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Version of the hypothesis implicating failure to generate more adipocytes in tissue expandability. The adipose tissue expandability hypothesis posits that metabolic dysregulation that appears to be caused by excess weight, such as type 2 diabetes [1] and non-alcoholic fatty liver disease, [2] are triggered when an individual's capacity for storing excess calories in the subcutaneous adipose ...
Adipose tissue (also known as body fat or simply fat) is a loose connective tissue composed mostly of adipocytes. [1] [2] It also contains the stromal vascular fraction (SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells and a variety of immune cells such as adipose tissue macrophages.
A large meta-analysis has shown that white adipose tissue cell size is dependent on measurement methods, adipose tissue depots, age, and body mass index; for the same degree of obesity, increases in fat cell size were also associated with the dysregulations in glucose and lipid metabolism. [2]
Abdominal obesity, excess fat cell accumulation in adipose tissue of the abdomen, is associated more strongly with meta-inflammation. [9] Evolutionarily, adipose tissue has been shown to function as an immune organ. [8] The immune cells located in adipose tissue are important for maintaining metabolic homeostasis.
The progression from visceral fat to increased TNF-α to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells, which play a role in inflammation. Chronic inflammation contributes to an increased risk of hypertension, atherosclerosis and ...
The adipokines, or adipocytokines (Greek adipo-, fat; cytos-, cell; and -kinos, movement) are cytokines (cell signaling proteins) secreted by adipose tissue.Some contribute to an obesity-related low-grade state of inflammation or to the development of metabolic syndrome, a constellation of diseases including, but not limited to, type 2 diabetes, cardiovascular disease and atherosclerosis. [1]
MHO individuals display less visceral adipose tissue, smaller adipocytes, and a reduced inflammatory profile relative to metabolically unhealthy obese individuals. [ 3 ] [ 4 ] [ 5 ] As a result, it has been argued that cardiometabolic risk might not improve significantly as a result of weight loss interventions.
Adiponectin is a protein hormone that modulates a number of metabolic processes, including glucose regulation and fatty acid oxidation. [10] [11] [12] Adiponectin is secreted from adipose tissue (and also from the placenta in pregnancy [13]) into the bloodstream and is very abundant in plasma relative to many hormones.