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Metabolic effects two years after renal denervation in insulin resistant hypertensive patients. The Re-Shape CV-risk study

医学 内科学 脂联素 胰岛素抵抗 动脉硬化 内分泌学 血压 定量胰岛素敏感性检查指数 动态血压 胰岛素 瘦素 心脏病学 代谢综合征 脂肪因子 回廊的 糖尿病 胰岛素敏感性 肥胖
作者
Atena Miroslawska,Petter Fosse Gjessing,Marit D. Solbu,Jon Viljar Norvik,Ole‐Martin Fuskevåg,Tove Aminda Hanssen,Terje Steigen
出处
期刊:Clinical Nutrition [Elsevier BV]
卷期号:40 (4): 1503-1509 被引量:5
标识
DOI:10.1016/j.clnu.2021.02.027
摘要

Background & aims Denervation of renal sympathetic nerves (RDN) is an invasive endovascular procedure introduced as an antihypertensive treatment with a potential beneficial effect on insulin resistance (IR). We have previously demonstrated a reduction in blood pressure (BP) six months after RDN, but severe hepatic and peripheral IR, assessed by glucose tracer and two step hyperinsulinemic-euglycemic clamp (HEC), did not improve. The aim of the current study was to evaluate IR and adipokines profiles in relation to BP and arterial stiffness changes two years after RDN. Methods In 20 non-diabetic patients with true treatment-resistant hypertension, ambulatory and office BP were measured after witnessed intake of medications prior to, six and 24 months after RDN. Arterial stiffness index (AASI) was calculated from ambulatory BP. Insulin sensitivity (IS) was assessed using an oral glucose tolerance test (OGTT), the Homeostasis Model Assessment (HOMA-IR), HOMA-Adiponectin Model Assessment (HOMA-AD), the Quantitative Insulin Sensitivity Check Index (QUICKI), the Triglyceride and Glucose Index (TyG) and the Leptin-to-Adiponectin Ratio (LAR). These surrogate indices of IS were compared with tracer/HEC measurements to identify which best correlated in this group of patients. Results All measured metabolic variables and IS surrogate indices remained essentially unchanged two years after RDN apart from a significant increase in HOMA-AD. OGTT peak at 30 min correlated best with reduction in endogenous glucose release (EGR) during low insulin HEC (r = −0.6, p = 0.01), whereas HOMA-IR correlated best with whole-body glucose disposal (WGD) (r = −0.6, p = 0.01) and glucose infusion rate (r = −0.6, p = 0.01) during high insulin HEC. BP response was unrelated to IS prior to RDN. Nocturnal systolic BP and arterial stiffness before RDN correlated positively with a progression in hepatic IR at six-month follow-up. Conclusion IR, adiponectin and leptin did not improve two years after RDN. There was no correlation between baseline IS and BP response. Our study does not support the notion of a beneficial metabolic effect of RDN in patients with treatment resistant hypertension.
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