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Long-term changes in adipose tissue in human disease
1Department of Biological Sciences, The Open University, Milton Keynes, UK. C.M.Pond@open.ac.uk
The Proceedings of the Nutrition Society
|October 30, 2001
Summary
Chronic diseases like HIV and Crohn's disease cause long-term changes in fat distribution. This review explores how immune system interactions with specific fat cells may explain these shifts and associated metabolic issues.
Area of Science:
- Endocrinology
- Immunology
- Metabolic Syndrome
Background:
- White adipose tissue redistribution is a chronic disease symptom.
- The link between short-term disease responses and long-term fat changes is unclear.
- HIV-associated adipose redistribution syndrome (HARS) and Crohn's disease show selective fat depot changes.
Purpose of the Study:
- Review explanations for adipose tissue redistribution in HIV and Crohn's disease.
- Critically assess theories for HARS.
- Propose mechanisms for selective fat depot enlargement.
Main Methods:
- Literature review of adipose tissue redistribution in HIV and Crohn's disease.
- Critical assessment of existing HARS theories.
- Analysis of perinodal adipocyte properties and immune cell interactions.
Main Results:
- HIV infection leads to gradual HARS, affecting untreated and treated patients.
- Local immune system interactions with perinodal adipocytes are implicated in HARS.
- Perinodal adipocytes possess unique properties enabling rapid fatty acid release to immune cells, potentially driving depot enlargement in Crohn's disease.
Conclusions:
- Prolonged immune stimulation of perinodal adipocytes may cause selective depot enlargement.
- Hypotheses for HARS and Crohn's mesenteric fat changes are proposed.
- Further investigation into immune-adipocyte interactions is warranted.
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