Balbo S L, Mathias P C, Bonfleur M L, Alves H F, Siroti F J, Monteiro O G, Ribeiro F B, Souza A C
Department of Cell Biology and Genetics, State University of Maringá, PR, Brazil.
Res Commun Mol Pathol Pharmacol. 2000 Nov-Dec;108(5-6):291-6.
In order to study the role of vagus nerve activity at the onset of obesity induced by monosodium glutamate (MSG), 30-day-old MSG-rats were vagotomized or sham operated. Body weight and food intake were recorded until animals were 90 days old and then sacrificed. Naso-anal length was recorded for all animals. Periepididymal and retroperitoneal fat pads were isolated and weighed. Reduction of body weight and naso-anal length were registered in 30-day-old MSG-rats. Obesity could also be observed, as increase of Lee index indicated. Results were most evident in 90-day-old MSG-rats. In both groups neither body weight gain nor food intake was changed by vagotomy. However, fat accumulation on tissues was reduced by vagotomy in MSG-rats. The results showed that MSG-obesity is not related to an increment in food intake behavior. Vagotonia might play a role at the onset of MSG-obesity.
为了研究迷走神经活动在味精（MSG）诱导的肥胖症发病过程中的作用，对30日龄的MSG大鼠进行迷走神经切断术或假手术。记录动物体重和食物摄入量直至90日龄，然后处死。记录所有动物的鼻肛长度。分离并称重附睾周围和腹膜后的脂肪垫。在30日龄的MSG大鼠中记录到体重和鼻肛长度的减少。如李氏指数增加所示，也可观察到肥胖。结果在90日龄的MSG大鼠中最为明显。在两组中，迷走神经切断术均未改变体重增加和食物摄入量。然而，迷走神经切断术减少了MSG大鼠组织中的脂肪堆积。结果表明，MSG诱导的肥胖与食物摄入行为的增加无关。迷走神经张力亢进可能在MSG诱导的肥胖症发病过程中起作用。
