An Update on the Innovative Mechanistic Modes for the Avoidance of Heart Failure with Preserved Ejection Fraction Using Glucagon Like Peptide 1 Receptor Agonism Particularly in Type 2 Diabetes Mellitus & Metabolic Syndrome: A Review

Review Article

Abstract

The aim of this review is to evaluate the manner obesity influences the pathophysiology of Heart failure with preserved ejection fraction (HFpEF) as well as concentrate on innovative mechanistic modes for the avoidance of HFpEF by utilization of glucagon like peptide 1(GLP-1)-1 receptor agonism(GLP-1RA). Obesity possess the capacity of causing HFpEF via mechanistic modes inclusive of low grade systemic inflammation, accrualof Visceral adipose tissue(VAT) pericardial along with epicardial adipose tissue(EAT) ,escalated myocardial fatquantities &fibrosis.GLP-1 portrays an incretin glucagon hormone whose liberation takes place from the enteroendocrine L cells of the gut. Continued liberation of GLP-1 occurs from the enteroendocrine cells with lesser baseline quantities in the fasting or interprandial status. GLP-1 controls quantities of blood glucose by stimulating insulin generation, repression of islet α cell working ,facilitating proliferation in addition differentiation of βcell, whereasdiminishing apoptosis GLP-1 regulates glycemic differences by escalating liberation of insulin along with diminishing glucagon liberation. Furthermore, slowing of gastric emptying as well as appetite ( food consumption) guarantees maximization of nutrients absorption along with restriction of weight accrual .GLP-1RA at present are getting evaluated for efficaciousness in obesity, or metabolic syndrome(MetS) or obese diabetic patients .Recent corroboration have illustrated GLP-1RA might be significantly efficacious in avoidance of HFpEF in patients of obesity, MetS /obese T2D.The modes behind such actions are (protective countercontrolling Renin-Angiotensin system(RAS) along with AMPK/mTORpathway)or hampering inimical remodeling modes (protein kinase A(PKA)/ Rho/ Rho kinase (ROCK) pathway, aldosterone quantities,or microinflammation.. Nonetheless greater work is required to work out the precise mechanistic modes via which GLP-1R agonists evoke their benefits as well as to generate their long-term safety in addition tothe efficaiousness in variable HFpEF populations.