Rohner-Jeanrenaud F, Jeanrenaud B
J Clin Invest. 1980 Apr;65(4):902-10. doi: 10.1172/JCI109744.
The existence of a relationship between the ventromedial hypothalamic area (VMH) and the activity of the endocrine pancreas has been shown previously. This relationship has been further tested and extended in the present study, using isolated perfused pancreases from rats previously lesioned (4-7 d) in the VMH. It was found that in isolated pancreases obtained from rats fed ad lib. for 4 d after VMH lesions (i.e., that were hyperphagic), the typical biphasic pattern of insulin secretion was observed following glucose stimulation (20 mM) and that the total insulin output was much greater than that of controls. The increased insulin output was not a result of hyperphagia because similar results were obtained using pancreases obtained from VMH-lesioned rats in which a food restriction matching exactly that of control rats was started either immediately of 3 d after the lesions. Pancreases from such food-restricted VMH-lesioned rats oversecreted insulin, when compared with controls fed the same amount, from 7 mM of glucose concentration in perfusion medium onwards. After the addition of arginine (10 mM), the total output of glucagon by pancreases from food-restricted VMH-lesioned rats was twice that of controls. Qualitatively, the arginine-induced glucagon secretion by pancreases from food-restricted VMH-lesioned rats retained its biphasic pattern. Similarly, epinephrine (0.1 muM) elicited a greater glucagon release by pancreases from food-restricted VMH-lesioned rats when compared with controls. These data further support the concept of a link (as yet undefined) between the hypothalamus and the endocrine pancreas, as lesions of the VMH area resulted in abnormal secretion not only of insulin, but of glucagon as well.
下丘脑腹内侧区（VMH）与内分泌胰腺的活动之间的关系此前已得到证实。在本研究中，使用先前在VMH中受损（4 - 7天）的大鼠的离体灌注胰腺，对这种关系进行了进一步的测试和扩展。结果发现，从VMH损伤后自由进食4天（即食欲亢进）的大鼠获得的离体胰腺中，在葡萄糖刺激（20 mM）后观察到典型的胰岛素分泌双相模式，并且总胰岛素输出量远高于对照组。胰岛素输出增加并非食欲亢进所致，因为使用从VMH损伤大鼠获得的胰腺也得到了类似结果，这些大鼠在损伤后立即或3天后开始进行与对照大鼠完全匹配的食物限制。与喂食相同量食物的对照组相比，来自这种食物限制的VMH损伤大鼠的胰腺从灌注培养基中葡萄糖浓度达到7 mM起就过度分泌胰岛素。添加精氨酸（10 mM）后，来自食物限制的VMH损伤大鼠的胰腺中胰高血糖素的总输出量是对照组的两倍。定性地说，来自食物限制的VMH损伤大鼠的胰腺中精氨酸诱导的胰高血糖素分泌保持其双相模式。同样，与对照组相比，肾上腺素（0.1 μM）引起来自食物限制的VMH损伤大鼠的胰腺释放更多的胰高血糖素。这些数据进一步支持了下丘脑与内分泌胰腺之间存在联系（尚未明确）的概念，因为VMH区域的损伤不仅导致胰岛素分泌异常，也导致胰高血糖素分泌异常。
