THE PARASYMPATHETIC NERVOUS-SYSTEM AND GLUCOCORTICOID-MEDIATED HYPERINSULINEMIA IN THE GENETICALLY-OBESE (FA FA) ZUCKER RAT
THE PARASYMPATHETIC NERVOUS-SYSTEM AND GLUCOCORTICOID-MEDIATED HYPERINSULINEMIA IN THE GENETICALLY-OBESE (FA FA) ZUCKER RAT
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DOI：
10.1677/joe.0.1180087
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发表时间：
1988-07-01
影响因子：
4
通讯作者：
MCKENZIE, N
中科院分区：
文献类型：
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作者：
FLETCHER, JM;MCKENZIE, N
在高胰岛素血症发作前，在18日龄（断奶前3天）时切除瘦（Fa/-）和遗传性肥胖（fa/fa）Zucker大鼠的肾上腺。在40-41日龄时，基础和葡萄糖刺激的胰岛素浓度在瘦大鼠和肥胖大鼠之间没有显著差异。血浆胰岛素和葡萄糖浓度较高的两种表型24小时后，皮质酮（2.0毫克，12小时的间隔）。皮质酮治疗的肥胖大鼠有较高的基础和葡萄糖刺激的胰岛素水平比类似的治疗瘦动物，虽然血浆葡萄糖浓度没有不同的表型。用皮质酮治疗肥胖大鼠24 h后，注射阿托品（0.3 mg）后15、30和45 min基础血浆胰岛素浓度降低，血糖水平无任何显著变化。葡萄糖负荷前20分钟注射阿托品（0.3毫克），可防止皮质酮治疗肥胖大鼠的血浆胰岛素浓度较类似治疗瘦动物更大的增量。阿托品管理（0.3毫克），以完整的肥胖大鼠在40天的年龄减少，但没有废除，他们的高胰岛素血症相比，完整的瘦动物。结论是：（1）断奶前肾上腺切除可防止遗传性肥胖大鼠发生高胰岛素血症，（2）仅24小时皮质酮替代可恢复肥胖大鼠的高胰岛素血症，（3）皮质酮对瘦大鼠和肥胖大鼠胰岛素分泌的不同作用是由副交感神经系统介导的，（4）副交感神经系统有助于，但不是完整肥胖大鼠中高胰岛素血症的唯一原因。
Lean (Fa/-) and genetically obese (fa/fa) Zucker rats were adrenalectomized at 18 days of age (3 days before weaning) before the onset of hyperinsulinaemia. At 40-41 days of age, basal and glucose stimulated insulin concentrations did not differ significantly between lean and obese rats. Plasma insulin and glucose concentrations were higher in both phenotypes 24 h after administration of corticosterone (2.0 mg at 12-h intervals). Corticosterone-treated obese rats had higher basal and glucose-stimulated insulin levels than similarly treated lean animals, although plasma glucose concentrations did not differ between phenotypes. The basal plasma insulin concentration of obese rats treated with corticosterone for 24 h was reduced 15, 30 and 45 min after injection of atropine (0.3 mg) without any significant change in the plasma glucose level. Injection of atropine (0.3 mg) 20 min before a glucose load prevented the greater increment in plasma insulin concentration of corticosterone-treated obese rats compared with similarly treated lean animals. Atropine administration (0.3 mg) to intact obese rats at 40 days of age reduced, but did not abolish, their hyperinsulinaemia compared with intact lean animals. It is concluded that (1) pre-weaning adrenalectomy prevents the development of hyperinsulinaemia in genetically obese rats, (2) corticosterone replacement for only 24 h restores the hyperinsulinaemia of obese rats, (3) the differential effects of corticosterone on insulin secretion by lean and obese rats are mediated by the parasympathetic nervous system and (4) the parasympathetic nervous system contributes to, but is not the only cause of hyperinsulinaemia in intact obese rats.