The Chronic Inflammatory Hypothesis for the Morbidity Associated with Morbid Obesity: Implications and Effects of Weight Loss
Abstract
Background Obesity is a worldwide pandemic that causes a multitude of co-morbid conditions.However, there has been slow progress in understanding the basic pathophysiology that underlies co-morbid conditions associated with obesity. Recently, there has been intense interest in the role of inflammation in obesity. Using the inflammatory hypothesis, many of the mechanisms by which co-morbid conditions are associated with obesity are being elucidated.Methods We searched the literature and reviewed all relevant articles. We focused on hormones and cytokines that have been associated with other inflammatory conditions such as sepsis and systemic inflammatory response syndrome.Findings Angiotensinogen (AGT), transforming growth factor beta (TGFbeta), tumor necrosis factor alpha (TNFalpha), and interleukin six (IL-6) are all elevated in obesity and correlate with several markers of adipocyte mass. These mediators have detrimental effects on hypertension, diabetes, dyslipidemia, thromboembolic phenomena, infections, and cancer. Weight loss results in a reduction of inflammatory mediators and a diminution of the associated co-morbid conditions.Conclusions The success of weight loss surgery in treating the complications associated with obesity is most probably related to the reduction of inflammatory mediators. While some aspects of bariatric physiology remain unclear, there appears to be a strong association between obesity and inflammation, thereby rendering obesity a chronic inflammatory state. A clearer understanding of the physiology of obesity will allow physicians who treat the obese to develop better strategies to promote weight loss and improve the well-being of millions of individuals.
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The molecular mechanisms that link inflammatory changes to the development, aggravation, maintenance, and resistance to treatment that characterize obesity states remain poorly understood.
“However, in spite of substantial evidence demonstrating the existence of a low-grade inflammatory component in obesity [5], the molecular mechanisms that link inflammatory changes to the development, aggravation, maintenance, and resistance to treatment that characterize obesity states remain poorly understood.”
From Adipose tissue transcriptomic signature highlights the pathological relevance of extracellular matrix in human obesity (2008) · cites this paper as [5]
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- Authors
- Cottam, D. R., Mattar, S. G., Barinas-Mitchell, E., Eid, G., Kuller, L., Kelley, D. E., & Schauer, P. R.
- Affiliations
- University of Pittsburgh (US)
- Venue
- Obesity Surgery
- Published
- 2004-05-01
- Volume
- 14
- Issue
- 5
- Pages
- 589-600
- ISSN
- 0960-8923 (ISSN-L)
- 1708-0428
- OpenAlex
- W2166558587
- Cited by
- 461
- References
- 150
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 13 · 2023: 13 · 2022: 17 · 2021: 23 · 2020: 11 · 2019: 27 · 2018: 16 · 2017: 24 · 2016: 22 · 2015: 25 · 2014: 21 · 2013: 22 · 2012: 25
- FWCI
- 19.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Obesity Surgery (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Surgery › Bariatric Surgery and Outcomes
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- obesity, chronic inflammation
- MeSH terms
- Acute-Phase Proteins, Adipose Tissue, Angiotensin II, Angiotensinogen, C-Reactive Protein, Humans, Inflammation, Insulin Resistance, Liver, Lymphotoxin-alpha, Morbidity, Obesity, Tumor Necrosis Factor-alpha, Weight Loss, Interleukin-6
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