Williams Kasey E, Washington Martha C, Johnson-Rouse Tanisha, Johnson Ruth E, Freeman Corren, Reed Chris, Heath John, Sayegh Ayman I
Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088, USA.
Gastroenterology Laboratory, Department of Biomedical Sciences, College of Veterinary Medicine, Tuskegee University, Tuskegee, AL 36088, USA.
Appetite. 2016 Jan 1;96:254-259. doi: 10.1016/j.appet.2015.09.030. Epub 2015 Sep 30.
Three experiments were done to better assess the gastrointestinal (GI) site(s) of action of GLP-1 on food intake in rats. First, near-spontaneous nocturnal chow meal size (MS), intermeal intervals (IMI) length and satiety ratios (SR = MS/IMI) were measured after infusion of saline, 0.025 or 0.5 nmol/kg GLP-1 into the celiac artery (CA, supplying the stomach and upper duodenum), cranial mesenteric artery (CMA, supplying small and all of the large intestine except the rectum), femoral artery (FA, control) or portal vein (PV, control). Second, infusion of 0.5 nmol/kg GLP-1 was tested after pretreatment with the GLP-1 receptor (GLP-1R) antagonist exendin-4(3-39) via the same routes. Third, the regional distribution of GLP-1R in the rat GI tract was determined using rtPCR. CA, CMA and FA GLP-1 reduced first MS relative to saline, with the CMA route more effective than the others. Only CMA GLP-1 prolonged the IMI. None of the infusions affected second MS or later eating. CA and CMA GLP-1 increased the SR, with the CMA route more effective than the CA route. CMA exendin-4 (3-39) infusion reduced the effect of CMA GLP-1. Finally GLP-1R expression was found throughout the GI tract. The results suggest that exogenous GLP-1 acts in multiple GI sites to reduce feeding under our conditions and that GLP-1R in the area supplied by the CMA, i.e., the small and part of the large intestine, plays the leading role.
进行了三项实验,以更好地评估胰高血糖素样肽-1(GLP-1)对大鼠食物摄入量的胃肠道(GI)作用部位。首先,在向腹腔动脉(CA,供应胃和十二指肠上部)、肠系膜上动脉(CMA,供应小肠和除直肠外的所有大肠)、股动脉(FA,对照)或门静脉(PV,对照)输注生理盐水、0.025或0.5 nmol/kg GLP-1后,测量近自发夜间进食餐量(MS)、餐间间隔(IMI)长度和饱腹感比率(SR = MS/IMI)。其次,通过相同途径用GLP-1受体(GLP-1R)拮抗剂艾塞那肽-4(3-39)预处理后,测试0.5 nmol/kg GLP-1的输注情况。第三,使用逆转录聚合酶链反应(rtPCR)确定大鼠胃肠道中GLP-1R的区域分布。与生理盐水相比,CA、CMA和FA输注的GLP-1首先降低了MS,CMA途径比其他途径更有效。只有CMA输注的GLP-1延长了IMI。所有输注均未影响第二次MS或后续进食。CA和CMA输注的GLP-1增加了SR,CMA途径比CA途径更有效。CMA输注艾塞那肽-4(3-39)降低了CMA输注GLP-1的效果。最后,在整个胃肠道中均发现了GLP-1R的表达。结果表明,在我们的实验条件下,外源性GLP-1在多个胃肠道部位发挥作用以减少进食,并且CMA供应区域(即小肠和部分大肠)中的GLP-1R起主要作用。