Inoue S, Bray G A, Mullen Y S
Am J Physiol. 1978 Sep;235(3):E266-71. doi: 10.1152/ajpendo.1978.235.3.E266.
The present experiments have tested the hypothesis that ventromedial hypothalamic (VMH) lesions enhance insulin secretion by neural mechanisms. Rats were made diabetic by injecting streptozotocin to destroy their own pancreatic beta-cells. Subsequently, transplants of fetal pancreatic tissue were placed under the renal capsule. VMH lesions were placed in rats whose diabetes was cured with transplants as well as sham-transplanted animals. The animals were followed for 4 wk. The lesioned rats with pancreatic transplants gained no more weight than the sham-operated controls. There was no significant rise in insulin in the transplanted rats after VMH lesioning, but the VMH lesioned rats with intact pancreatic tissue showed the expected rise in insulin. Food intake rose 71% in the VMH lesioned rats with intact beta-cells, but only 23% in the VMH lesioned rats with transplants. Hypertrophy of the pancreatic islets was also observed in the VMH lesioned rats with an intact pancreas, but was not found in the VMH lesioned rats with a transplanted pancreas. Thus, transplantation of pancreatic tissue beneath the renal capsule of diabetic rats prevented the characteristic hyperphagia, hyperinsulinemia, and obesity in VMH lesioned rats whose pancreas was free from intact innervation. The results support the hypothesis that neural mediation of the rise in insulin is the primary factor in the development of hypothalamic obesity.
下丘脑腹内侧核（VMH）损伤通过神经机制增强胰岛素分泌。通过注射链脲佐菌素破坏大鼠自身的胰腺β细胞使其患糖尿病。随后，将胎儿胰腺组织移植到肾被膜下。对糖尿病已通过移植治愈的大鼠以及假移植动物进行VMH损伤。对这些动物进行了4周的跟踪观察。接受胰腺移植的损伤大鼠体重增加幅度并不比假手术对照组大。VMH损伤后，移植大鼠的胰岛素水平没有显著升高，但胰腺组织完整的VMH损伤大鼠胰岛素水平出现了预期的升高。胰腺β细胞完整的VMH损伤大鼠食物摄入量增加了71%，但接受移植的VMH损伤大鼠食物摄入量仅增加了23%。在胰腺组织完整的VMH损伤大鼠中也观察到胰岛肥大，但在接受胰腺移植的VMH损伤大鼠中未发现。因此，将胰腺组织移植到糖尿病大鼠的肾被膜下，可防止胰腺无完整神经支配的VMH损伤大鼠出现典型的食欲亢进、高胰岛素血症和肥胖。这些结果支持了以下假设：胰岛素升高的神经介导是下丘脑性肥胖发生的主要因素。
