Xinxin Hu, Brendon John Yee, Craig Phillips, Julia Chapman, Ronald Grunstein
{"title":"Incretins for management of obesity and obstructive sleep apnea.","authors":"Xinxin Hu, Brendon John Yee, Craig Phillips, Julia Chapman, Ronald Grunstein","doi":"10.1080/17476348.2025.2513516","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Recent trials have demonstrated the efficacy of incretin-based pharmacotherapy in obstructive sleep apnea (OSA) in obese patients. In addition to improving sleep indices, these agents also led to sustained weight loss and improvements in cardiometabolic profile. Given cardiovascular mortality remains the most common cause of death among patients with OSA, these agents represent a potential paradigm shift toward more holist management approach toward patients with OSA.</p><p><strong>Areas covered: </strong>This article provides an overview of OSA pathophysiology, in particular, its overlapping risk factors with obesity. The physiology of the incretin axis is covered with reference to molecular targets of current therapies. Key trials in the use of incretins for diabetes and OSA are presented with critical discussion of knowledge gaps and scope for future research. The article focuses on newer incretin agents which appear to have dual activity against obesity and its cardiometabolic complications. Comparisons between incretin-based agents and current treatment modalities are explored including identification of knowledge gaps and future directions for research.</p><p><strong>Expert opinion: </strong>Incretin-based pharmacotherapy has the potential to transform the therapeutic landscape for OSA through their dual action on sleep-disordered breathing and obesity-related complications. Scope for future research remains to optimize patient selection, drug delivery, dosing, and equitable access and identify future molecular targets for OSA.</p>","PeriodicalId":94007,"journal":{"name":"Expert review of respiratory medicine","volume":" ","pages":"775-787"},"PeriodicalIF":2.7000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Expert review of respiratory medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/17476348.2025.2513516","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/6/3 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: Recent trials have demonstrated the efficacy of incretin-based pharmacotherapy in obstructive sleep apnea (OSA) in obese patients. In addition to improving sleep indices, these agents also led to sustained weight loss and improvements in cardiometabolic profile. Given cardiovascular mortality remains the most common cause of death among patients with OSA, these agents represent a potential paradigm shift toward more holist management approach toward patients with OSA.
Areas covered: This article provides an overview of OSA pathophysiology, in particular, its overlapping risk factors with obesity. The physiology of the incretin axis is covered with reference to molecular targets of current therapies. Key trials in the use of incretins for diabetes and OSA are presented with critical discussion of knowledge gaps and scope for future research. The article focuses on newer incretin agents which appear to have dual activity against obesity and its cardiometabolic complications. Comparisons between incretin-based agents and current treatment modalities are explored including identification of knowledge gaps and future directions for research.
Expert opinion: Incretin-based pharmacotherapy has the potential to transform the therapeutic landscape for OSA through their dual action on sleep-disordered breathing and obesity-related complications. Scope for future research remains to optimize patient selection, drug delivery, dosing, and equitable access and identify future molecular targets for OSA.