## 4 The Anatomy of Obesity
### Local Effects of Adipose Surplus  
The adverse functional effects of excess adipose tissue are related to the secretion of proinflammatory and orthorhombic adipokines [40; 41], local hypoxia [42], fibrosis [43], and mitochondrial function alteration [44]. Several localizations present a series of particularities worth noting, in lieu of their prominent noxious local effects that also have a systemic resonance. The effects of perihepatic adipose surplus have already been previously described. Excess adiposity is, however, also associated with the intracellular accumulation of fatty deposits, in the form of triglycerides within hepatic cells, with injurious effects upon their function. The resulting pathological entity is defined as non-alcoholic fatty liver disease, which is frequently associated with metabolic syndrome and weight excess [45; 46]. Increased intracellular triglyceride deposits can also be found within striated muscular cells, which may play a role in increasing insulin resistance and may predispose to developing dyslipidemia [47]. A further example of relevant local effects of adipose surplus is with regard to epicardial adipose tissue. In physiological conditions, the epicardial adipose tissue has an important role in the energetic balance of the heart. Through the uptake of excess free fatty acids, it offers a metabolic support for the myocardium during ischemia. In addition, this tissue is responsible for the thermal insulation of the heart, isolating it, andmaintaining the ideal temperature for the optimal functioning of the enzymatic apparatus within the cardiomyocytes. Furthermore, the connective tissue surrounding the epicardium has an important structural role and is maintained by the synthesis of adiponectin and adrenomedullin. Excess adipose tissue surrounding the heart, however, leads to the decrease in adiponectin, an increase in inflammatory markers, myocardial fibrosis and hypertrophy, and cardiomyocyte apoptosis. These mechanisms could help explain the association between increased epicardial adiposity and ischemic heart disease, heart failure, hypertension, left ventricular hypertrophy, dysplasia, and insulin resistance [48, 49, 50, 51, 52, 53]. Local macrophage accumulation and angiogenesis within epicardial adipose tissue also seem to play an important part in the inflammatory-mediated mechanisms that link increased epicardial fat to worse outcomes in patients with coronary artery disease [54]. Perivascular adipose tissue is defined by a series of particular characteristics involved in the mechanisms behind the obesity-associated cardiovascular risk. The histological distinction between brown and white adipose tissue is of relevance concerning this matter. While brown fatty tissue has a significant thermogenic role, particularly important in newborns, white adipose tissue serves mostly as a deposit for energetic surplus in the form of lipids, releasing them into the circulation and thus making them available to tissues in need, when such a need arises. White adipose tissue is mostly responsible for the mechanisms involved in metabolic obesity-related disease. In certain conditions, white adipose tissue has shown the capacity of transforming into brown adipose tissue (mostly due to exposure to very low temperatures). Differently localized vessels in the organism present different proportions between white and brown adipose tissue. This variability may be in conjecture with the different predominant functions of perivascular tissue according to localization. Large central vessels, for example, such as the aorta and its main ramifications, are mostly surrounded by brown adipose tissue, thus playing a key part in maintaining central temperature within normal ranges. Peripherally increased perivascular adipose tissue, on the other hand, has been associated with increased insulin resistance [55]. Excessive perirenal adipose tissue can lead to the increase in intrarenal pressure, with potential involvement in the development of microalbuminuria.