Published online Sep 15, 2018. doi: 10.4239/wjd.v9.i9.141
Peer-review started: April 21, 2018
First decision: June 8, 2018
Revised: June 19, 2018
Accepted: June 28, 2018
Article in press: June 28, 2018
Published online: September 15, 2018
Processing time: 147 Days and 8.6 Hours
Epicardial adipose tissue is defined as a deposit of adipocytes with pathophysiological properties similar to those of visceral fat, located in the space between the myocardial muscle and the pericardial sac. When compared with subcutaneous adipose tissue, visceral adipocytes show higher metabolic activity, lipolysis rates, increased insulin resistance along with more steroid hormone receptors. The epicardial adipose tissue interacts with numerous cardiovascular pathways via vasocrine and paracrine signalling comprised of pro- and anti-inflammatory cytokines excretion. Both the physiological differences between the two tissue types, as well as the fact that fat distribution and phenotype, rather than quantity, affect cardiovascular function and metabolic processes, establish epicardial fat as a biomarker for cardiovascular and metabolic syndrome. Numerous studies have underlined an association of altered epicardial fat morphology, type 2 diabetes mellitus (T2DM) and adverse cardiovascular events. In this review, we explore the prospect of using the epicardial adipose tissue as a therapeutic target in T2DM and describe the underlying mechanisms by which the antidiabetic drugs affect the pathophysiological processes induced from adipose tissue accumulation and possibly allow for more favourable cardiovascular outcomes though epicardial fat manipulation.
Core tip: In this review, we aim to create a concise overview of the pathophysiology concerning the epicardial fat deposits on a type 2 diabetic individual, while, delving into the intricacies of each antidiabetic drug and exploring the manner by which it interacts with visceral fat accumulation in the sub-pericardial space.