The pathophysiology of abdominal adipose tissue depots in health and disease

Abstract

Obesity is currently the most important contributor to ill health and expenditure worldwide. More alarming is the fact that the pediatric population parallels adults, with obesity closely associated to type 2 diabetes mellitus (T2D), cardiovascular disease, hypertension, non-alcoholic fatty liver disease, vitamin D deficiency (VDD) and certain types of cancer. The observation in the early 1950s that android or truncal adipose tissue (AT) distribution compared to gynoid had a greater association with metabolic dysfunction, in particular T2D and cardiovascular disease risk, led to the hypothesis that obesity-associated complications are not associated with fat mass per se, but the pattern of fat distribution. This concept was further supported by groups of individuals with metabolic dysfunction despite a lean phenotype, and healthy obese people protected from metabolic dysfunction. It is now well recognized that an increase in visceral AT is an independent risk factor for the development of obesity-associated comorbidities with AT depot distribution, their anatomic, cellular and molecular features defining their role. The differences and the plasticity of subcutaneous, visceral and ectopic ATs to store and release fatty acids and to synthesize and secrete adipokines, defines the metabolic outcomes. The present review will examine the phenotypic and pathophysiological differences between the different AT depots, with a particular focus on the abdominal depots and their link to metabolic complications.

Irisin plasma concentration in PCOS and healthy subjects is related to body fat content and android fat distribution

“…It is commonly accepted that obesity-associated disorders are related to the type of fat distribution [22]. Individuals with excess of a visceral (android or truncal) adipose tissue but with normal BMI, called MONW (metabolically obese but normal weight), are burdened with obesity-related disease as well as patients with MS (type 2 diabetes, hypertension, dyslipidemia and coronary heart disease) [23].…”

Prospective study of body fat distribution and the risk of endometrial cancer

“…Abdominal fat is hypothesized to be biologically different from other fat in the body with characteristics favoring cell proliferation or vascularization [11, 12]. The biologic effect of adipose tissue may vary depending on its location in terms of functional activity to store and release fatty acids and to synthesize and secrete adipokines [21], which subsequently can discriminate the carcinogenic potential of fat tissue. Another hypothesis suggesting the role of abdominal fatness in carcinogenesis is that the abdominal adiposity is mainly composed of white adipose tissue with little brown adipose tissue.…”

The adipokine chemerin amplifies electrical field-stimulated contraction in the isolated rat superior mesenteric artery

“…This artery was chosen for several reasons. 1) The superior mesenteric artery is in the viscera, and it is visceral fat that is associated with the greatest cardiovascular risk (21,46,47).…”