胰淀素
内科学
医学
胰岛素抵抗
内分泌学
糖尿病
胰岛素
2型糖尿病
帕金森病
稳态模型评估
疾病
小岛
作者
Almudena Sánchez-Gómez,Gema Alcarraz-Vizán,Manel Fernández,Rubén Fernández‐Santiago,Mario Ezquerra,Ana Cámara,M. Serrano,Anna Novials,Esteban Muñoz,Francesc Valldeoriola,Yaroslau Compta,Marı́a José Martı́
标识
DOI:10.1016/j.parkreldis.2020.08.018
摘要
Background Type-2-diabetes (T2D) has surfaced as a potential risk factor for Parkinson's disease (PD) in some epidemiological studies. Evidence of glucose metabolism alterations in PD from molecular studies remains conflicting. Amylin, the T2D amyloid protein, has been implicated in PD in pathological studies. We aimed to assess peripheral levels of amylin and insulin in PD patients and control subjects (Cs). Methods We conducted an observational cross-sectional study of 111 participants: 73 PD and 38 Cs, similar in age, sex and body mass index. All underwent motor (UPDRS-MDS-III), non-motor (NMSS) and cognitive (MDRS) scales as well as determination of four parameters: fasting glycaemia, glycated haemoglobin, fasting plasma insulin (FPI) and fasting plasma amylin (FPA). Results FPI was significantly lower in PD than Cs (p = 0.034). In participants with age above cohort-median-age, FPA was higher in PD than Cs (p = 0.046). The FPA/FPI ratio (FPAIR) was significantly higher in PD than Cs (p = 0.024). In PD, modest correlation was found between higher insulin-resistance and NMSS scores. Conclusions PD patients had lower FPI and increased FPAIR. In older PD subgroup, FPA was increased. The more the insulin resistance, the higher the non-motor scores. These findings provide an additional link between pathophysiology of diabetes and PD. This might be related to a dissociated insulin and amylin secretion in PD, in line with recent evidence of endocrine pancreas role in PD pathogeny.
科研通智能强力驱动
Strongly Powered by AbleSci AI