Tomasik Przemyslaw J, Sztefko Krystyna, Starzyk Jerzy
Department of Clinical Biochemistry, University Children 's Hospital, Jagiellonian University, Krakow, Poland.
J Pediatr Endocrinol Metab. 2004 Dec;17(12):1623-31. doi: 10.1515/jpem.2004.17.12.1623.
Cholecystokinin (CCK), glucose dependent insulinotropic peptide (GIP), and glucagon-like peptide 1 (GLP-1) regulate satiety as enterogastrons and incretins. They also directly affect the satiety centers. Therefore, these peptides may participate in the pathogenesis of eating disorders. CCK, GIP, and GLP-1 secretion were studied in 13 adolescent girls suffering from simple obesity, 13 girls with anorexia nervosa, and 10 healthy girls. Each girl was subjected to an oral glucose tolerance test (OGTT) and standard meal test. Blood was collected before stimulation and at 15, 30, 60, and 120 min. The concentrations of all peptides were determined by RIA commercial kits. Fasting and postprandial levels of these peptides as well as integrated outputs were measured. High postprandial levels of CCK observed in the girls with anorexia may aggravate the course of this disease by intensifying nausea and vomiting. Low postprandial level of GLP-1 in girls with simple obesity may be responsible for excessive ingestion of food and weaker inhibition of gastric emptying, which also leads to obesity.
胆囊收缩素（CCK）、葡萄糖依赖性促胰岛素多肽（GIP）和胰高血糖素样肽1（GLP-1）作为肠抑胃素和肠促胰岛素调节饱腹感。它们还直接影响饱腹感中枢。因此，这些肽可能参与饮食失调的发病机制。对13名患有单纯性肥胖的青春期女孩、13名神经性厌食症女孩和10名健康女孩的CCK、GIP和GLP-1分泌情况进行了研究。每位女孩均接受口服葡萄糖耐量试验（OGTT）和标准餐试验。在刺激前以及刺激后15、30、60和120分钟采集血液。所有肽的浓度均通过放射免疫分析商业试剂盒测定。测量了这些肽的空腹和餐后水平以及综合分泌量。神经性厌食症女孩餐后CCK水平较高，可能通过加剧恶心和呕吐而加重该病的病程。单纯性肥胖女孩餐后GLP-1水平较低，可能是导致食物摄入过多和胃排空抑制减弱的原因，这也会导致肥胖。
