Visceral Adipose Tissue Indicates the Severity of Cardiometabolic Risk in Patients with and without Type 2 Diabetes: Results from the INSPIRE ME IAA Study

Background: Visceral adiposity is an important correlate of cardiometabolic risk, yet its association after the diagnosis of type 2 diabetes remains unclear. Methods: Our objective was to assess the independent and combined associations of visceral adiposity and type 2 diabetes to cardiometabolic risk. The INternational Study of Prediction of Intra-abdominal adiposity and its RElationships with cardioMEtabolic risk/Intra-Abdominal Adiposity (INSPIRE ME IAA) is a cross-sectional computed tomography imaging study with data collected from June 2006 to May 2008. General physicians, cardiologists, and diabetologists (n = 297) in 29 countries recruited 4144 (51.8% men) men (39-71 yr) and women (44-71 yr). Patients were categorized according to visceral adiposity tertiles, type 2 diabetes status, and sex. All results were adjusted for age, body mass index, region, and physician's specialty. Results: Markers of insulin resistance, lipid/lipoproteins, inflammatory markers, and liver fat increased with visceral adiposity in men and women with and without type 2 diabetes. Prevalent cardiovascular disease increased with visceral adiposity tertiles, regardless of type 2 diabetes status. Visceral adiposity [odds ratio = 1.25 (1.09-1.44) for men and 1.78 (1.50-2.12) for women] was positively associated with type 2 diabetes, whereas liver attenuation (inversely related to liver fat) was negatively associated with type 2 diabetes [odds ratio = 0.66 (0.59-0.75) for men and 0.63 (0.55-0.72) for women]. Subcutaneous adipose tissue was inversely related to type 2 diabetes in women [0.76 (0.0.66-0.88)] and not associated with type 2 diabetes in men [0.97 (0.85-1.11)]. Conclusions: Visceral, but not sc, abdominal adiposity is strongly related to cardiometabolic risk factors and to the prevalence of cardiovascular disease and may be an important driver of cardiometabolic risk in patients regardless of type 2 diabetes status. (J Clin Endocrinol Metab 97: 1517-1525, 2012)