title: 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.
  
  
  RESULTS
  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.
authors.affiliation: Department of Surgery, The University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
authors.forename: Daniel R
authors.initials: DR
authors.lastname: Cottam
authors.forename: Samer G
authors.initials: SG
authors.lastname: Mattar
authors.forename: Emma
authors.initials: E
authors.lastname: Barinas-Mitchell
authors.forename: George
authors.initials: G
authors.lastname: Eid
authors.forename: Lewis
authors.initials: L
authors.lastname: Kuller
authors.forename: David E
authors.initials: DE
authors.lastname: Kelley
authors.forename: Philip R
authors.initials: PR
authors.lastname: Schauer
mesh_terms: D000209:Acute-Phase Proteins / Q000502:physiology; D000273:Adipose Tissue / Q000502:physiology; D000804:Angiotensin II / Q000502:physiology; D000808:Angiotensinogen / Q000502:physiology; D002097:C-Reactive Protein / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000502:physiology; D008099:Liver / Q000502:physiology; D008233:Lymphotoxin-alpha / Q000502:physiology; D009017:Morbidity; D009765:Obesity / Q000453:epidemiology* / Q000378:metabolism / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D015431:Weight Loss / Q000502:physiology
chemical_list: D000209:Acute-Phase Proteins; D015850:Interleukin-6; D008233:Lymphotoxin-alpha; D014409:Tumor Necrosis Factor-alpha; D000808:Angiotensinogen; D000804:Angiotensin II; D002097:C-Reactive Protein