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1 Division of Endocrinology, Indiana University School of Medicine, Indianapolis, Indiana 46202; 2 Department of Medicine, Kuopio University Hospital, Kuopio, Finland 70210; and 3 Division of Endocrinology, Department of Medicine, University of California San Diego Veterans Affairs Medical Center, San Diego, California 92161
We hypothesized that the
vasodilation observed during insulin stimulation is closely coupled to
the rate of glucose metabolism. Lean (L, n = 13), obese
nondiabetic (OB, n = 13), and obese type 2 diabetic
subjects (Type 2 DM, n = 16) were studied. Leg blood flow (LBF) was examined under conditions of euglycemic hyperinsulinemia (EH) and hyperglycemic hyperinsulinemia (HH), which produced a steady-state whole body glucose disposal rate (GDR) of ~2,000 µmol · m
2 · min
1. At this
GDR, under both conditions, subjects across the range of insulin
sensitivity exhibited equivalent LBF (l/min EH: L, 0.42 ± 0.03;
OB, 0.43 ± 0.03; Type 2 DM, 0.38 ± 0.07; P = 0.72 by ANOVA. HH: L, 0.44 ± 0.04; OB, 0.39 ± 0.05; Type
2 DM, 0.41 ± 0.04; P = 0.71). The continuous
relationship between LBF and GDR did not differ across subject groups
[slope × 10
5
l/(µmol · m
2 · min
1) by
ANOVA. EH: L, 8.6; OB, 9.2; Type 2 DM, 7.9; P = 0.91. HH: L, 4.2; OB, 2.5; Type 2 DM, 4.1; P = 0.77],
although this relationship did differ between the EH and HH conditions
(P = 0.001). These findings support a physiological
coupling of LBF and insulin-mediated glucose metabolism. The
mechanism(s) linking substrate delivery and metabolism appears to be
intact in insulin-resistant states.
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