Abstract
BackgroundDiabetes mellitus (DM) and hypertension (HTN) are accused of being responsible for the development of the cardiac fibrosis due to severe cardiomyopathy.MethodsBlood glucose (BG) test was carried out, lipid concentrations, tumor necrosis factor alpha (TNF-α), transforming growth factor beta (TGF-β), matrix metalloproteinase (MMP-2), collagen-I and collagen-III were measured in male Albino rats weighing 179-219 g. The rats were divided into five groups, kept on either control diet or high fat diet (HFD), and simultaneously treated with rosiglitazone (PPAR-gamma) only for one group with 3 mg/kg/day via oral route for 30 days, and with rosiglitazone and felodipine combination for another group with 3 mg/kg/day and 5 mg/kg/day, respectively via oral route for 30 days.ResultsDiabetic hypertensive (DH) rats which fed on a HFD, injected with streptozotocin (STZ) (i.p.) and obstruction for its right kidney was occurred develop hyperglycemia, hypertension, cardiac fibrosis, hypertriglyceridemia, hypercholesterolemia, increased TNF-α, increased TGF-β, decreased MMP-2, increased collagen-I and increased collagen-III, when compared to rats fed on control diet. Treating the DH rats with rosiglitazone only causes a significant decrease for BG levels by 52.79%, triglycerides (TGs) by 24.05%, total cholesterol (T-Chol) by 30.23%, low density lipoprotein cholesterol (LDL-C) by 40.53%, TNF-α by 20.81%, TGF-β by 46.54%, collagen-I by 48.11% and collagen-III by 53.85% but causes a significant increase for MMP-2 by 272.73%. Moreover, Treating the DH rats with rosiglitazone and felodipine combination causes a significant decrease for BG levels by 61.08%, blood pressure (BP) by 16.78%, TGs by 23.80%, T-Chol by 33.27%, LDL-C by 45.18%, TNF-α by 22.82%, TGF-β by 49.31%, collagen-I by 64.15% and collagen-III by 53.85% but causes a significant increase for MMP-2 by 290.91%. Rosiglitazone alone failed to decrease the BP in DH rats in the current dosage and duration.ConclusionOur results indicate that the co-existence of diabetes and hypertension could induce cardiomyopathy which could further result in cardiac fibrosis, and that combination treatment with rosiglitazone and felodipine has a great protective role against the metabolic abnormalities, meanwhile, the treatment with rosiglitazone alone has a protective role with a minimal effect against these abnormalities and has no effect on decreasing BP in these cases which may lead to coronary artery diseases (CADs) in future.
Highlights
Diabetic cardiomyopathy, the leading cause of death in diabetic patients, is characterized by both systolic and diastolic dysfunction, due to reduced contractility, prolonged relaxation, and decreased compliance [1,2]
We investigate the role of Calcium channel blockers (CCBs) and Peroxisome Proliferator-Activated Receptors (PPAR)-gamma modulators on blood glucose level, blood pressure, lipid profile, tumor necrosis factor alpha (TNF-a), TGF-b1, MMP-2, collagen-I and collagen-III in Diabetic hypertensive (DH) rats
There is no significance between groups even with rosiglitazone only (group R) and Diabetic Hypertensive Control group (DHC) data in its blood pressure (BP) levels
Summary
The leading cause of death in diabetic patients, is characterized by both systolic and diastolic dysfunction, due to reduced contractility, prolonged relaxation, and decreased compliance [1,2]. Interstitial fibrosis has been regarded as an important pathogenic factor of the heart’s impaired functional integrity [5]; altered substrate supply and use by cardiac myocytes could be the primary injury in the pathogenesis of this specific heart muscle disease. Structural and functional impairment of myocytes, which occurs already in the first week of diabetes, precedes cardiac fibrosis and remains the key step in impairing contractile performance, inducing heart failure [6]. The diagnosis of a diabetic cardiomyopathy is made in patients in whom no other known etiological factors, such as coronary artery disease, or hypertension, are present [7]. Diabetes mellitus (DM) and hypertension (HTN) are accused of being responsible for the development of the cardiac fibrosis due to severe cardiomyopathy
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