Brown versus white fat: are they really playing a role in obesity and cardiometabolic risk?

Abstract

Cardiometabolic risk (CMR) is given by a cluster of risk factors, modifiable or not, that may lead to the development of metabolic and/or cardiovascular diseases, for example, glucose intolerance, Type 2 diabetes (T2DM), atherosclerosis, hypertension, myocardial infarction and stroke. Among non-modifiable cardiometabolic risk factors there are age and family history, while the most important modifiable factors are obesity, elevated blood pressure, hyperlipidemia and smoking [1,2]. Excess caloric intake and sedentary lifestyle are associated with fat overflow that accumulates preferentially in subcutaneous adipose tissue (SAT). However, the possibility of expansion of SAT is limited, and excess glucose and lipids are either taken up by SAT adipocytes (enlarging lipid droplets and making them hypertrophic) or promoting visceral (VF), cardiac and ectopic fat (i.e., in liver, muscle and pancreas) deposition [1]. CMR is strongly associated not only with obesity and total fat, but also with fat distribution; in particular CMR is increased proportionally to VF, cardiac and ectopic fat (i.e., in liver, muscle and pancreas) [1,2]. Subjects with increased VF, cardiac and ectopic fat are, in general, more insulin resistant, display increased lipolysis, plasma concentrations of free fatty acids, triglycerides (TGs), VLDLs, proinflammatory factors, increased atherosclerosis, carotid rigidity, cardiac and endothelial dysfunction [1,2]. VF releases free fatty acid (FFA) directly into the portal vein making the liver the first target of unsuppressed lipolysis and promoting hepatic TG synthesis and accumulation. Current research is focusing the attention on the mechanisms of fat deposition and adipose tissue composition in order to prevent and/or reduce CMR and related pathologies.