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Diabetes 54:2720-2726, 2005
© 2005 by the American Diabetes Association, Inc.

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

A Positron-Emitting Tomography Study

Kirsi A. Virtanen1, Patricia Iozzo1,2, Kirsti Hällsten1, Risto Huupponen3,4, Riitta Parkkola5, Tuula Janatuinen1, Fredrik Lönnqvist6, Tapio Viljanen1, Tapani Rönnemaa7, Peter Lönnroth8, Juhani Knuuti1, Ele Ferrannini2,9, and Pirjo Nuutila1,7

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

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-[18F]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 intra-abdominal fat mass in a curvilinear fashion. When regional glucose uptake was multiplied by tissue mass, total glucose uptake per fat depot was similar irrespective of abdominal obesity or type 2 diabetes, and its contribution to whole-body glucose uptake increased by ~40% in obese nondiabetic and nonobese diabetic men and was doubled in obese diabetic subjects. We conclude that 1) in abdominal obesity, insulin-stimulated glucose uptake rate is markedly reduced in skeletal muscle and in all fat depots; 2) in target tissues, this reduction is reciprocally (and nonlinearly) related to the amount of intra-abdominal fat; 3) mild, recent diabetes adds little insulin resistance to that caused by abdominal obesity; and 4) despite fat insulin resistance, an expanded fat mass (especially subcutaneous) provides a sink for glucose, resulting in a compensatory attenuation of insulin resistance at the whole-body level in men.

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

Key Words: FFA, free fatty acid • [18F]FDG, [18F]fluorodeoxyglucose • MRI, magnetic resonance imaging • PET, positron emission tomography • ROI, region of interest


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