No abstract

Title Diabetes-induced chronic heart failure is due to defects in calcium transporting and regulatory contractile proteins: cellular and molecular evidence Type Article URL https://clok.uclan.ac.uk/43996/ DOI ##doi## Date 2022 Citation Rupee

Diabetes mellitus can induce substantial damage to the conduction system of the heart, especially the sinoatrial node. This is due to hyperglycemia leading to bradyarrhythmia. DM, via the elevation of HG, generates the production of a number of insulting agents in the myocardium known as reactive oxygen species and reactive carbonyl species, which elicit direct damage to neuro-filament-M and β2-adrenergic receptors in the conducting system as well as a number of cardiac contractile, cation transporting and channel proteins. One cation channel protein is the hyperpolarization-activated cyclic nucleotide-gated potassium channel. It encodes the protein responsible for the hyperpolarizing-activated current or the “funny current” that participates in spontaneous diastolic membrane depolarization in sinoatrial node cells. Gene expression of these proteins and their physiological functions are decreased in the diabetic heart, which affects the generation of electrical impulses or action potentials resulting in increases in RR and PR intervals and QRS complex duration of the electrocardiogram. The heart rate and force of contraction of the myocardium are decreased leading to bradyarrhythmia and sudden cardiac death. This review attempts to explain the cellular mechanism(s) involved in diabetes-induced bradyarrhythmia with emphasis on cation-transporting proteins, especially the hyperpolarization-activated cyclic nucleotide-gated channels pacemaker current channels.

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/m 2 are considered to be overweight while obesity is the term used when the BMI is 30 kg/m 2 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 , 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.

More than 450 million people worldwide have diabetes mellitus (DM), a metabolic disorder characterized by an increase in blood glucose level (hyperglycemia) that arises from insufficient insulin secretion or resistance to insulin’s action. More than 70% of individuals with chronic DM will develop cardiovascular diseases (CVDs) including atherosclerosis and coronary artery diseases (CADs), hypertension, cardiac arrhythmias, cardiomyopathy (heart failure), stroke, and chronic kidney disease. A significant number of these individuals will also succumb to sudden cardiac death (SCD). SCD usually occurs in early morning from abnormal heart rhythms or arrhythmias and ventricular fibrillation. When the pumping action of the heart becomes erratic, a reduction in oxygenated blood to the brain leads to unconsciousness and brain damage. SCD is independent of age and sex and positively correlates with impairment in cardiac metabolism, muscle damage, fibrosis, apoptosis, hypertrophy, ischemia, and deranged cation signaling. This review centers on mechanisms by which intracellular cations (Na+, K+, and Ca2+) handling, inflammation, and oxidative and carbonyl stresses due to diabetes-induced hyperglycemia can lead to the deterioration of excitation/contraction coupling (ECC), impaired contractility, arrhythmias, and SCD in DM patients. It also discusses the beneficial effects of exercise training to attenuate the risk of SCD.