Contraction and Intracellular Calcium Transport in Epicardial and Endocardial Ventricular Myocytes from Streptozotocin-Induced Diabetic Rat

Introduction: Diabetes mellitus (DM) is a global health problem. According to the International Diabetes Federation, 424.9 million people suffered from DM in 2017 and this number is expected to rise to 628.6 million by 2045. Although diabetes can affect every organ in the body, cardiovascular disease is a major cause of death and disability in people with diabetes. Diabetic patients frequently suffer from systolic and diastolic dysfunction. Within the ventricles, the electromechanical properties of cardiac myocytes vary transmurally. Aims and Objectives: The aim of this study was to investigate contraction and Ca2+ transport in epicardial (EPI) and endocardial (ENDO) myocytes from the left ventricle in the streptozotocin (STZ) “ induced diabetic rat heart. Materials and Methods: Experiments were performed 5-6 months after STZ treatment. Ventricular myocytes were isolated by enzymic and mechanical dispersal techniques from EPI and ENDO regions of the left ventricle. Contraction and free intracellular Ca2+ concentration [Ca2+]i were measured by video edge detection and fluorescence photometry techniques, respectively. Results: Myocyte length and calculated surface area were smaller in EPI-STZ compared to EPI-CON. Time to peak (TPK) shortening was prolonged in EPI-STZ compared to EPI-CON and in ENDO-STZ compared to ENDO-CON myocytes. Time to half (THALF) relaxation of shortening was prolonged in EPI-STZ compared to EPI-CON. TPK Ca2+ transient was prolonged in EPI-STZ compared to EPI-CON, ENDO-STZ compared to ENDO-CON, ENDO-STZ compared to EPI-STZ and in ENDO-CON compared to EPI-CON myocytes. THALF decay of the Ca2+ transient was prolonged in ENDO-STZ compared to ENDO-CON. Fractional release of Ca2+ was increased in ENDO-STZ compared to ENDO-CON and in ENDO-STZ compared to EPI-STZ. Recovery of the Ca2+ transient was prolonged in ENDO-STZ compared to ENDO-CON. Conclusion: In conclusion the kinetics of contraction and Ca2+ transient and fractional release of Ca2+ from the sarcoplasmic reticulum are altered to different extents in EPI and ENDO myocytes from STZ-induced diabetic rat

The Role of Oxidative Stress in the Development of Diabetic Cardiomyopathy

Diabetes mellitus (DM) is a major global health problem, currently affecting about 460 million people while another billion have prediabetes, all costing the governments of the world over $1 trillion USAD to diagnose and treat diabetic patients, so that they can enjoy a better quality of life. DM induces hyperglycemia (HG), which in turn plays a significant role in the development of diabetic cardiomyopathy (DCM), which is responsible for over 80% of diabetic mortality. The exact mechanisms underlying DCM remain incompletely clear, although several pathological mechanisms responsible for DCM have been proposed in the literature. One such mechanism is oxidative stress (OS), which is widely considered as one of the major causes for the pathogenesis of the disease. There is a growing scientific and public interest in connecting oxidative stress with a variety of pathological conditions, including DM as well as other human diseases. HG-induced oxidative stress is a major risk factor for the development of micro-vascular pathogenesis in the diabetic myocardium, resulting in myocardial cell death, hypertrophy, fibrosis, abnormalities of calcium homeostasis and endothelial dysfunction. The aim of this review is to highlight the role of oxidative stress in the development of DCM

Medicinal and anti-oxidant effects of Bitter Melon (Momordica charantia) in the treatment of diabetic cardiomyopathy

Obesity is a major risk factor for diabetes mellitus (DM), which is a major global metabolic health disorder currently affecting over 460 million people and this number is rising rapidly. Heart failure (HF) is the major cause of death among diabetic patients. The disorder is due to elevated blood glucose or hyperglycemia (HG) beyond physiological level, which in turn leads to a number of long-term or end-organ complications over time and over 80% of all diabetics will eventually die from either HF or cardiomyopathy if left untreated. Treatment of DM is very costly and as such, patients turn to non-pharmacological or alternative forms of treatment, including weight loss, diet modifications and plant-based medicines, which are more cost-effective. There are several medicinal plants, which are currently used to treat for DM and they are known to exhibit anti-diabetic properties. One such plant is Momordica charantia, or bitter melon, which is used in many tropical countries as a traditional functional food and medicine, especially for the treatment of obesity, DM, hypertension and cancer. This review is related to the anti-oxidant beneficial effect of Momordica charantia in the treatment of diabetic cardiomyopathy (DCM). The beneficial effects of Momordica charantia in the treatment of obesity, diabetes and cardiovascular diseases (CVDs) have been reported in clinical and experimental animal studies and this review addresses some of these useful effects. However, the cellular and molecular mechanisms underlying its therapeutic antidiabetic effects of M charantia via its anti-oxidant activities are not fully known and further research studies need to be done

