Aukan Marthe Isaksen, Nymo Siren, Haagensli Ollestad Karoline, Akersveen Boyesen Guro, DeBenedictis Julia Nicole, Rehfeld Jens Frederik, Coutinho Silvia, Martins Catia
Obesity Research Group, Department of Clinical and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology NTNU, 7491, Trondheim, Norway.
Obesity Research Group, Department of Clinical and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology NTNU, 7491, Trondheim, Norway; Nord-Trøndelag Hospital Trust, Clinic of Surgery, Namsos Hospital, Norway; Centre of Obesity and Innovation ObeCe, Clinic of Surgery, St. Olav University Hospital, 7006, Trondheim, Norway.
Appetite. 2022 Apr 1;171:105940. doi: 10.1016/j.appet.2022.105940. Epub 2022 Jan 19.
The aim of this study was to compare gastrointestinal (GI) hormones and subjective ratings of appetite among obesity classes, and between classes of obesity and controls. Ninety-eight adult individuals with obesity, divided into class I (n = 35), II (n = 44) and III (n = 19), together with 45 controls without obesity were included in this cross-sectional analysis. Body weight/composition, and basal and postprandial (after a 600 kcal fixed breakfast) plasma concentrations of acylated ghrelin, active glucagon-like peptide 1 (GLP-1), total peptide YY (PYY), cholecystokinin (CCK) and insulin, as well as subjective ratings of hunger, fullness, desire to eat (DTE) and prospective food consumption (PFC) were measured. There were no differences in the plasma concentration of GI hormones (either basal or postprandial) among obesity classes, except for insulin. In general, obesity was associated with impaired secretion of GI hormones. Ghrelin secretion did not decline postprandially in class-III obesity. GLP-1 peak for obesity class I and II was early and lower, while class III showed no postprandial GLP-1 response. Postprandial PYY response for obesity class II and III was absent, and class III showed a delayed and shortened postprandial CCK response. Obesity class II and III had greater basal insulin concentration compared to controls and postprandial insulin was greater in obesity class III versus class II, class I and controls. No differences were found for appetite ratings among obesity classes. In conclusion, obesity is characterized by impaired secretion of GI hormones, with reduced postprandial satiety, particularly in individuals with obesity class III. This abnormal pattern may lead to overeating.
本研究旨在比较不同肥胖等级之间以及肥胖等级与对照组之间的胃肠(GI)激素和食欲主观评分。98名肥胖成人被分为I级(n = 35)、II级(n = 44)和III级(n = 19),并纳入45名非肥胖对照者进行这项横断面分析。测量了体重/身体成分,以及酰基化胃饥饿素、活性胰高血糖素样肽1(GLP-1)、总肽YY(PYY)、胆囊收缩素(CCK)和胰岛素的基础及餐后(600千卡固定早餐后)血浆浓度,以及饥饿、饱腹感、进食欲望(DTE)和预期食物摄入量(PFC)的主观评分。除胰岛素外,不同肥胖等级之间的胃肠激素血浆浓度(基础或餐后)没有差异。总体而言,肥胖与胃肠激素分泌受损有关。III级肥胖者餐后胃饥饿素分泌未下降。I级和II级肥胖者的GLP-1峰值出现早且较低,而III级肥胖者餐后无GLP-1反应。II级和III级肥胖者餐后无PYY反应,III级肥胖者餐后CCK反应延迟且缩短。与对照组相比,II级和III级肥胖者的基础胰岛素浓度更高,III级肥胖者的餐后胰岛素水平高于II级、I级肥胖者和对照组。不同肥胖等级之间的食欲评分没有差异。总之,肥胖的特征是胃肠激素分泌受损,餐后饱腹感降低,尤其是III级肥胖者。这种异常模式可能导致暴饮暴食。