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- Title
Increased fat mass compensates for insulin resistance in abdominal obesity and type 2 diabetes: a positron-emitting tomography study.
- Authors
Virtanen, Kirsi A.; Iozzo, Patricia; Hällsten, Kirsti; Huupponen, Risto; Parkkola, Riitta; Janatuinen, Tuula; Lönnqvist, Fredrik; Viljanen, Tapio; Rönnemaa, Tapani; Lönnroth, Peter; Knuuti, Juhani; Ferrannini, Ele; Nuutila, Pirjo; Hällsten, Kirsti; Lönnqvist, Fredrik; Rönnemaa, Tapani; Lönnroth, Peter
- 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-[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. Diabetes 54: 2720-2726, 2005
- Subjects
INSULIN resistance; OBESITY; TYPE 2 diabetes; ABDOMEN; ADIPOSE tissues; GLUCOSE
- Publication
Diabetes, 2005, Vol 54, Issue 9, p2720
- ISSN
0012-1797
- Publication type
Academic Journal
- DOI
10.2337/diabetes.54.9.2720