scholarly journals Diabetes and Heart Failure: Multi-Omics Approaches

2021 ◽  
Vol 12 ◽  
Author(s):  
Akram Tayanloo-Beik ◽  
Peyvand Parhizkar Roudsari ◽  
Mostafa Rezaei-Tavirani ◽  
Mahmood Biglar ◽  
Ozra Tabatabaei-Malazy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Type 2 Diabetes ◽  
Molecular Mechanisms ◽  
Medical Systems ◽  
Global Issues ◽  
Glucose Levels ◽  
Glycation End Products ◽  
Amplifying Effect

Diabetes and heart failure, as important global issues, cause substantial expenses to countries and medical systems because of the morbidity and mortality rates. Most people with diabetes suffer from type 2 diabetes, which has an amplifying effect on the prevalence and severity of many health problems such as stroke, neuropathy, retinopathy, kidney injuries, and cardiovascular disease. Type 2 diabetes is one of the cornerstones of heart failure, another health epidemic, with 44% prevalence. Therefore, finding and targeting specific molecular and cellular pathways involved in the pathophysiology of each disease, either in diagnosis or treatment, will be beneficial. For diabetic cardiomyopathy, there are several mechanisms through which clinical heart failure is developed; oxidative stress with mediation of reactive oxygen species (ROS), reduced myocardial perfusion due to endothelial dysfunction, autonomic dysfunction, and metabolic changes, such as impaired glucose levels caused by insulin resistance, are the four main mechanisms. In the field of oxidative stress, advanced glycation end products (AGEs), protein kinase C (PKC), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) are the key mediators that new omics-driven methods can target. Besides, diabetes can affect myocardial function by impairing calcium (Ca) homeostasis, the mechanism in which reduced protein phosphatase 1 (PP1), sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a), and phosphorylated SERCA2a expressions are the main effectors. This article reviewed the recent omics-driven discoveries in the diagnosis and treatment of type 2 diabetes and heart failure with focus on the common molecular mechanisms.

Oxidative stress in patients with chronic heart failure and type 2 diabetes mellitus

2007 ◽  
Vol 143 (2) ◽  
pp. 207-209 ◽  
Author(s):  
N. E. Arzamastseva ◽  
V. Z. Lankin ◽  
G. G. Konovalova ◽  
A. K. Tikhaze ◽  
F. T. Ageev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Heart Failure ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Chronic Heart Failure

scholarly journals Canagliflozin Prevents Intrarenal Angiotensinogen Augmentation and Mitigates Kidney Injury and Hypertension in Mouse Model of Type 2 Diabetes Mellitus

2019 ◽  
Vol 49 (4) ◽  
pp. 331-342 ◽  
Author(s):  
T. Cooper Woods ◽  
Ryousuke Satou ◽  
Kayoko Miyata ◽  
Akemi Katsurada ◽  
Courtney M. Dugas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
High Blood Pressure ◽  
Kidney Injury ◽  
Renal Tubules ◽  
Glucose Levels

