scholarly journals Aldosterone and the autocrine modulation of potassium currents and oxidative stress in the diabetic rat heart

2008 ◽  
Vol 154 (3) ◽  
pp. 675-687 ◽  
Author(s):  
Y Shimoni ◽  
K Chen ◽  
T Emmett ◽  
G Kargacin
2014 ◽  
Vol 92 (10) ◽  
pp. 827-837 ◽  
Author(s):  
Varun Saran ◽  
Vijay Sharma ◽  
Richard Wambolt ◽  
Violet G. Yuen ◽  
Michael Allard ◽  
...  

Metabolic disturbances and oxidative stress have been highlighted as potential causative factors for the development of diabetic cardiomyopathy. The β-blocker metoprolol is known to improve function in the diabetic rat heart and ameliorates the sequelae associated with oxidative stress, without lowering oxidative stress. The antioxidant ascorbic acid is known to improve function in the diabetic rat heart. We tested whether a combination of ascorbic acid and metoprolol treatment would improve function further than each drug individually. Control and streptozotocin-induced diabetic Wistar rats were treated with metoprolol (15 mg·(kg body mass)−1·day−1, via an osmotic pump) and (or) ascorbic acid (1000 mg·(kg body mass)−1·day−1, via their drinking water). To study the effect of treatment on the development of dysfunction, we examined time points before (5 weeks diabetic) and after (7 weeks diabetic) development of overt systolic dysfunction. Echocardiography and working-heart-perfusion were used to assess cardiac function. Blood and tissue samples were collected to assess the severity of disease and oxidative stress. While both drugs improved function, only ascorbic acid had effects on oxidative damage. Combination treatment had a more pronounced improvement in function. Our β-blocker + antioxidant treatment strategy focused on oxidative stress, not diabetes specifically; therefore, it may prove useful in other diseases where oxidative stress contributes to the pathology.


2005 ◽  
Vol 567 (1) ◽  
pp. 177-190 ◽  
Author(s):  
Y. Shimoni ◽  
D. Hunt ◽  
M. Chuang ◽  
K. Y. Chen ◽  
G. Kargacin ◽  
...  

Diabetologia ◽  
1995 ◽  
Vol 38 (10) ◽  
pp. 1157-1168 ◽  
Author(s):  
P. R�sen ◽  
T. Ballhausen ◽  
W. Bloch ◽  
K. Addicks

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.


PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0171544 ◽  
Author(s):  
Pilar Rodríguez-Rodríguez ◽  
Angel L. López de Pablo ◽  
Concha F. García-Prieto ◽  
Beatriz Somoza ◽  
Begoña Quintana-Villamandos ◽  
...  

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