Increased Fat Mass Compensates for Insulin Resistance in Abdominal Obesity and Type 2 Diabetes

Increased Fat Mass Compensates for Insulin Resistance in Abdominal Obesity and Type 2 Diabetes A Positron-Emitting Tomography Study Kirsi A. Virtanen 1 , Patricia Iozzo 1 2 , Kirsti Hällsten 1 , Risto Huupponen 3 4 , Riitta Parkkola 5 , Tuula Janatuinen 1 , Fredrik Lönnqvist 6 , Tapio Viljanen 1 , Tapani Rönnemaa 7 , Peter Lönnroth 8 , Juhani Knuuti 1 , Ele Ferrannini 2 9 and Pirjo Nuutila 1 7 1 Turku PET Centre, Turku, Finland 2 Position Emission Tomography (PET) Laboratory, National Research Council Institute of Clinical Physiology, Pisa, Italy 3 Department of Pharmacology and Clinical Pharmacology, University of Turku, Finland 4 Department of Pharmacology and Toxicology, University of Kuopio and Kuopio University Hospital, Kuopio, Finland 5 Department of Radiology, Turku University Hospital, Turku, Finland 6 Karolinska Institutet, Stockholm, Sweden 7 Department of Medicine, Turku University Hospital, Turku, Finland 8 Department of Medicine, University of Gothenburg, Gothenburg, Sweden 9 Department of Internal Medicine, University of Pisa School of Medicine, Pisa, Italy Address correspondence and reprint requests to Dr. Kirsi Virtanen, Turku PET Centre, University of Turku, P.O. Box 52 20521, Turku, Finland. E-mail: kirsi.virtanen{at}utu.fi Abstract To evaluate the relative impact of abdominal obesity and newly diagnosed type 2 diabetes on insulin action in skeletal muscle and fat tissue, we studied 61 men with ( n = 31) or without ( n = 30) diabetes, subgrouped into abdominally obese or nonobese according to the waist circumference. Adipose tissue depots were quantified by magnetic resonance imaging, and regional glucose uptake was measured using 2-[ 18 F]fluoro-2-deoxyglucose/positron emission tomography during euglycemic hyperinsulinemia. Across groups, glucose uptake per unit tissue weight was higher in visceral (20.5 ± 1.4 μmol · min −1 · kg −1 ) than in abdominal (9.8 ± 0.9 μmol min −1 · kg −1 , P < 0.001) or femoral (12.3 ± 0.6 μmol · min −1 · kg −1 , P < 0.001) subcutaneous tissue and ∼40% lower than in skeletal muscle (33.1 ± 2.5 μmol · min −1 · kg −1 , P < 0.0001). Abdominal obesity was associated with a marked reduction in glucose uptake per unit tissue weight in all fat depots and in skeletal muscle ( P < 0.001 for all regions). Recent type 2 diabetes per se had little additional effect. In both intra-abdominal adipose ( r = −0.73, P < 0.0001) and skeletal muscle ( r = −0.53, P < 0.0001) tissue, glucose uptake was reciprocally related to intr