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Adiposopathy

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Adiposopathy (or sick fat) is a hypothetical condition proposed by Harold Bays, an endocrinologist and director of the Louisville Metabolic and Atherosclerosis Research Center, Inc. According to the hypothesis, pathologic fat tissue may contribute to CVD risk and metabolic syndrome.[1]

Pathophysiology[edit]

Anatomy[edit]

Subcutaneous fat tissue found in the abdominal region has the potential to contribute to metabolic disease.[2] 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.[3]

In humans, the observation of leptin-induced hypertension is not as yet conclusive.[4]

Physiology[edit]

Fat tissue is an active body organ involved in many processes critical to human health, 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, Bays suggests that 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.[5] When excessive body weight leads to adiposopathy, this represents a hormone or endocrine disease.[6] Additionally, fat cells and fat tissue also produce many different types of immune factors.[7] 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:[8] (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 [8] 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.[5]

History[edit]

It has been known since the 1940s that if fat gain occurs in the belly or abdominal (visceral) region, this may promote metabolic diseases.[9][verification needed] Finally, if fat growth exceeds its blood vessel supply, then the lack of oxygen delivery by the blood may also result in pathologic responses from fat tissue.[10] In summary, it has been known for decades that adverse changes in fat cell and fat tissue anatomy may predict metabolic disease. More recently, an additional event that has prompted the concept and term of "adiposopathy" is the evolving recognition of the profound hormone and immune importance of fat tissue. In the past, fat cells and fat tissue were considered by many as being inert, or hormonally and immunologically inactive. However, this has been proven incorrect, and it is now generally accepted that fat tissue produces hormones[8] and has a role in immune function.[7] Yet another historical event that moved medical science towards recognizing fat tissue as an underlying cause of metabolic disease has been the problematic issues that have arisen with the "metabolic syndrome". The metabolic syndrome is a commonly used medical term to describe atherosclerotic coronary heart disease risk factors that tend to cluster together. Over the years, there have been at least 15 other similar terms used to generally describe the same clustering.[11] According to one common definition, a patient is said to have "metabolic syndrome" if he or she has 3 or more the 5 following criteria: (1) abdominal obesity, (2) elevated triglycerides, (3) reduced high density lipoprotein cholesterol levels, (4) high blood pressure, and (5) high blood sugar.[12] However, different scientific and medical organizations have different definitions for the "metabolic syndrome". Also, the term "metabolic syndrome" does not describe, nor is it intended to describe a unifying cause of any disease.[13] Since "metabolic syndrome" is not a disease, regulatory agencies (such as the Food and Drug Administration) do not approve drugs to treat metabolic syndrome, as a specific indicated use. Finally, the "metabolic syndrome" may be no better at predicting atherosclerotic coronary heart disease than an assessment of its individual components.[14] As such, major scientific and medical organizations have questioned the usefulness of the metabolic syndrome, sometimes in open conflict with other major scientific and medical organizations.[13][15]

See also[edit]

References[edit]

This article incorporates material from the Citizendium article "Adiposopathy", which is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License but not under the GFDL.

