Circulating leptin correlates with left ventricular mass in morbid (grade III) obesity before and after weight loss induced by bariatric surgery: A potential role for leptin in mediating human left ventricular hypertrophy
Circulating leptin correlates with left ventricular mass in morbid (grade III) obesity before and after weight loss induced by bariatric surgery: A potential role for leptin in mediating human left ventricular hypertrophy
复制标题
DOI：
10.1210/jc.2004-1963
复制
发表时间：
2005-07-01
影响因子：
5.8
通讯作者：
Pontiroli, AE
中科院分区：
文献类型：
--
作者：
Perego, L;Pizzocri, P;Pontiroli, AE
背景：肥胖经常与左心室肥厚相关，即使不合并高血压或糖尿病也是如此。目的：探讨无并发症、病态(3级)肥胖患者的瘦素水平与左心室重量的关系，以及心脏内瘦素受体和细胞内信号蛋白的存在。设计：对血压正常的III级肥胖患者(世界卫生组织分级)，分别于基线和1年后行减重手术[腹腔镜可调胃束带术(LAGB)]，通过心电图读数计算左心室重量(LVM)。对照组由健康、瘦弱、血压正常的受试者组成。研究对象：31例3级肥胖症患者和30例正常血压、年龄和性别匹配的健康非肥胖者。干预：肥胖者接受LAGB诱导体重减轻，并在基线和1年后进行评估。结果：肥胖组LVM、血浆瘦素、血糖、胰岛素水平和稳态模型评估指数均高于瘦对照组(P<；0.01)；单因素回归分析显示，LVM与体重指数、瘦素和稳态模型评估指数相关；多元回归分析显示，LVM仅与瘦素水平相关(P=0.001)。当肥胖患者的体重指数从46.2+/-1.24降至36.6+/-1.05 kg/m(2)(P<；0.01)时，肥胖者在LAGB后1年进行重新评估；LVM的下降仅与瘦素水平的下降相关(P<；0.01)。我们通过RT-PCR和/或免疫细胞化学的方法证明瘦素受体的长、短亚型以及介导瘦素信号的细胞内蛋白在人的心脏中都有表达。结论：这些数据提示瘦素可能参与了人类左室肥厚。
Context: Obesity is frequently associated with left ventricular hypertrophy, even when uncomplicated by hypertension or diabetes mellitus. Left ventricular hypertrophy is an important risk factor for congestive heart failure.Objective: The objective of this study was to evaluate the relationship between leptin and left ventricular mass in uncomplicated, morbid (grade 3) obesity and the existence of leptin receptors and intracellular signaling proteins in the human heart.Design: Left ventricular mass (LVM) was calculated through electrocardiogram reading in normotensive grade III obese patients (World Health Organization classification) undergoing bariatric surgery [laparoscopic adjustable gastric banding (LAGB)] at baseline and 1 yr later. The control group was composed of healthy lean normotensive subjects. Leptin receptors were detected by PCR and immunocytochemistry in human heart biopsies.Setting: This study was performed at university hospitals.Patients: Thirty-one grade 3 obese patients and 30 healthy nonobese normotensive, age- and sex-matched control subjects were studied.Intervention: Obese subjects underwent LAGB to induce weight loss and were evaluated at baseline and after 1 yr.Results: LVM, plasma leptin, glucose, insulin levels, and homeostasis model assessment index were higher in obese than in lean controls (P < 0.01); at univariate regression analysis, LVM correlated with body mass index, leptin, and homeostasis model assessment index; at multiple regression analysis, LVM only correlated with leptin levels (P = 0.001). Obese subjects were reevaluated 1 yr after LAGB, when their body mass index changed from 46.2 +/- 1.24 to 36.6 +/- 1.05 kg/m(2) (P < 0.01); the decrease in LVM correlated only with the decrease in leptin levels (P < 0.01). We demonstrated that long and short isoforms of the leptin receptor and intracellular proteins mediating leptin signaling were expressed in human heart by RT-PCR, immunocytochemistry, or both methods.Conclusions: These data suggest that leptin could contribute to the left ventricular hypertrophy in humans.