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Influence of Growth Hormone on Glucose-Induced Glucose Uptake in Normal Men as Assessed by the Hyperglycemic Clamp Technique^*

First (L.Ø., O.S., J.A., N.A.) and Second (J.O.L.J., J.S.C.) University Clinics of Internal Medicine Kommunehospitalet, Denmark
The Institute of Experimental Clinical Research, University of Aarhus (H.Ø) Aarhus, Denmark
The Department of Medicine, University of Newcastle (K.G.M.M.A.), Newcastleupon-Tyne NE2 4HH, England

Address requests for reprints to: Lotte Ørskov, M.D., Department of Medicine, Aarhus Kommunehospital, DK-8000 Aarhus C, Denmark.

To determine whether physiological increments in circulating GH concentrations influence glucose-induced glucose uptake (GIGU), two-step sequential hyperglycemic clamp (plasma glucose, 6 and 14 mmol/L) studies were performed in six normal subjects with and without GH infusion (40 ng/kg·min). The latter resulted in serum GH levels of 15 ± 1 (±SE) µg/L. Infusion of somatostatin (250 µg/h during step 1 and 750 µg/h during step 2) together with a replacement dose of insulin (1.1 pmol/kg·min) resulted in serum insulin levels comparable to basal levels in both studies. The GIGU ([3–³H]glucose), assessed as the difference between steps 2 and 1 glucose utilization during the final 60 min of each step (150 min) was markedly impaired during GH infusion (with GH, 1.1 ± 0.2 mg/kg·min; without GH, 3.1 ± 0.3 mg/kg-min; P < 0.001). Moreover, the percent increase in glucose uptake was considerably reduced during hypersomatotropinemia (with GH, 44 ± 9%; without GH, 97 ± 11%; P < 0.01). In the GH infusion as well as control studies, endogenous glucose production (EGP) was similar at the two levels of glycemia, whereas GH infusion approximately doubled EGP [2.3 ± 0.2 vs. 1.1 ± 0.3 mg/kg·min and 2.0 ± 0.4 vs. 1.1 ± 0.4 mg/kg·min (step 1 and 2, respectively)].

We conclude that moderate hypersomatotropinemia for several hours is characterized by impaired GIGU as well as augmented EGP.

^* This work was supported by the Danish Diabetes Association, the British Diabetic Association, the Institute of Experimental Clinical Research, and the Research Council of the University of Aarhus.

Received March 4, 1988.

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