Appetite Regulation and Allostatic Load Across Prediabetes Phenotypes

糖尿病前期表型中的食欲调节和异质性负荷

阅读:1

Abstract

Allostatic load is a physiological measure of chronic stress, and stress is implicated in disrupting appetite regulation. Individuals with obesity and type 2 diabetes have higher allostatic load compared to lean counterparts. However, whether allostatic load differs across prediabetes phenotypes and relates to appetite is unknown. PURPOSE: Test whether prediabetes phenotypes differ in allostatic load in relation to altered appetite regulation. METHODS: Individuals with obesity were recruited, and prediabetes was determined using American Diabetes Association (ADA) criteria (75 g OGTT) for this cross-sectional study. After an overnight fast, appetite hormones (ghrelin and PYY), insulin, and glucose were measured every 30 min up to 120 min of the OGTT. Perception of hunger and fullness as well as desire for sweet and fatty foods were assessed using a visual analog scale. Allostatic load was calculated from physiologic markers. Aerobic fitness (VO(2)max), body composition (DXA), clinical labs, and quality-of-life questionnaires were also collected. RESULTS: Participants with impaired fasting glucose (IFG) + impaired glucose tolerance (IGT) had a higher allostatic load, obesity, and insulin resistance compared with IFG or IGT (all p < 0.05), independent of fitness. IFG + IGT also had lower fasting ghrelin (p < 0.05) and no difference in fasting PYY. Hunger, fullness, and sweet ratings were comparable across groups, but fatty food ratings tended to be higher in IFG + IGT than NGT. CONCLUSIONS: Allostatic load was associated with altered fasting ghrelin levels in individuals with IFG + IGT, along with elevated body weight and insulin resistance. These findings suggest stress is a potential mechanism underlying appetite dysregulation in different forms of prediabetes.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。