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- W1767165379 abstract "Objective: To review current consensus and controversy regarding whether obesity is a ‘disease’, examine the pathogenic potential of adipose tissue to promote metabolic disease and explore the merits of ‘adiposopathy’ and ‘sick fat’ as scientifically and clinically useful terms in defining when excessive body fat may represent a ‘disease’. Methods: A group of clinicians and researchers, all with a background in endocrinology, assembled to evaluate the medical literature, as it pertains to the pathologic and pathogenic potential of adipose tissue, with an emphasis on metabolic diseases that are often promoted by excessive body weight. Results: The data support pathogenic adipose tissue as a disease. Challenges exist to convince many clinicians, patients, healthcare entities and the public that excessive body fat is often no less a ‘disease’ than the pathophysiological consequences related to anatomical abnormalities of other body tissues. ‘Adiposopathy’ has the potential to scientifically define adipose tissue anatomic and physiologic abnormalities, and their adverse consequences to patient health. Adiposopathy acknowledges that when positive caloric balance leads to adipocyte hypertrophy and visceral adiposity, then this may lead to pathogenic adipose tissue metabolic and immune responses that promote metabolic disease. From a patient perspective, explaining how excessive caloric intake might cause fat to become ‘sick’ also helps provide a rationale for patients to avoid weight gain. Adiposopathy also better justifies recommendations of weight loss as an effective therapeutic modality to improve metabolic disease in overweight and obese patients. Conclusion: Adiposopathy (sick fat) is an endocrine disease." @default.
- W1767165379 created "2016-06-24" @default.
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- W1767165379 date "2008-08-04" @default.
- W1767165379 modified "2023-10-12" @default.
- W1767165379 title "Is adiposopathy (sick fat) an endocrine disease?" @default.
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- W1767165379 doi "https://doi.org/10.1111/j.1742-1241.2008.01848.x" @default.
- W1767165379 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2658008" @default.
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