Adiposopathy: why do adiposity and obesity cause metabolic disease?

In the adipocentric paradigm, fat health affects patient health. Adiposopathy ('pathos' of adipose tissue or fat dysfunction) is more directly associated with excessive fat-related metabolic disease (EFRMD) than adiposity (increased fat mass) alone. Examples of adipocyte factors whose dysmetabolism may contribute to Type 2 diabetes mellitus include: 11 beta-hydroxysterold dehydrogenase type 1, acylation-stimulating protein, adiponectin, adipsin, anglotensinogen, autotaxin, ceramide, free fatty acids, hormone-sensitive lipase, interieukin-6, insulin-like growth factor-1, leptin, lipin, lysophospholipids, perillpin, phosphoenolpyrovate carboxykinase, plasminogen activator inhibitor-1, resistin, retinol-bincling protein, tumor necrosis factor-a, visceral adipose tissue-derived serpin and visfatin. Excessive body fat may lead to hypertension due to physical compression of kidneys, sleep apnea, and other mechanisms. Examples of adipocyte factors whose dysmetabolism may contribute to hypertension include: 11 beta-hydroxysteroid dehydrogenase type 1, adiponectin, angiotensinogen, anglotensin I and II, angiotensin-converting enzyme, renin, cathepsin, chymase, free fatty acids, interleukin-6 and leptin. Examples of adipocyte factors whose dysmetabolism may contribute to dyslipidemia include: 11 beta-hydroxysterold dehydrogenase type 1, acylation-stimulating protein, adipophilin, adiponectin, adipsin, cholesteryl ester-transfer protein, free fatty acids, hormone-sensitive lipase, leptin, lipoprotein lipase, perilipin, phosphollpid transfer protein, sex hormones and tumor necrosis factor-a. Numerous other adipocyte factors may directly affect atherosclerosis and cardiomyopathy, A better understanding and recognition of how fat weight gain contributes to EFRMD will substantially affect the research and development of therapeutic interventions that may treat or prevent adiposopathy, and dramatically influence which patients with EFRMD are best treated and how.