Structural determination, dielectric and photoluminescence properties of Ba0.975Ln(0.017)(Ti(0.95-x)ZrxSn(0.05))O-3 (Ln = Eu, Ho; x=0.05, 0.20)

International audienceLead-free compounds with formula Ba0.975Ln0.017(Ti0.90Zr0.05Sn0.05)O3 (BLnZ5TS) and Ba0.975Ln0.017(Ti0.75Zr0.20Sn0.05)O3 (BLnZ20TS) [Ln = Eu, Ho] were synthesized using the solid-state reaction technique. Scanning electron micrographs of ceramics showed a decrease in the average grain size as the Ln3+ radii increases. The structural study allowed the identification of tetragonal and cubic symmetries at room temperature for BLnZ5TS and BLnZ20TS, respectively. Dielectric measurements were carried out as a function of temperature and frequency. The results revealed that BLnZ5TS exhibited normal ferroelectric behavior with diffuse phase transition, whereas BLnZ20TS displayed relaxor ferroelectric properties. The diffuse phase transition parameters were determined from the modified Curie-Weiss law, while the relaxor behavior in BLnZ20TS was highlighted by a good fit to the Vogel-Fulcher relationship. The photoluminescence of the prepared specimens was investigated and the results showed that these compositions bear interest for green and red emission

Cellular and Biochemical Mechanisms Driving the Susceptibility of Obese Subjects to Covid-19 Infection

Overweight is a major global health problem currently affecting almost 2 billion people worldwide. An additional 800 million are obese. These figures showed that 40% of the global adult population aged 18 years, and over are overweight while 14% are obese. What is now worrying is that more than 40 million children worldwide, as young as 5 years of age are either overweight or obese. Individuals with a body mass index (BMI) of 25–29 kg/m2 are considered to be overweight while obesity is the term used when the BMI is 30 kg/m2 and over. Obesity is an imbalance between calorie intake and calorie expenditure. In general, obesity can be caused by excessive eating and reduced physical activity. Obesity is a major risk factor for non-communicable diseases such as diabetes mellitus, respiratory and liver dysfunctions, sleep apnea, chronic inflammation, compromised immune system, renal failure, cancer, musculoskeletal disorders, cardiovascular diseases and others. Obesity is also a major risk factor for coronavirus disease 19 (Covid-19), which can induce severe cases of pneumonia and sepsis or acute respiratory distress syndrome. In many cases, Covid-19 causes severe and long-lasting damage to the lungs and other vital organs of the body resulting in death. This review describes the cellular and biochemical mechanism(s) whereby obese patients become susceptible to Covid-19 infection. It also outlines how obesity on its own can affect the lungs, which in turn become more compromised in cases of Covid-19 disease resulting in the imminent death of the patient

Voltage dependence of the Ca2+ transient in endocardial and epicardial myocytes from the left ventricle of Goto-Kakizaki type 2 diabetic rats

Diabetes mellitus is a major global health disorder and, currently, over 450 million people have diabetes with 90% suffering from type 2 diabetes. Left untreated, diabetes may lead to cardiovascular diseases which are a leading cause of death in diabetic patients. Calcium is the trigger and regulator of cardiac muscle contraction and derangement in cellular Ca2+ homeostasis, which can result in heart failure and sudden cardiac death. It is of paramount importance to investigate the regional involvement of Ca2+ in diabetes-induced cardiomyopathy. Therefore, the aim of this study was to investigate the voltage dependence of the Ca2+ transients in endocardial (ENDO) and epicardial (EPI) myocytes from the left ventricle of the Goto-Kakizaki (GK) rats, an experimental model of type 2 diabetes mellitus. Simultaneous measurement of L-type Ca2+ currents and Ca2+ transients was performed by whole-cell patch clamp techniques. GK rats displayed significantly increased heart weight, heart weight/body weight ratio, and non-fasting and fasting blood glucose compared to controls (CON). Although the voltage dependence of L-type Ca2+ current was unaltered, the voltage dependence of the Ca2+ transients was reduced to similar extents in EPI-GK and ENDO-GK compared to EPI-CON and ENDO-CON myocytes. TPK L-type Ca2+ current and Ca2+ transient were unaltered. THALF decay of L-type Ca2+ current was unaltered; however, THALF decay of the Ca2+ transient was shortened in ENDO and EPI myocytes from GK compared to CON rat hearts. In conclusion, the amplitude of L-type Ca2+ current was unaltered; however, the voltage dependence of the Ca2+ transient was reduced to similar extents in EPI and ENDO myocytes from GK rats compared to their respective controls, suggesting the possibility of dysfunctional sarcoplasmic reticulum Ca2+ transport in the GK diabetic rat hearts