Background: Hypertension and renal injury are common complications of type 2 diabetes mellitus (T2DM). Hyperglycemia stimulates renal proximal tubular angiotensinogen (AGT) expression via elevated oxidative stress contributing to the development of high blood pressure and diabetic nephropathy. The sodium glucose cotransporter 2 (SGLT2) in proximal tubules is responsible for the majority of glucose reabsorption by renal tubules. We tested the hypothesis that SGLT2 inhibition with canagliflozin (CANA) prevents intrarenal AGT augmentation and ameliorates kidney injury and hypertension in T2DM. Methods: We induced T2DM in New Zealand obese mice with a high fat diet (DM, 30% fat) with control mice receiving regular fat diet (ND, 4% fat). When DM mice exhibited > 350 mg/dL blood glucose levels, both DM- and ND-fed mice were treated with 10 mg/kg/day CANA or vehicle by oral gavage for 6 weeks. We evaluated intrarenal AGT, blood pressure, and the development of kidney injury. Results: Systolic blood pressure in DM mice (133.9 ± 2.0 mm Hg) was normalized by CANA (113.9 ± 4.0 mm Hg). CANA treatment ameliorated hyperglycemia-associated augmentation of renal AGT mRNA (148 ± 21 copies/ng RNA in DM, and 90 ± 16 copies/ng RNA in DM + CANA) and protein levels as well as elevation of urinary 8-isoprostane levels. Tubular fibrosis in DM mice (3.4 ± 0.9-fold, fibrotic score, ratio to ND) was suppressed by CANA (0.9 ± 0.3-fold). Furthermore, CANA attenuated DM associated increased macrophage infiltration and cell proliferation in kidneys of DM mice. Conclusions: CANA prevents intrarenal AGT upregulation and oxidative stress and which may mitigate high blood pressure, renal tubular fibrosis, and renal inflammation in T2DM.

Comment on: acute and chronic fluctuations in blood glucose levels can increase oxidative stress in type 2 diabetes mellitus

2012 ◽  
Vol 50 (5) ◽  
pp. 825-826
Author(s):  
Turgay Ulas ◽  
Mehmet Sinan Dal ◽  
Irfan Tursun ◽  
Mehmet Emin Demir ◽  
Hakan Buyukhatipoglu
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Blood Glucose ◽  
Glucose Levels ◽  
Blood Glucose Levels

scholarly journals Characterization of Blood Oxidative Stress in Type 2 Diabetes Mellitus Patients: Increase in Lipid Peroxidation and SOD Activity

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Suziy de M. Bandeira ◽  
Glaucevane da S. Guedes ◽  
Lucas José S. da Fonseca ◽  
André S. Pires ◽  
Daniel P. Gelain ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Lipid Peroxidation ◽  
Diabetic Patients ◽  
Sod Activity ◽  
Glucose Levels ◽  
Significant Difference ◽  
Close Relationship

This study evaluated the oxidative stress through enzymatic and nonenzymatic biomarkers in diabetic patients with and without hypertension and prediabetics. The SOD and CAT (in erythrocytes) and GPx (in plasma) enzymatic activities, plasma levels of lipid peroxidation, and total thiols were measured in the blood of 55 subjects with type 2 diabetes and 38 subjects without diabetes (9 pre-diabetics and 29 controls) aged 40–86 years. The total SOD activity and the lipid peroxidation were higher in diabetics compared to nondiabetics. In stratified groups, the total SOD activity was different for the hypertensive diabetics compared to the prediabetics and normotensive controls. Lipid peroxidation was significantly higher in both groups of diabetics (hypertensive and normotensive) compared to prediabetic groups and hypertensive and normotensive controls. There was no significant difference in the CAT and GPx activities, as well as in the concentration of total thiols in the groups studied. Present data strongly suggest the involvement of oxidative stress in the pathophysiology of diabetes, revealing that the increased lipid peroxidation has a close relationship with high glucose levels, as observed by the fasting glucose and HbA1c levels. The results evidence the correlation between lipid peroxidation and DM, irrespective of the presence of hypertension.

scholarly journals Exercise Training-Induced Changes in MicroRNAs: Beneficial Regulatory Effects in Hypertension, Type 2 Diabetes, and Obesity

2018 ◽  
Vol 19 (11) ◽  
pp. 3608 ◽  
Author(s):  
Alex Improta Caria ◽  
Carolina Nonaka ◽  
Ciro Pereira ◽  
Milena Soares ◽  
Simone Macambira ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Exercise Training ◽  
Insulin Signaling ◽  
Molecular Mechanisms ◽  
Phenotypic Change ◽  
Glucose Levels ◽  
Physiological Processes ◽  
Regulatory Effects

