Pathogenic potential of adipose tissue and metabolic consequences of adipocyte hypertrophy and increased visceral adiposity

Abstract

When caloric intake exceeds caloric expenditure, the positive caloric balance and storage of energy in adipose tissue often causes adipocyte hypertrophy and visceral adipose tissue accumulation. These pathogenic anatomic abnormalities may incite metabolic and immune responses that promote Type 2 diabetes mellitus, hypertension and dyslipidemia. These are the most common metabolic diseases managed by clinicians and are all major cardiovascular disease risk factors. 'Disease' is traditionally characterized as anatomic and physiologic abnormalities of an organ or organ system that contributes to adverse health consequences. Using this definition, pathogenic adipose tissue is no less a disease than diseases of other body organs. This review describes the consequences of pathogenic fat cell hypertrophy and visceral adiposity, emphasizing the mechanistic contributions of genetic and environmental predispositions, adipogenesis, fat storage, free fatty acid metabolism, adipocyte factors and inflammation. Appreciating the full pathogenic potential of adipose tissue requires an integrated perspective, recognizing the importance of 'cross-talk' and interactions between adipose tissue and other body systems. Thus, the adverse metabolic consequences that accompany fat cell hypertrophy and visceral adiposity are best viewed as a pathologic partnership between the pathogenic potential adipose tissue and the inherited or acquired limitations and/or impairments of other body organs. A better understanding of the physiological and pathological interplay of pathogenic adipose tissue with other organs and organ systems may assist in developing better strategies in treating metabolic disease and reducing cardiovascular disease risk.

Macrophage gene expression is related to obesity and the metabolic syndrome in human subcutaneous fat as well as in visceral fat

“…Since then, intense research on the factors initiating adipose tissue inflammation and promoting obesity-related metabolic abnormalities such as type 2 diabetes has been ongoing, but the problem remains imperfectly understood especially in humans. The term the metabolic syndrome was introduced to denote a cluster of metabolic disorders with an atherogenic, prothrombotic and inflammatory profile [3,4]. The key components of the metabolic syndrome are insulin resistance and abdominal adiposity, with a predominance of intra-abdominal visceral fat accumulation [5].…”

“…The pathogenic potential of adipose tissue seems to be determined, besides total adiposity as such, by specific anatomic location [3,6] or phenotypic and functional differences between subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT). Indeed, although abdominal SAT and VAT are associated with metabolic risk profile [7], it has previously been reported [7][8][9] and recently confirmed in the Framingham Heart Study [10] that high VAT has a stronger correlation with metabolic risk factors and the metabolic syndrome than SAT.…”

Regulation of Adipocyte Formation by GLP-1/GLP-1R Signaling

“…Obesity, characterized by an excessive accumulation of adipose tissue, is a key component of the metabolic syndrome, often associated with the development of type 2 diabetes mellitus, atherosclerosis, and hyperlipidemia (1)(2)(3)(4). The growth of adipose tissue involves cellular hypertrophy (cell size increase) and hyperplasia (cell number increase) (5).…”

The Partial Replacement of Lard by Caryocar brasiliense Oil in a Western Diet improves Cardiovascular Risk Factors in Rats

“…This is an important result, since visceral fat accumulation is highly associated to metabolic disturbances [33]. Indeed, it has been postulated that fat topography and body distribution impact more than the body weight in CVD development [34].…”