King B M, Frohman L A
Neurosci Biobehav Rev. 1982 Summer;6(2):205-14. doi: 10.1016/0149-7634(82)90056-2.
Evidence that the obesity syndrome which follows ventromedial hypothalamic (VMH) lesions is at least partially the result of a primary metabolic dysfunction is reviewed, as are proposals that the altered metabolism is due to enhanced vagally-mediated insulin release. This hypothesis was based largely on experiments demonstrating the complete reversal of hypothalamic obesity by subdiaphragmatic vagotomy, but subsequent studies have revealed that hypothalamic obesity is not always prevented by prior vagal transections. Interpretation of these discrepant results has been made difficult because of the frequent use of gastric secretion, behavioral, or other indirect tests for completeness of vagotomy. A review of more recent studies which have employed either direct assessment of vagotomy effects on insulin levels, pharmacological blockade of vagal efferent activity, or selective vagotomies indicates that vagally-mediated hyperinsulinemia can account for no more than 40% of the weight gain observed in animals with VMH lesions fed ad libitum, and may not be involved in the obesity that results from some parasagittal VMH knife cuts. It is concluded that vagally-mediated hyperinsulinemia does make a substantial, although not exclusive, contribution to the increased carcass lipid content observed in VMH animals that are food-restricted or pair-fed with control animals.
本文回顾了腹内侧下丘脑（VMH）损伤后出现的肥胖综合征至少部分是原发性代谢功能障碍所致的证据，以及关于代谢改变是由于迷走神经介导的胰岛素释放增强的提议。这一假设主要基于膈下迷走神经切断术可使下丘脑性肥胖完全逆转的实验，但随后的研究表明，先前的迷走神经横断术并不总能预防下丘脑性肥胖。由于频繁使用胃分泌、行为或其他间接测试来评估迷走神经切断术的完整性，这些相互矛盾的结果难以解释。对最近的研究进行回顾，这些研究要么直接评估迷走神经切断术对胰岛素水平的影响，要么对迷走神经传出活动进行药理学阻断，要么进行选择性迷走神经切断术，结果表明，在自由进食的VMH损伤动物中，迷走神经介导的高胰岛素血症最多只能解释所观察到的体重增加的40%，并且可能与某些矢状旁VMH刀切所致的肥胖无关。得出的结论是，迷走神经介导的确对食物受限或与对照动物配对喂养的VMH动物中观察到的胴体脂质含量增加有很大贡献，尽管不是唯一的贡献。
