Gender Differences in the Aldosterone Level of Young Obese Patients With Hypertension 1 1 1 Li-jun Li, Xiao-ling Hou, Xiao-wen Geng, and Yun-dai Chen Department of Cardiology, Chinese PLA General Hospital, Beijing, China. Correspondence: Yun-dai Chen (email@example.com). Objective: To investigate gender differences in aldosterone levels of young obese patients with hypertension. Methods: A total of 319 young inpatients with hypertension were enrolled in this study, and there were 217 male and 102 female. Obesity was defined as body mass index (BMI) ≥28 kg/m according to the diagnostic criteria of obesity for the Asia- Pacific region. All the patients underwent fasting blood tests and the recumbent-upright test, and the levels of angiotensin and aldosterone were detected during hospitalization. Results: e le Th vel of supine aldosterone in female obese patients with hypertension was significantly lower than that in the male obese patients with hypertension (407.37 ± 169.59 vs. 470.09 ± 159.67 pmol/l, P < 0.05). In young male patients with hypertension, supine aldosterone levels were significantly increased in the obese group compared to the nonobese group (470.09 ± 159.67 vs. 416.21 ± 126.05 pmol/l, P < 0.05). While in young female patients with hypertension, there were no significant differences in supine aldosterone levels between obese and nonobese group (407.37 ± 169.59 vs. 402.37 ± 126.37 pmol/l, P > 0.05). In young male patients with hypertension, the aldosterone level was positively correlated with BMI and systolic blood pressure (r = 0.195, 0.216, both P < 0.05). Conclusion: Young male obese patients with hypertension have higher aldosterone levels than their nonobese counterparts. However, aldosterone levels are similar between obese and nonobese hypertensive patients in young females. Epicardial Adipose Tissue-Derived Leptin Promotes Cardiac Fibroblast Proliferation in High-Fat Diet Induced Obese Rats 1 1 1 1 1 Min Li, Lei Liu, Yan Song, Gang Tian, and Dan-jun Zhu Department of Cardiology, The First Affiliated Hospital, Xi’an Jiaotong University, Xi’an Shaanxi, China. Correspondence: Dan-jun Zhu (firstname.lastname@example.org), Gang Tian (email@example.com). Objective: To investigate the effects of epicardial adipose tissue-derived leptin on cardiac fibroblast (CF) proliferation and its possible mechanism. Methods: Adult Wistar rats were randomly divided to feed with a high fat diet (obesity group, n = 7) or a standard diet (con- trol group, n = 7) for 12 weeks. Body weight, blood pressure, and serum leptin levels were measured. CFs were cultured in the epicardial adipose tissue-conditioned medium with and without leptin, leptin triple antagonist (leptin-tA), extracellular signal-regulated kinases (ERK) 1/2 inhibitor or p38 inhibitor. Cell proliferation was assessed by methylthiazolyl tetrazolium (MTT) assay. Levels of leptin and leptin receptors in the epicardial adipose tissue, and phosphorylation of ERK1/2 and p38 in cultured cells were determined by Western blot analysis. Results: Compared with control group, serum leptin levels and the expression of leptin and leptin receptors in the epicardial adipose tissue were significantly higher in the obese group (all P < 0.05). In vitro, leptin levels in epicardial adipose tissue- conditioned medium were significantly higher from obese rats compared to those from control rats ( P < 0.05). The obese rats epicardial adipose tissue-conditioned medium significantly increased CF cell proliferation ( P < 0.05), and phosphorylation of ERK1/2 and p38 (all P < 0.05). Treatment with leptin-tA, an ERK1/2, or p38 inhibitor significantly decreased CF cell pro - liferation (all P < 0.05). Conclusion: Epicardial adipose tissue-derived leptin from obese rats promotes CF cell proliferation via ERK1/2 and p38 signaling pathways. 750 American Journal of Hypertension 31(6) June 2018 Downloaded from https://academic.oup.com/ajh/article-abstract/31/6/750/4993502 by Ed 'DeepDyve' Gillespie user on 20 June 2018
American Journal of Hypertension – Oxford University Press
Published: May 7, 2018
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