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1 Lundberg Laboratory for Diabetes Research and 2 Wallenberg Laboratory, Sahlgrenska University Hospital, S-413 45 Goteborg, Sweden
Previous measurement of insulin in
human muscle has shown that interstitial muscle insulin and glucose
concentrations are ~30-50% lower than in plasma during
hyperinsulinemia in normal subjects. The aims of this study were to
measure interstitial muscle insulin and glucose in patients with type 2 diabetes to evaluate whether transcapillary transport is part of the
peripheral insulin resistance. Ten patients with type 2 diabetes and
ten healthy controls matched for sex, age, and body mass index were investigated. Plasma and interstitial insulin, glucose, and lactate (measured by intramuscular in situ-calibrated microdialysis) in the
medial quadriceps femoris muscle were analyzed during a
hyperinsulinemic euglycemic clamp. Blood flow in the contralateral
calf was measured by vein plethysmography. At steady-state
clamping, at 60-120 min, the interstitial insulin
concentration was significantly lower than arterial insulin in
both groups (409 ± 86 vs. 1,071 ± 99 pmol/l,
P < 0.05, in controls and 584 ± 165 vs.
1,253 ± 82 pmol/l, P < 0.05, in
diabetic subjects, respectively). Interstitial insulin concentrations did not differ significantly between diabetic
subjects and controls. Leg blood flow was significantly higher in
controls (8.1 ± 1.2 vs. 4.4 ± 0.7 ml · 100 g
1 · min1 in diabetics,
P < 0.05). Calculated glucose uptake was less in diabetic patients compared with controls (7.0 ± 1.2 vs. 10.8 ± 1.2 µmol · 100 g1 · min1, P < 0.05, respectively). Arterial and interstitial lactate concentrations were both higher in the control group (1.7 ± 0.1 vs. 1.2 ± 0.1, P < 0.01, and 1.8 ± 0.1 vs. 1.2 ± 0.2 mmol/l, P < 0.05, in controls and diabetics,
respectively). We conclude that, during hyperinsulinemia, muscle
interstitial insulin and glucose concentrations did not differ between
patients with type 2 diabetes and healthy controls despite a
significantly lower leg blood flow in diabetic subjects. It is
suggested that decreased glucose uptake in type 2 diabetes is caused by
insulin resistance at the cellular level rather than by a deficient
access of insulin and glucose surrounding the muscle cell.
insulin resistance; skeletal muscle; insulin uptake; glucose uptake; microdialysis
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