Anatomy Diseased fat tissue surrounding various organs can cause illness, such as fat surrounding the heart, muscle, vessels, eyes, and bone. Some have suggested that diseased fat tissue surrounding the heart and vessels can contribute to inflammation and plaque rupture. Although not as well recognized, even the so-called "protective" subcutaneous fat tissue has the potential to be "sick" and contribute to metabolic disease. A prime example would be subcutaneous fat tissue found in the abdominal region. Accumulation of fat tissue in this region may have hormonal and immune activity, and thus the potential to cause metabolic disease, between that of visceral fat tissue and other areas of subcutaneous fat tissue. However, other subcutaneous fat tissues also might contribute to metabolic disease, if the fat cells become too enlarged and "sick." Admittedly, subcutaneous fat cells typically are larger, and capable of storing more fat when needed. However, subcutaneous fat tissue represents the largest proportion of fat tissue in the body, and is the major source of leptin. One potentially unfavorable effect of leptin is to increase blood pressure, as observed in animals. In humans, the observation of leptin-induced hypertension is not as yet conclusive. But to the extent that leptin may increase blood pressure, then the increase in leptin with subcutaneous fat cells (particularly when they become enlarged) could hardly be characterized as "protective". Other potentially detrimental effects of enlarged subcutaneous fat tissue relate to free fatty acids. During fasting, the body can obtain energy through the release of free fatty acids from the triglycerides in fat cells. The fatty acids thus become available for release into the blood. If too high a concentration of certain fatty acids accumulates in the blood because of sick fat tissue, and the body is unable to recruit more healthy fat cells, then existing healthy fat cells become engorged (and thus also sick). The result is that blood fatty acid concentrations increase to levels toxic to tissues such as liver, muscle, and pancreas, and lead to a range of pathological metabolic conditions. There are grounds for suspicion that sick abdominal fat tissue may produce factors that cause subcutaneous fat tissue to also become "sick" and further contribute to metabolic diseases. In summary, although abdominal or visceral fat tissue is best described to contribute to metabolic disease, abdominal fat is by no means the only fat tissue depot that has the potential to become "sick" and capable of contributing to metabolic ill health. Physiology Fat tissue is an active body organ involved in many processes critical to human health,8 including: (1) promotion of blood vessel formation (angiogenesis); (2) fat cell recruitment and development adipogenesis; (3) dissolving and reforming the structures around fat tissue (extracellular matrix); (4) generation, storage and release of fat; (5) growth factor production; (6) glucose metabolism; (6) production of factors that affect blood pressure (such as those associated with the renin–angiotensin system); (7) fat and cholesterol metabolism; (8) enzyme production; (9) hormone production; (10) steroid metabolism; (11) blood clotting (hemostasis); (12) element binding; (13) and immune response (described below). When fat cells and fat tissue remain healthy during fat weight gain, patients may avoid metabolic ill health. However, if enlargement of fat cells and fat tissue causes them to become "sick", then important fat tissue functions are disrupted, and deranged responses contribute to metabolic disease. When excessive body weight leads to<unk> , this represents a hormone or endocrine disease. Additionally, fat cells and fat tissue also produce many different types of immune factors. Inflammation is a contributing cause to metabolic disease, and the ultimate contribution of fat tissue to inflammation is determined by the production of both inflammatory and anti-inflammatory factors. From a pro-inflammatory standpoint, fat tissue (which includes fat cells and other cells, such as immune cells) produces factors including: (1) adipokines with cytokine activity such as leptin, interleukins, and tumor necrosis factor alpha; (2) acute phase proteins / reactants such as C-reactive protein; (3) adipokines of the alternative complement system; (4) chemotactic/chemoattractant adipokines; and prostaglandins (eicosanoids). From an anti-inflammatory standpoint, fat tissue produces various anti-inflammatory factors with the most commonly described being adiponectin. If fat cells or fat tissue becomes "sick", then the release of too many pro-inflammatory factors and a decrease in too many anti-inflammatory factors often result in a net pro-inflammatory response can contribute to metabolic disease.
Adiposopathy
Sarcopenic obesity
Normal weight obesity
Abdominal obesity
Exercise addiction
Metabolic syndrome
Metabolically healthy obesity
Body fat redistribution syndrome