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Submitted on February 13, 2007
Accepted on May 3, 2007
Department of Internal Medicine and CNR Institute of Clinical Physiology, University of Pisa, Pisa, Italy, INSERM U 780-IFR69, Villejuif, France, Academic Medical Unit, The Royal London Hospital, London, UK, EMGO Institute, VU University Medical Center, Amsterdam, The Netherlands, CNR Institute of Biomedical Engineering, Padova, Italy, Department of Medicine, Trinity College, Dublin, Ireland, Department of Medicine, University of Newcastle upon Tyne, UK, Department of Endocrinology M, Odense University Hospital, Odense, Denmark
* To whom correspondence should be addressed. E-mail: ferranni{at}ifc.cnr.it.
Context. Insulin resistance (IR) and obesity, especially abdominal obesity, are regarded as central pathophysiological features of a cluster of cardiovascular risk factors (CVRF), but their relative roles remain undefined. Moreover, the differential impact of IR viz insulin response has not been evaluated.
Objective. To dissect out the impact of obesity, abdominal obesity and insulin resistance/insulin response on CVRF.
Design. Cross-sectional
Setting. Nineteen clinical research centres in Europe
Subjects. Cohort of 1,308 non-diabetic subjects (825 women and 483 men, age 30-60 years, BMI 17-44 kg.m-2).
Main outcome measures. We measured IR (by a standardised euglycaemic insulin clamp), waist girth, insulin response to an OGTT and major CVRF and analysed their associations by multivariate models and factor analysis.
Results. BMI was positively related to all CVRF, waist circumference was related to higher blood pressure and serum triglycerides and lower HDL-cholesterol, IR to reduced glucose tolerance, higher FFA, triglyceride and LDL-cholesterol, and lower HDL-cholesterol, and insulin response to higher heart-rate, blood pressure and fasting glucose and the same dyslipidaemic profile as IR (p
0.05 for all). By factor analysis, three main factors - related to IR, age and fatness, respectively - appeared to underlie this pattern of associations. Each of BMI, waist girth, IR and insulin response was independently associated with total CVRF load (all p<0.001).
Conclusions. When IR, fat mass and distribution, and insulin response are measured simultaneously in a large cohort, no one factor stands out as the sole driving force of the CVRF cluster, each being associated with one or more physiological pathways according to known cause-effect relationships.
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