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Glucose Turnover in Hyperthyroid Patients with Normal Glucose Tolerance^*

SVEN-GUNNAR KARLANDER, AKHTAR KHAN, ALEXANDRE WAJNGOT, OVE TORRING, MLADEN VRANIC and SUAD EFENDI

Department of Endocrinology, Karolinska Hospital, Stockholm Sweden
The Departments of Physiology and Medicine, University of Toronto (M. V.) Toronto, Ontario, Canada

Address requests for reprints to: Dr. S. Efendi, Department Endocrinology, Karolinska Hospital, S-104 01 Stockholm, Sweden.

To determine the diabetogenic effect(s) of thyroid hormones, we simultaneously measured glucose turnover in six hyperthyroid patients and six normal subjects. All had normal fasting blood glucose concentration and oral glucose tolerance test values. We determined hepatic total glucose output (HTGO) and total glucose phosphorylation with [2-³H]glucose and hepatic glucose production (HGP) and irreversible glucose uptake using [6’³H]glucose. The difference between the two turnover rates indicates the extent of hepatic glucose cycling (glucose glucose-6-phosphate). Measurements were made both in the postabsorptive steady state and during a 2-h glucose infusion (11.1 µmol/kg·min). The postabsorptive HTGO and total glucose phosphorylation were increased in the hyperthyroid patients [13.5 ± 0.8 (±SE) vs. 11.3 ± 0.4 µmol/kg · min; P < 0.05]. HGP and irreversible glucose uptake also were slightly but not significantly higher. During the glucose infusion, HTGO and HGP were less suppressed in the hyperthyroid patients than in the normal subjects, while the increments in peripheral glucose uptake were normal. In hyperthyroidism, glucose cycling was increased both postabsorptively (2.35 ± 0.27 vs. 1.17 ± 0.25 µmol/kg·min; P < 0.025) and during glucose infusion (2.57 ± 0.34 vs. 1.31 ± 0.35 µmol/kg·min; P < 0.05). We conclude that increases in HTGO and HGP are important features of hyperthyroidism, especially during glucose infusion. The increase in GC indicates increased activities of both glucokinase and glucose-6-phosphatase. The diabetogenic effect of hyperthyroidism, as revealed most markedly by [2-³H] glucose, could be accounted for by augmented glucose production, possibly due to increased glucose-6-phosphatase activity. (J Clin Endocrinol Metab 68: 780,1989)

^* This work was supported by the Swedish Medical Research Council 00034), the Nordic Insulin Foundation (Gentofte, Denmark), the Riksbankens Jubileums Fond, the Swedish Diabetes Association, the Magnus Bergvalls Foundation, and the Medical Research Council Canada).

Received June 28, 1988.

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