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The Association between Abdominal Visceral Fat and Carotid Stiffness Is Mediated by Circulating Inflammatory Markers in Uncomplicated Type 2 Diabetes

Departments of Endocrinology (M.D.) and Clinical Epidemiology and Biostatistics (P.J.K.), VU University Medical Center, 1007 MB Amsterdam, The Netherlands; Departments of Endocrinology (M.D., J.K.R.), Radiology (H.J.L., E.L.E.), General Internal Medicine (M.A.v.d.R.), and General Practice (Y.G.), Leiden University Medical Center, 2300 RC Leiden, The Netherlands; and Julius Center for Health and Sciences and Primary Care (M.L.B.), University Medical Center Utrecht, 3508 GA Utrecht, The Netherlands

Address all correspondence and requests for reprints to: Dr. Michaela Diamant, Department of Endocrinology/Diabetes Center, VU University Medical Center, De Boelelaan 1117, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands. E-mail: m.diamant{at}vumc.nl.

Central obesity, insulin resistance, inflammation, as well as vascular changes are common in patients with type 2 diabetes. In this study we assessed the relationship among stiffness of the carotid artery, visceral fat, and circulating inflammatory markers in type 2 diabetic subjects. Carotid stiffness, quantified as the distensibility coefficient (DC), was measured by ultrasound in asymptomatic, normotensive patients with uncomplicated, well-controlled type 2 diabetes and in controls. Body fat distribution was quantified by magnetic resonance imaging. In patients, the carotid DC was inversely associated with visceral fat area (r = –0.660; P = 0.005) and plasma levels of C-reactive protein (CRP; r = –0.687; P = 0.002), but most strongly with plasma IL-6 (r = –0.766; P < 0.001). In multivariate analysis, the association between DC and visceral fat disappeared after adjustment for CRP and IL-6. Correction for age, body mass index, blood pressure, glycosylated hemoglobin, or fasting plasma glucose did not affect the association between carotid DC and inflammatory markers. Thus, carotid stiffness is associated with visceral obesity in patients with uncomplicated type 2 diabetes, but this association seems to be mediated by circulating IL-6 and CRP, of which IL-6, at least in part, originates from adipose tissue and stimulates hepatic CRP production.

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