de Andrade Iracema Senna, Gonzalez João Carlos Gonzalez, Hirata Aparecida Emiko, Carneiro Glaucia, Amado Débora, Cavalheiro Esper Abrão, Dolnikoff Miriam Sterman
Department of Physiology, Division of Neurophysiology and Endocrine Physiology, Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, SP 04023-060, Brazil.
Neurosci Lett. 2006 May 1;398(1-2):6-11. doi: 10.1016/j.neulet.2005.12.043. Epub 2006 Jan 6.
In the present study, newborn male Wistar rats were injected, subcutaneously, five times, every other day, with monosodium glutamate (MSG, 4 g/kg bw) or saline (as control, C), during the neonatal period. MSG animals developed destruction of the arcuate nuclei (ARC) with absence of NPY-immunoreactive cell bodies, which impaired both the food intake (baseline) and the 2-deoxy-D-glucose (2DG) glucoprivic feeding response. Increases in the immunoreactivity of corticotropin-releasing hormone-cell bodies in the paraventricular nuclei might have developed to compensate for the atrophy of the pituitary in MSG-treated rats. After systemic 2DG injection, neither the C nor the MSG rats increased their food intake, but they showed similar hyperglycemic responses, whereas plasma free fatty acids (FFA) increased only in the C group. In other groups, 2DG, norepinephrine (NE), neostigmine (NEO) and saline were intracerebroventricularly (i.c.v.) administered. In this condition, impairment of the hyperglycemic and food intake responses, associated to a lower increase in plasma FFA levels, were observed. As opposed to this, the MSG treatment gives support to NE effects, enhancing food intake, as well as plasma glucose and FFA levels. After NEO, plasma glucose increased only in the MSG group, while plasma FFA levels were elevated in the C rats. Taken together, the results obtained after MSG treatment point to a separate neural control of the hyperglycemic response and of the lipid mobilization when stimulated by central 2DG, NE or NEO administration. It seems likely that the excitatory neural pathway that controls lipid metabolism and is present in C rats was destroyed by the MSG treatment.
在本研究中，新生雄性Wistar大鼠在新生期每隔一天皮下注射五次味精（MSG，4 g/kg体重）或生理盐水（作为对照，C）。味精处理组动物出现弓状核（ARC）破坏，缺乏神经肽Y免疫反应性细胞体，这损害了食物摄入量（基线）和2-脱氧-D-葡萄糖（2DG）糖缺乏性摄食反应。室旁核中促肾上腺皮质激素释放激素细胞体的免疫反应性增加可能是为了补偿味精处理大鼠垂体的萎缩。全身注射2DG后，C组和味精处理组大鼠均未增加食物摄入量，但它们表现出相似的高血糖反应，而血浆游离脂肪酸（FFA）仅在C组中增加。在其他组中，脑室内（i.c.v.）给予2DG、去甲肾上腺素（NE）、新斯的明（NEO）和生理盐水。在这种情况下，观察到高血糖和食物摄入反应受损，同时血浆FFA水平升高幅度较小。与此相反，味精处理增强了NE的作用，增加了食物摄入量以及血浆葡萄糖和FFA水平。注射NEO后，仅味精处理组血浆葡萄糖升高，而C组大鼠血浆FFA水平升高。综上所述，味精处理后的结果表明，当通过中枢给予2DG、NE或NEO刺激时，高血糖反应和脂质动员存在独立的神经控制。似乎C组大鼠中存在的控制脂质代谢的兴奋性神经通路被味精处理破坏了。
