suggested the parasympathetic nervous system plays a role in genetically obese fa/fa rats in bringing about an early increased substrate-induced insulin release, a defect which could be one of the causes involved in the development of their obesity syndrome. In adult animals, the involvement of the parasympathetic nervous system in insulin oversecretion is less clear probably due to the presence of an increased B cell mass. However, using three different experimental approaches, it could be seen that an increased vagal tone acting at the B cells in obese animals participate to their insulin hypersecretion.

中文翻译：

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迷走神经在遗传性肥胖fa / fa大鼠的病因和维持高胰岛素血症中的作用。

研究表明，在断奶前（17天大）进行肥胖研究的祖克大鼠，在与瘦肉对照组没有区别的时候，与瘦肉同窝相比，对葡萄糖或精氨酸给​​药的人分泌的胰岛素过多。正常基础胰岛素水平。当使用精氨酸作为刺激物时，显示肥胖前的幼犬分泌高分泌的胰高血糖素以及胰岛素，胰岛素和胰高血糖素过度分泌的最终结果可能是这些动物的正常血糖。此外，可以通过用胆碱能抑制剂阿托品对肥胖前期大鼠进行急性预处理，将这些早期的底物诱导的胰腺激素分泌增加降低至正常值。提示副交感神经系统在遗传肥胖的fa / fa大鼠中起着作用，导致早期的底物诱导的胰岛素释放增加，该缺陷可能是肥胖症候群发展的原因之一。在成年动物中，副交感神经系统是否参与胰岛素分泌过多尚不清楚，这可能是由于B细胞质量增加所致。但是，使用三种不同的实验方法，可以发现，肥胖动物中作用于B细胞的迷走神经音调增强参与了他们的胰岛素分泌过多。副交感神经系统是否参与胰岛素分泌过多尚不清楚，可能是由于B细胞质量增加所致。但是，使用三种不同的实验方法，可以发现，肥胖动物中作用于B细胞的迷走神经音调增强参与了他们的胰岛素分泌过多。副交感神经系统是否参与胰岛素分泌过多尚不清楚，可能是由于B细胞质量增加所致。但是，使用三种不同的实验方法，可以发现，肥胖动物中作用于B细胞的迷走神经音调增强参与了他们的胰岛素分泌过多。