全胃切除术会严重改变大鼠食物摄入的中枢调节。
Total gastrectomy severely alters the central regulation of food intake in rats.
作者信息
Zittel Tilman T, Glatzle Jörg, Müller Mario, Kreis Martin E, Raybould Helen E, Becker Horst D, Jehle Ekkehard C
机构信息
University Hospital, Department of General and Transplantation Surgery, University of Tübingen, Germany.
出版信息
Ann Surg. 2002 Aug;236(2):166-76. doi: 10.1097/00000658-200208000-00004.
OBJECTIVE
To investigate the central regulation of food intake by quantifying neuron activation of the nucleus of the solitary tract (NTS) after injection of cholecystokinin (CCK) or food intake in gastrectomized rats.
SUMMARY BACKGROUND DATA
Total gastrectomy is followed by early satiety, low calorie intake, and weight loss in the majority of patients. The etiology of these effects is unknown. Sixty percent to 70% of patients remain underweight after total gastrectomy, the weight loss averaging 25% of preoperative body weight. About two thirds of gastrectomized patients report early satiety, and about 60% do not reach the recommended daily calorie intake. The NTS is a brain stem center involved in the regulation of food intake; thus, the extent and pattern of neuronal activation provide information on the process involved in the initiation of satiation and the regulation of food intake.
METHODS
The authors investigated neuronal activation in the NTS using c-fos immunohistochemistry following CCK injection or food intake in healthy control rats, sham-operated control rats, age-matched control rats, weight-matched control rats, and vagotomized or gastrectomized rats.
RESULTS
Neuronal activation in the NTS after CCK injection was significantly decreased 21 days after total gastrectomy, but increased by up to 51% 3 months and by up to 102% 12 months after surgery compared to age-matched unoperated control rats. Neuronal activation in the NTS in response to feeding was markedly increased up to fivefold in gastrectomized rats. This increase was early in onset and sustained, and occurred despite significantly reduced food intake. Administration of MK329, a CCK-A receptor antagonist, significantly reduced the number of postprandially activated neurons in both gastrectomized and control rats.
CONCLUSIONS
The early postprandial activation of NTS neurons after total gastrectomy in rats may correspond to early satiety reported by patients, while the sustained activation of NTS neurons after a meal could contribute to a reduced daily calorie intake. These data suggest that a disturbed central regulation of food intake might contribute to early satiety, reduced food intake, and weight loss after total gastrectomy.
目的
通过量化胆囊收缩素（CCK）注射后或胃切除大鼠进食后孤束核（NTS）的神经元激活情况，研究食物摄入的中枢调节。
总结背景数据
大多数患者在全胃切除术后会出现早饱、低热量摄入和体重减轻。这些影响的病因尚不清楚。60%至70%的患者在全胃切除术后体重仍低于正常，体重减轻平均为术前体重的25%。约三分之二的胃切除患者报告有早饱现象，约60%的患者未达到推荐的每日热量摄入量。NTS是参与食物摄入调节的脑干中枢；因此，神经元激活的程度和模式提供了有关饱腹感起始过程和食物摄入调节的信息。
方法
作者使用c-fos免疫组织化学方法，研究了健康对照大鼠、假手术对照大鼠、年龄匹配对照大鼠、体重匹配对照大鼠以及迷走神经切断或胃切除大鼠在注射CCK或进食后NTS中的神经元激活情况。
结果
与年龄匹配的未手术对照大鼠相比，全胃切除术后21天，注射CCK后NTS中的神经元激活显著降低，但在术后3个月增加了51%，在术后12个月增加了102%。胃切除大鼠对进食的反应中，NTS中的神经元激活显著增加，高达五倍。这种增加在早期开始并持续存在，尽管食物摄入量显著减少。给予CCK-A受体拮抗剂MK329可显著减少胃切除大鼠和对照大鼠餐后激活神经元的数量。
结论
大鼠全胃切除术后NTS神经元的早期餐后激活可能与患者报告的早饱现象相对应，而进食后NTS神经元的持续激活可能导致每日热量摄入减少。这些数据表明，食物摄入的中枢调节紊乱可能导致全胃切除术后的早饱、食物摄入减少和体重减轻。
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