Drug-induced metabolic alterations in adipose tissue - with an emphasis in epicardial adipose tissue

Currently, research on understanding adipose tissue (AT) metabolism has increased significantly. AT is an endocrine organ, that releases proteins, specific metabolites, hormones, micro-RNAs and signaling lipids, all involved in a network of inter-organ communication. Among other effects, AT dysfunction contributes to a proinflammatory and diabetogenic state, from an early stage in the disease development. Overweight and obesity have reached epidemic proportions worldwide, which has been linked to the development and progression of high-comorbidity and diseases, such as insulin resistance, type 2 diabetes mellitus, hypertension, and cardiovascular diseases (CVD). Therefore, therapeutic strategies have been devised to modulate the composition of fat stores, including changes in lifestyle and/or pharmacological treatment for weight management or attenuation of cardiometabolic risk factors. As a result, life expectancy has been increasing. However, the population is being overmedicated and secondary adverse effects due to drug usage can be serious. Commonly prescribed drugs for immunosuppression and psychiatric disorders, such as severe depression and anxiety, are known to alter metabolism, particularly, in AT depots. In this review, we discuss important molecular mechanisms in AT, especially in epicardial AT (EAT), that are highly modulated by these drugs, and put forth EAT as a potential therapeutic target for CVD.