1. The association between abdominal visceral fat and carotid stiffness is mediated by circulating inflammatory markers in uncomplicated type 2 diabetes.
- Author
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Diamant M, Lamb HJ, van de Ree MA, Endert EL, Groeneveld Y, Bots ML, Kostense PJ, and Radder JK
- Subjects
- Abdomen, Adipose Tissue pathology, Biomarkers blood, Body Composition, C-Reactive Protein metabolism, Carotid Artery Diseases complications, Carotid Artery Diseases immunology, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 immunology, Female, Humans, Interleukin-6 blood, Magnetic Resonance Imaging, Male, Middle Aged, Multivariate Analysis, Obesity complications, Obesity immunology, Obesity metabolism, Viscera, Adipose Tissue metabolism, Carotid Artery Diseases metabolism, Diabetes Mellitus, Type 2 metabolism
- Abstract
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.
- Published
- 2005
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