Tian Zi-Bin, Deng Run-Jun, Sun Gui-Rong, Wei Liang-Zhou, Kong Xin-Juan, Ding Xue-Li, Jing Xue, Zhang Cui-Ping, Ge Yin-Lin
Zi-Bin Tian, Run-Jun Deng, Liang-Zhou Wei, Xin-Juan Kong, Xue-Li Ding, Xue Jing, Cui-Ping Zhang, Department of Gastroenterology, Affiliated Hospital of Medical College of Qingdao University, Qingdao 266003, Shandong Province, China.
World J Gastroenterol. 2014 Jun 14;20(22):6897-905. doi: 10.3748/wjg.v20.i22.6897.
To determine the expression levels of gastrointestinal nesfatin-1 in ventromedial hypothalamic nucleus (VMH)-lesioned (obese) and ventrolateral hypothalamic nucleus (VLH)-lesioned (lean) rats that exhibit an imbalance in their energy metabolism and gastric mobility.
Male Wistar rats were randomly divided into a VMH-lesioned group, a VLH-lesioned group, and their respective sham-operated groups. The animals had free access to food and water, and their diets and weights were monitored after surgery. Reverse transcription-polymerase chain reaction and immunostaining were used to analyse the levels of NUCB2 mRNA and nesfatin-1 immunoreactive (IR) cells in the stomach, duodenum, small intestine, and colon, respectively. Gastric emptying was also assessed using a modified phenol red-methylcellulose recovery method.
The VMH-lesioned rats fed normal chow exhibited markedly greater food intake and body weight gain, whereas the VLH-lesioned rats exhibited markedly lower food intake and body weight gain. NUCB2/nesfatin-1 IR cells were localised in the lower third and middle portion of the gastric mucosal gland and in the submucous layer of the enteric tract. Compared with their respective controls, gastric emptying was enhanced in the VMH-lesioned rats (85.94% ± 2.27%), whereas the VLH lesions exhibited inhibitory effects on gastric emptying (29.12% ± 1.62%). In the VMH-lesioned rats, the levels of NUCB2 mRNA and nesfatin-1 protein were significantly increased in the stomach and duodenum and reduced in the small intestine. In addition, the levels of NUCB2 mRNA and nesfatin-1 protein in the VLH-lesioned rats were decreased in the stomach, duodenum, and small intestine.
Our study demonstrated that nesfatin-1 level in the stomach and duodenum is positively correlated with body mass. Additionally, there is a positive relationship between gastric emptying and body mass. The results of this study indicate that gastrointestinal nesfatin-1 may play a significant role in gastric mobility and energy homeostasis.
确定在腹内侧下丘脑核(VMH)损伤(肥胖)和腹外侧下丘脑核(VLH)损伤(消瘦)的大鼠中胃肠道nesfatin-1的表达水平,这些大鼠表现出能量代谢和胃动力失衡。
将雄性Wistar大鼠随机分为VMH损伤组、VLH损伤组及其各自的假手术组。动物可自由获取食物和水,术后监测其饮食和体重。分别采用逆转录-聚合酶链反应和免疫染色分析胃、十二指肠、小肠和结肠中NUCB2 mRNA水平和nesfatin-1免疫反应(IR)细胞。还采用改良的酚红-甲基纤维素回收法评估胃排空。
喂食普通饲料的VMH损伤大鼠表现出明显更高的食物摄入量和体重增加,而VLH损伤大鼠表现出明显更低的食物摄入量和体重增加。NUCB2/nesfatin-1 IR细胞位于胃黏膜腺的下三分之一和中部以及肠道的黏膜下层。与各自的对照组相比,VMH损伤大鼠的胃排空增强(85.94%±2.27%),而VLH损伤对胃排空有抑制作用(29.12%±1.62%)。在VMH损伤大鼠中,胃和十二指肠中NUCB2 mRNA和nesfatin-1蛋白水平显著升高,而小肠中则降低。此外,VLH损伤大鼠胃、十二指肠和小肠中NUCB2 mRNA和nesfatin-1蛋白水平降低。
我们的研究表明,胃和十二指肠中nesfatin-1水平与体重呈正相关。此外,胃排空与体重之间存在正相关关系。本研究结果表明,胃肠道nesfatin-1可能在胃动力和能量稳态中发挥重要作用。