Brown D F, McGuirk J P, Larsen S P, Minter S D
Department of Anatomy, University of Health Sciences, Kansas City, MO 64124.
Physiol Behav. 1991 Jan;49(1):41-6. doi: 10.1016/0031-9384(91)90227-f.
It has been demonstrated that the ventromedial hypothalamus (VMH) of alloxan-induced diabetic mice is protected from subsequent gold thioglucose (GTG)-induced lesions. Another compound, 3,3'-methyliminobis-(N-methylpropylamine) (MIMPA), a triamine structurally unrelated to GTG, has been shown to cause similar VMH lesions in mice. We chose to investigate the effect of alloxan-induced diabetes on VMH lesion formation in MIMPA-treated mice. In this study CF-1 female mice were made diabetic by a simple intravenous (IV) injection of alloxan and subsequently treated with MIMPA by subcutaneous injection (SC). Contrary to studies which showed that GTG-induced VMH lesions are insulin dependent, an insulin deficiency did not inhibit MIMPA-induced lesions in the VMH of mice. Our data suggests, albeit GTG is suspected to induce VMH necrosis by attaching to glucoreceptors and insulin-sensitive neurons, MIMPA works by a different and as yet unknown mechanism. We conclude that MIMPA-induced lesions in the VMH of mice are not insulin dependent.
已证实,四氧嘧啶诱导的糖尿病小鼠的腹内侧下丘脑(VMH)可免受随后金硫葡萄糖(GTG)诱导的损伤。另一种化合物3,3'-亚氨基二(N-甲基丙胺)(MIMPA),一种结构上与GTG无关的三胺,已被证明可在小鼠中引起类似的VMH损伤。我们选择研究四氧嘧啶诱导的糖尿病对MIMPA处理的小鼠VMH损伤形成的影响。在本研究中,通过简单静脉注射四氧嘧啶使CF-1雌性小鼠患糖尿病,随后通过皮下注射(SC)用MIMPA进行处理。与表明GTG诱导的VMH损伤是胰岛素依赖性的研究相反,胰岛素缺乏并未抑制小鼠VMH中MIMPA诱导的损伤。我们的数据表明,尽管怀疑GTG通过附着于葡萄糖受体和胰岛素敏感神经元诱导VMH坏死,但MIMPA的作用机制不同且尚不清楚。我们得出结论,MIMPA诱导的小鼠VMH损伤不是胰岛素依赖性的。