Rohner-Jeanrenaud F, Jeanrenaud B
Ann Endocrinol (Paris). 1983;44(4):217-27.
Some results suggesting the existence of gluco- and/or insulin-sensitive sites within the central nervous system (CNS) are recalled. In summary, it seems that when these sites are activated by the presence of glucose or insulin, there is an activation of the parasympathetic nervous system which is responsible for an increased peripheral insulin secretion and/or an hypoglycemia. This could possibly favour glucose disposal. Inversely, when the CNS lacks energy substrates, a cascade of events occurs which tend to increase peripheral glycemia. Bilateral lesions of the ventromedial hypothalamus (VMH) bring about a very early occurring hypersecretion of insulin which can be rapidly and completely abolished by vagotomy. It has also been shown that genetically pre-obese rats (fa/fa) do hypersecrete insulin in response to an i.v. glucose load. This suggests that hypersecretion of insulin of these animals could play a causative role in the development of their obesity. Moreover, this hypersecretion of insulin observed in genetic pre-obesity is abolished by acute atropine administration indicating the involvement of the parasympathetic nervous system in the development of their hyperinsulinemia and subsequent obesity. Cephalic phase insulin secretion seems to "optimalize" insulin secretion that occurs following a meal, as it appears to permit adequate glucose utilization and therefore glucose tolerance. Indeed, animals which are lacking cephalic phase insulin secretion do hypersecrete insulin while remaining hyperglycemic for a longer period of time when compared to animals which have a cephalic phase insulin secretion. Hypothalamic factors present in the ventromedial or the ventrolateral hypothalamus have been shown to have insulin secretion promoting activity when administered in vivo or in vitro to donor rats. It remains to be shown whether such factors are indeed released into the blood (humoral factors) or whether they are neuromodulators and/or neurotransmitters.
本文回顾了一些表明中枢神经系统（CNS）内存在葡萄糖和/或胰岛素敏感位点的研究结果。总之，当这些位点因葡萄糖或胰岛素的存在而被激活时，副交感神经系统会被激活，进而导致外周胰岛素分泌增加和/或低血糖。这可能有利于葡萄糖的代谢。相反，当中枢神经系统缺乏能量底物时，会引发一系列事件，导致外周血糖升高。双侧腹内侧下丘脑（VMH）损伤会导致胰岛素过早分泌增加，而迷走神经切断术可迅速且完全消除这种现象。研究还表明，遗传性肥胖前期大鼠（fa/fa）静脉注射葡萄糖后确实会出现胰岛素分泌过多的情况。这表明这些动物的胰岛素分泌过多可能在其肥胖的发生中起因果作用。此外，急性给予阿托品可消除遗传性肥胖前期动物中观察到的胰岛素分泌过多现象，这表明副交感神经系统参与了其高胰岛素血症及随后肥胖的发生。头期胰岛素分泌似乎能“优化”餐后发生的胰岛素分泌，因为它似乎能使葡萄糖得到充分利用，从而改善葡萄糖耐量。实际上，与具有头期胰岛素分泌的动物相比，缺乏头期胰岛素分泌的动物在较长时间内血糖仍会升高，同时会出现胰岛素分泌过多的情况。当将腹内侧或腹外侧下丘脑存在的下丘脑因子在体内或体外给予供体大鼠时，已显示其具有促进胰岛素分泌的活性。这些因子是否确实释放到血液中（体液因子），或者它们是否为神经调节剂和/或神经递质，仍有待进一步研究。
