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dc.contributor.authorSam, Susanen_US
dc.contributor.authorHaffner, Stevenen_US
dc.contributor.authorDavidson, Michael H.en_US
dc.contributor.authorD'Agostino, Ralph B.en_US
dc.contributor.authorFeinstein, Stevenen_US
dc.contributor.authorKondos, Georgeen_US
dc.contributor.authorPerez, Alfonsoen_US
dc.contributor.authorMazzone, Theodoreen_US
dc.date.accessioned2011-12-29T23:03:40Z
dc.date.available2011-12-29T23:03:40Z
dc.date.issued2009-2-19
dc.identifier.citationSam, Susan, Steven Haffner, Michael H. Davidson, Ralph B. D'Agostino, Steven Feinstein, George Kondos, Alfonso Perez, Theodore Mazzone. "Relation of Abdominal Fat Depots to Systemic Markers of Inflammation in Type 2 Diabetes" Diabetes Care 32(5): 932-937. (2009)
dc.identifier.issn1935-5548
dc.identifier.urihttps://hdl.handle.net/2144/2633
dc.description.abstractOBJECTIVE: Both visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) have been linked to systemic inflammation in nondiabetic cohorts. We examined the relationships between VAT and SAT and systemic inflammatory markers in a large well-characterized cohort of subjects with type 2 diabetes. RESEARCH DESIGN AND METHODS: Three hundred eighty-two subjects with type 2 diabetes in the CHICAGO (Carotid Intima-Media Thickness in Atherosclerosis Using Pioglitazone) study cohort underwent abdominal computed tomography to determine SAT and VAT distribution. Fasting blood was obtained for measurement of inflammatory markers. The relationships between inflammatory markers and BMI, SAT, and VAT were examined using regression models adjusted for age, sex, diabetes treatment, duration of diabetes, smoking, statin use, and A1C. RESULTS: VAT was positively related to CRP, monocyte chemoattractant protein (MCP), intracellular adhesion molecule (ICAM)-1, and plasminogen activator inhibitor type 1 (PAI-1) antigen before adjustment for BMI. After adjustment for BMI, the relationship to CRP was lost but positive associations with MCP (P < 0.01), PAI-1 (P < 0.0001), ICAM-1 (P < 0.01), and vascular cell adhesion molecule (P = 0.01) were evident. BMI was positively related to CRP (P < 0.0001) and IL-6 (P < 0.01) even after adjustment for VAT and SAT. SAT was not related to any inflammatory marker after adjustment for BMI. CONCLUSIONS: In this large group of subjects with type 2 diabetes, BMI was most strongly associated with CRP and IL-6 levels. SAT was not associated with markers of systemic inflammation. The size of the VAT depot provided information additional to that provided by BMI regarding inflammatory markers that are strongly related to vascular wall remodeling and coagulation. Our findings suggest that adipose tissue distribution remains an important determinant of systemic inflammation in type 2 diabetes.en_US
dc.description.sponsorshipNational Institutes of Health (DK-71711); University of Illinois at Chicagoen_US
dc.language.isoen
dc.publisherAmerican Diabetes Associationen_US
dc.titleRelation of Abdominal Fat Depots to Systemic Markers of Inflammation in Type 2 Diabetesen_US
dc.typeArticleen_US
dc.identifier.doi10.2337/dc08-1856
dc.identifier.pmid19228869
dc.identifier.pmcid2671130


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