MicroRNAs are small non-coding RNAs that regulate gene expression post-transcriptionally. They are involved in the regulation of physiological processes, such as adaptation to physical exercise, and also in disease settings, such as systemic arterial hypertension (SAH), type 2 diabetes mellitus (T2D), and obesity. In SAH, microRNAs play a significant role in the regulation of key signaling pathways that lead to the hyperactivation of the renin-angiotensin-aldosterone system, endothelial dysfunction, inflammation, proliferation, and phenotypic change in smooth muscle cells, and the hyperactivation of the sympathetic nervous system. MicroRNAs are also involved in the regulation of insulin signaling and blood glucose levels in T2D, and participate in lipid metabolism, adipogenesis, and adipocyte differentiation in obesity, with specific microRNA signatures involved in the pathogenesis of each disease. Many studies report the benefits promoted by exercise training in cardiovascular diseases by reducing blood pressure, glucose levels, and improving insulin signaling and lipid metabolism. The molecular mechanisms involved, however, remain poorly understood, especially regarding the participation of microRNAs in these processes. This review aimed to highlight microRNAs already known to be associated with SAH, T2D, and obesity, as well as their possible regulation by exercise training.

Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome

2008 ◽  
Vol 114 (3) ◽  
pp. 195-210 ◽  
Author(s):  
Heiko Bugger ◽  
E. Dale Abel
Keyword(s):  
Heart Failure ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Coronary Artery Disease ◽  
Metabolic Syndrome ◽  
Molecular Mechanisms ◽  
Contractile Dysfunction ◽  
The Metabolic Syndrome ◽  
Artery Disease

The metabolic syndrome represents a cluster of abnormalities, including obesity, insulin resistance, dyslipidaemia and Type 2 diabetes, that increases the risk of developing cardiovascular diseases, such as coronary artery disease and heart failure. The heart failure risk is increased even after adjusting for coronary artery disease and hypertension, and evidence is emerging that changes in cardiac energy metabolism might contribute to the development of contractile dysfunction. Recent findings suggest that myocardial mitochondrial dysfunction may play an important role in the pathogenesis of cardiac contractile dysfunction in obesity, insulin resistance and Type 2 diabetes. This review will discuss potential molecular mechanisms for these mitochondrial abnormalities.

scholarly journals Effect of oxidative stress on endothelium in patients with heart failure and type 2 diabetes ­mellitus

2020 ◽  
Vol 101 (1) ◽  
pp. 13-17
Author(s):  
F I Mammadova
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Heart Failure ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Chronic Heart Failure ◽  
Endothelial Dysfunction ◽  
Control Group

Aim. To estimate the severity of endothelial dysfunction and effects of nitric oxide, thiol status and cystatin on the progression of chronic heart failure and chronic heart failure in type 2 diabetes mellitus. Methods. 80 patients (men and women) with chronic heart failure were included. All patients were divided into two groups: the first group 39 patients with chronic heart failure, the second 41 people with chronic heart failure and type 2 diabetes mellitus. The control group consists of 20 healthy donors. To obtain statistically significant differences with the control group the minimum sample size for observations was determined based on the target variance of a small sample (n=10). The lipid profile and carbohydrate metabolism, endothelin-1, cystatin, nitric oxide were evaluated. Statistical processing was performed using Microsoft Office Excel and IBM SPSS Statistics 20 software. Results. Changes in lipid metabolism were found in both groups, while an increase in carbohydrate metabolism was observed in patients with chronic heart failure with type 2 diabetes mellitus. Under conditions of oxidative stress in patients with chronic heart failure, a decrease in the content of thiol status and an increase in the amount of nitric oxide in the blood serum were recorded. The endothelin-1 level was elevated, particularly in the second group, which indicates a more serious endothelial dysfunction with increased glucose content in patients with chronic heart failure. Conclusion. The level of cystatin C as an atherogenic risk factor was equally increased in the studied patients, possibly it affected by the rate of disease progression; feasible to use these markers to detect the progression of chronic heart failure in the early stages.

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