Role of endogenous GLP-1 on arterial stiffness and renal haemodynamics following bariatric surgery

IF 4.4 3区 医学 Q1 MEDICINE, GENERAL & INTERNAL
D. Moriconi, R. M. Bruno, E. Rebelos, S. Armenia, S. Baldi, L. Bonvicini, S. Taddei, M. Nannipieri
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引用次数: 0

Abstract

Background

Cardiovascular trials have revealed the positive impact of GLP-1 receptor agonists (GLP-1 RAs) on cardiovascular outcomes in type 2 diabetes (T2D). However, the specific effects of endogenous GLP-1 on arterial stiffness and renal function remain understudied. This study aimed to explore the influence of endogenous GLP-1 response post-bariatric surgery on arterial stiffness and renal haemodynamic.

Methods

Thirty individuals with morbid obesity and without T2D, scheduled for Roux-en-Y Gastric Bypass (RYGB), were included. Clinical parameters, 3-hour oral glucose tolerance test (OGTT) with serial sampling for glycaemia, GLP-1 and insulin, carotid-femoral pulse wave velocity (cf-PWV), carotid distensibility coefficient (carotid-DC) and renal resistive index (RRI) measurements were conducted pre-surgery and 1-year post-surgery. Participants were categorized into high-response and low-response groups based on their post-surgery increase in GLP-1 (median increase of 104% and 1%, respectively, pre- vs. post-surgery).

Results

Post-surgery, high-response group demonstrated a greater reduction in cf-PWV (p = .033) and a greater increase (p = .043) in carotid DC compared to low-response group. These enhancements were observed independently of weight loss or blood pressure changes. High-response group exhibited a reduction in RRI (p = .034), although this association was influenced by improvement in pulse pressure. Finally, a multivariate stepwise regression analysis indicated that the percentage increase of GLP1, Δ-GLP1(AUC)%, was the best predictor of percentage decrease in cf-PWV (p = .014).

Conclusions

Elevated endogenous GLP-1 response following RYGB was associated with improved arterial stiffness and renal resistances, suggesting potential cardio-renal benefits. The findings underscore the potential role of endogenous GLP-1 in influencing vascular and renal haemodynamics independent of traditional weight loss.

减肥手术后内源性 GLP-1 对动脉僵化和肾血流动力学的作用。
背景:心血管试验显示,GLP-1 受体激动剂(GLP-1 RAs)对 2 型糖尿病(T2D)患者的心血管预后有积极影响。然而,内源性 GLP-1 对动脉僵化和肾功能的具体影响仍未得到充分研究。本研究旨在探讨减肥手术后内源性 GLP-1 反应对动脉僵化和肾血流动力学的影响:方法:研究人员纳入了 30 名计划接受 Roux-en-Y 胃旁路手术(RYGB)的病态肥胖且无 T2D 患者。在手术前和手术后 1 年分别进行了临床参数、3 小时口服葡萄糖耐量试验(OGTT)及血糖、GLP-1 和胰岛素连续采样、颈动脉-股动脉脉搏波速度(cf-PWV)、颈动脉舒张系数(carotid-DC)和肾阻力指数(RRI)测量。根据参与者手术后 GLP-1 的增加情况(手术前与手术后的中位增加率分别为 104% 和 1%),将其分为高反应组和低反应组:结果:与低反应组相比,手术后高反应组的 cf-PWV 降低幅度更大(p = .033),颈动脉直流增加幅度更大(p = .043)。这些改善与体重减轻或血压变化无关。高反应组的 RRI 有所下降(p = .034),尽管这种关联受到脉压改善的影响。最后,多变量逐步回归分析表明,GLP1 增加的百分比(Δ-GLP1(AUC)%)是预测 cf-PWV 百分比下降的最佳指标(p = .014):结论:RYGB术后内源性GLP-1反应的升高与动脉僵化和肾脏阻力的改善有关,这表明GLP-1对心血管和肾脏有潜在的益处。这些发现强调了内源性 GLP-1 在影响血管和肾血流动力学方面的潜在作用,而与传统的体重减轻无关。
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来源期刊
CiteScore
9.50
自引率
3.60%
发文量
192
审稿时长
1 months
期刊介绍: EJCI considers any original contribution from the most sophisticated basic molecular sciences to applied clinical and translational research and evidence-based medicine across a broad range of subspecialties. The EJCI publishes reports of high-quality research that pertain to the genetic, molecular, cellular, or physiological basis of human biology and disease, as well as research that addresses prevalence, diagnosis, course, treatment, and prevention of disease. We are primarily interested in studies directly pertinent to humans, but submission of robust in vitro and animal work is also encouraged. Interdisciplinary work and research using innovative methods and combinations of laboratory, clinical, and epidemiological methodologies and techniques is of great interest to the journal. Several categories of manuscripts (for detailed description see below) are considered: editorials, original articles (also including randomized clinical trials, systematic reviews and meta-analyses), reviews (narrative reviews), opinion articles (including debates, perspectives and commentaries); and letters to the Editor.
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