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Second Department of Internal Medicine (G.D., P.M., V.L., E.B., N.T., T.E., S.A.R.), Research Institute and Diabetes Center, Athens University Medical School, "Attikon" University Hospital, GR-12462 Haidari, Greece; Hellenic National Center for Research, Prevention and Treatment of Diabetes Mellitus and Its Complications (E.M., S.A.R.), GR-10675 Athens, Greece; Department of Endocrinology (E.K.), Elena Venizelou Hospital, GR-11521 Athens, Greece; and Department of Nutrition Science-Dietetics (D.P.), Harokopio University, GR-17671 Athens, Greece
Address all correspondence and requests for reprints to: George Dimitriadis, M.D., D.Phil., Second Department of Internal Medicine, Research Institute and Diabetes Center, Athens University, Attikon University Hospital, 1 Rimini Street, GR-12462 Haidari, Greece. E-mail: gdimi{at}ath.forthnet.gr; or gdimitr{at}med.uoa.gr.
Background: In hyperthyroidism, although hepatic insulin resistance is well established, information on the effects of insulin on glucose uptake in skeletal muscle is variable.
Methods: To investigate this, a meal was given to nine hyperthyroid (HR) and seven euthyroid (EU) subjects. Blood was withdrawn for 360 min from a forearm deep vein and the radial artery for measurements of insulin and glucose. Forearm blood flow (BF) was measured with strain-gauge plethysmography. Glucose flux was calculated as arteriovenous difference multiplied by BF and fractional glucose extraction as arteriovenous difference divided by arterial glucose concentrations.
Results: Both groups displayed comparable postprandial glucose levels, with the HR having higher insulin levels than the EU. In the forearm of HR vs. EU: 1) glucose flux was similar [area under the curve (AUC)0–360 673 ± 143 vs. 826 ± 157 µmol per 100 ml tissue]; 2) BF was increased (AUC0–360 3076 ± 338 vs. 1745 ± 145 ml per 100 ml tissue, P = 0.005); and 3) fractional glucose extraction was decreased (AUC0–360 14.5 ± 3 vs. 32 ± 5%min, P = 0.03).
Conclusions: These results suggest that, in hyperthyroidism, insulin-stimulated glucose uptake in muscle is impaired; this defect is corrected, at least in part, by the increases in BF.
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