Relation of Abdominal Fat Depots to Systemic Markers of Inflammation in Type 2 Diabetes
- Susan Sam, MD1,
- Steven Haffner, MD2,
- Michael H. Davidson, MD3,
- Ralph B. D'Agostino, Sr., MD4,
- Steven Feinstein, MD5,
- George Kondos, MD6,
- Alfonso Perez, MD7 and
- Theodore Mazzone, MD1
- 1Department of Medicine, Section of Endocrinology, Diabetes, and Metabolism, University of Illinois at Chicago, Chicago, Illinois;
- 2Department of Medicine, University of Texas Health Science Center, San Antonio, Texas;
- 3Pritzker School of Medicine, The University of Chicago, Chicago, Illinois;
- 4Statistics and Consulting Unit, Department of Mathematics and Statistics, Boston University, Boston, Massachusetts;
- 5Department of Medicine, Section of Cardiology, Rush University Medical Center, Chicago, Illinois;
- 6Department of Medicine, Section of Cardiology, University of Illinois College of Medicine, Chicago, Illinois;
- 7Takeda Global Research & Development, Deerfield, Illinois.
- Corresponding author: Theodore Mazzone, tmazzone{at}uic.edu
Abstract
OBJECTIVE 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.
Footnotes
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- Received October 13, 2008.
- Accepted February 5, 2009.
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Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
- © 2009 by the American Diabetes Association.
