Obesity and its cardiovascular effects

Abstract

Obesity is described in terms of body fat percentage or body mass index (BMI), despite the fact that these measures do not give full insight about the body fat distribution. It is presently a consistently growing universal challenge since it has tripled in the last 10 years, killing approximately 28 million people each year. In this review, we aim to clarify the different results of obesity on the working and physiology of the cardiovascular system and to reveal changes in the obesity "paradox"-a variety of cardiovascular outcomes in typical/overweight people. Central fat build-up in ordinary/overweight populaces has been related to expanded occurrences of myocardial infarction, heart failure, or all-cause mortality when contrasted with the obese populace. These discoveries are additionally clarified as the abundance and prolonged vulnerability to free fatty acids (FFAs) in obesity. This has been believed to cause the myocardial substrate to move from glucose to FFAs digestion, which causes lipid gathering in cardiomyocytes, spilling over to other lean tissues, and prompting a general atherogenic impact. This cardiomyocyte lipid aggregation has been demonstrated to cause insulin resistance and cardiovascular hypertrophy, and to lessen the heart functions in general. There is a proof backing the fact that fat tissue is not only an energy reservoir, it also coordinates hormones and proinflammatory cytokines and deals with the energy transition of the body by putting away abundant lipids in diverse tissues.

Circulating branched‐chain amino acids and incident heart failure in type 2 diabetes: The Hong Kong Diabetes Register

“…People with T2D and/or obesity often have unhealthy or imbalanced diet, which together with beta‐cell dysfunction and other neurohormonal dysregulation (such as leptin resistance and activation of sympathetic nervous system and renin‐angiotensin system [RAS]) may contribute to abnormal energy metabolism. Despite the importance of protein in cellular metabolism, there is a paucity of data on the risk association of BCAAs and diabetes‐related complications such as HF.…”

“…Our detailed analyses with careful adjustments for confounders supported potential adverse effects of BCAAs in T2D‐associated HF, although the underlying mechanisms require further elucidation. Multiple factors including abnormal myocardial energy metabolism, coronary atherosclerosis, arrhythmia, diastolic dysfunction (associated with ageing, epicardial fat deposition with proinflammatory effect, and reduced coronary microvascular density), and renal dysfunction can predispose to HF . Herein, effective substrate utilization and ATP synthesis, transfer, and consumption are critically important for optimal myocardial function .…”

“…Insufficient insulin action (quantity and/or quality) is the hallmark of T2D with reduced peripheral glucose uptake and increased formation of FFA and ketone bodies, especially in organs with high energy demand such as the myocardium . While increased blood glucose and FFA levels can increase myocardial steatosis and insulin resistance, these fuel substrates compete with circulating BCAAs and BCKAs for a limited supply of acetyl‐CoA, resulting in impaired ATP synthesis through the TCA cycle, which can be worsened by impaired BCAAs metabolism . High circulating levels of BCAAs can also lead to widespread abnormal cellular function.…”

“…In individuals with high‐intensity resistance training or poor nutritional status, increased BCAAs intake may confer health benefits, although its indiscriminate or excessive use as health supplements may potentially cause harm . Dysregulation of energy metabolism due to excessive calorie intake and/or reduced energy expenditure can lead to obesity and type 2 diabetes (T2D), which are the leading causes of atherosclerotic cardiovascular disease (ASCVD) . With better control of cardiometabolic‐renal risk factors, use of cardioprotective drugs, and coronary interventions, we and others have witnessed declining trends of myocardial infarction and its complications, especially in high‐income countries .…”

“…Traditionally, HF is considered a consequence of long‐standing hypertension and coronary heart disease (CHD), although people with T2D may have subclinical cardiomyopathy for years due to predominantly metabolic causes . Given the high energy demand of myocardium, HF can be caused by abnormal utilization of energy substrate . In T2D and obesity, insulin resistance and beta‐cell dysfunction can lead to inefficient uptake of glucose for energy production and non‐suppression of lipolysis with increased release of free fatty acids (FFAs) .…”