Bueno Marta, Boixadera-Planas Ester, Blanco-Hinojo Laura, Esteba-Castillo Susanna, Giménez-Palop Olga, Torrents-Rodas David, Pujol Jesús, Corripio Raquel, Deus Joan, Caixàs Assumpta
Endocrinology and Nutrition Department, University Hospital Arnau de Vilanova, Obesity, Diabetes and Metabolism (ODIM) Research Group, IRBLleida, University of Lleida, 25198 Lleida, Spain.
Servei d'Estadística Aplicada, Universitat Autònoma de Barcelona, 08193 Cerdanyola, Spain.
J Clin Med. 2021 Nov 4;10(21):5170. doi: 10.3390/jcm10215170.
Hyperphagia is one of the main problems of patients with Prader-Willi syndrome (PWS) to cope with everyday life. The underlying mechanisms are not yet well understood. Gut-brain hormones are an interrelated network that may be at least partially involved. We aimed to study the hormonal profile of PWS patients in comparison with obese and healthy controls. Thirty adult PWS patients (15 men; age 27.5 ± 8.02 years; BMI 32.4 ± 8.14 kg/m), 30 obese and 30 healthy controls were studied before and after eating a hypercaloric liquid diet. Plasma brain-derived neurotrophic factor (BDNF), leptin, total and active ghrelin, peptide YY (PYY), pancreatic polypeptide (PP), Glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and amylin were determined at times 0', 30', 60' and 120'. Cluster analysis was used. When considering all peptides together, two clusters were established according to fasting hormonal standardized concentrations. Cluster 1 encompassed most of obese (25/30) and healthy controls (28/30). By contrast, the majority of patients with PWS were located in Cluster 2 (23/27) and presented a similar fasting profile with hyperghrelinemia, high levels of leptin, PYY, GIP and GLP-1, compared to Cluster 1; that may reflect a dysfunction of these hunger/satiety hormones. When peptide behavior over the time was considered, PP concentrations were not sustained postprandially from 60 min onwards in Cluster 2. BDNF and amylin did not help to differentiate the two clusters. Thus, cluster analysis could be a good tool to distinguish and characterize the differences in hormone responses between PWS and obese or healthy controls.
食欲亢进是普拉德-威利综合征(PWS)患者应对日常生活的主要问题之一。其潜在机制尚未完全明确。肠脑激素是一个相互关联的网络,可能至少部分参与其中。我们旨在研究PWS患者与肥胖及健康对照者的激素谱。对30名成年PWS患者(15名男性;年龄27.5±8.02岁;体重指数32.4±8.14kg/m)、30名肥胖者和30名健康对照者在进食高热量流质饮食前后进行了研究。在0分钟、30分钟、60分钟和120分钟时测定血浆脑源性神经营养因子(BDNF)、瘦素、总胃饥饿素和活性胃饥饿素、肽YY(PYY)、胰多肽(PP)、胰高血糖素样肽-1(GLP-1)、葡萄糖依赖性促胰岛素多肽(GIP)和胰淀素。采用聚类分析。当综合考虑所有肽类时,根据空腹激素标准化浓度建立了两个聚类。聚类1包括大多数肥胖者(25/30)和健康对照者(28/30)。相比之下,大多数PWS患者位于聚类2(23/27),与聚类1相比,呈现出类似的空腹特征,伴有高胃饥饿素血症、高水平的瘦素、PYY、GIP和GLP-1;这可能反映了这些饥饿/饱腹感激素的功能障碍。当考虑肽类随时间的变化时,聚类2中PP浓度在餐后60分钟后未持续升高。BDNF和胰淀素无助于区分这两个聚类。因此,聚类分析可能是区分和表征PWS患者与肥胖或健康对照者激素反应差异的良好工具。