  1. Bays, Harold E. (2011-06-21). "Adiposopathy is "sick fat" a cardiovascular disease?". Journal of the American College of Cardiology. 57 (25): 2461–2473. doi:10.1016/j.jacc.2011.02.038. ISSN 1558-3597. PMID 21679848.
  2. Weyer, C; Foley, JE; Bogardus, C; Tataranni, PA; Pratley, RE (2000). "Enlarged subcutaneous abdominal adipocyte size, but not obesity itself, predicts type II diabetes independent of insulin resistance". Diabetologia. 43 (12): 1498–506. doi:10.1007/s001250051560. PMID 11151758.
  3. Bays, H; Blonde, L; Rosenson, R (2006). "Adiposopathy: how do diet, exercise and weight loss drug therapies improve metabolic disease in overweight patients?". Expert Review of Cardiovascular Therapy. 4 (6): 871–95. doi:10.1586/14779072.4.6.871. PMID 17173503. Unknown parameter |s2cid= ignored (help)
  4. Brook, RD; Bard, RL; Bodary, PF; Eitzman, DT; Rajagopalan, S; Sun, Y; Depaoli, AM (2007). "Blood pressure and vascular effects of leptin in humans" (PDF). Metabolic Syndrome and Related Disorders. 5 (3): 270–4. doi:10.1089/met.2006.0023. hdl:2027.42/63121. PMID 18370781.
  5. 5.0 5.1 Bays, H; Ballantyne, C. (2006). "Adiposopathy: why do adiposity and obesity cause metabolic disease?". Future Lipidology. 1 (4): 389–420. doi:10.2217/17460875.1.4.389.
  6. Bays, HE; González-Campoy, JM; Henry, RR; Bergman, DA; Kitabchi, AE; Schorr, AB; Rodbard, HW; Adiposopathy Working, Group (2008). "Is adiposopathy (sick fat) an endocrine disease?". International Journal of Clinical Practice. 62 (10): 1474–83. doi:10.1111/j.1742-1241.2008.01848.x. PMC 2658008. PMID 18681905.
  7. 7.0 7.1 Schäffler, A; Müller-Ladner, U; Schölmerich, J; Büchler, C (2006). "Role of adipose tissue as an inflammatory organ in human diseases". Endocrine Reviews. 27 (5): 449–67. doi:10.1210/er.2005-0022. PMID 16684901.
  8. 8.0 8.1 8.2 Bays, HE; González-Campoy, JM; Bray, GA; Kitabchi, AE; Bergman, DA; Schorr, AB; Rodbard, HW; Henry, RR (2008). "Pathogenic potential of adipose tissue and metabolic consequences of adipocyte hypertrophy and increased visceral adiposity". Expert Review of Cardiovascular Therapy. 6 (3): 343–68. doi:10.1586/14779072.6.3.343. PMID 18327995.
  9. Vague J. La differentiation sexuelle, facteur determinant des formes de l'obesite. Presse Med 1947;30:339-40.
  10. Wang, B; Wood, IS; Trayhurn, P (2007). "Dysregulation of the expression and secretion of inflammation-related adipokines by hypoxia in human adipocytes". Pflügers Archiv: European Journal of Physiology. 455 (3): 479–92. doi:10.1007/s00424-007-0301-8. PMC 2040175. PMID 17609976.
  11. Bays, H (2005). "Adiposopathy, metabolic syndrome, quantum physics, general relativity, chaos and the Theory of Everything". Expert Review of Cardiovascular Therapy. 3 (3): 393–404. doi:10.1586/14779072.3.3.393. PMID 15889967. Unknown parameter |s2cid= ignored (help)
  12. Grundy, SM; Cleeman, JI; Daniels, SR; Donato, KA; Eckel, RH; Franklin, BA; Gordon, DJ; Krauss, RM; et al. (2005). "Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement". Circulation. 112 (17): 2735–52. doi:10.1161/CIRCULATIONAHA.105.169404. PMID 16157765.
  13. 13.0 13.1 Kahn, R; Buse, J; Ferrannini, E; Stern, M; American Diabetes, Association; European Association for the Study of Diabetes (2005). "The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes". Diabetes Care. 28 (9): 2289–304. doi:10.2337/diacare.28.9.2289. PMID 16123508.
  14. Stern, MP; Williams, K; Gonzalez-Villalpando, C; Hunt, KJ; Haffner, SM (November 2004). "Does the metabolic syndrome improve identification of individuals at risk of type 2 diabetes and/or cardiovascular disease?". Diabetes Care. 27 (11): 2676–81. doi:10.2337/diacare.27.11.2676. PMID 15505004.
  15. Grundy, SM (2006). "Does a diagnosis of metabolic syndrome have value in clinical practice?". The American Journal of Clinical Nutrition. 83 (6): 1248–51. doi:10.1093/ajcn/83.6.1248. PMID 16762931.


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