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Glucose and Lipid Fluxes in the Adipose Tissue after Meal Ingestion in Hyperthyroidism

Second Department of Internal Medicine (G.D., P.M., V.L., E.B., S.A.R.), Research Institute and Diabetes Center, Athens University Medical School, 12462 Haidari, Greece; Hellenic National Diabetes Center (E.M., S.A.R.), 106 75 Athens, Greece; and Department of Endocrinology, "Elena Venizelou" (E.K.) and "Evangelismos" (M.T., N.T.) Hospitals, Athens, Greece

Address all correspondence and requests for reprints to: George Dimitriadis, M.D., DPhil, Second Department of Internal Medicine, Research Institute and Diabetes Center, Athens University, "Attikon" University Hospital, 1 Rimini Street, GR-12462 Haidari, Greece. E-mail: gdim{at}internet.gr.

Background: Although insulin resistance is well established in hyperthyroidism, information on the effects of insulin on adipose tissue (AD) is limited.

Methods: To investigate this, a meal was given to 12 hyperthyroid (HR) and 10 euthyroid (EU) subjects. Blood was withdrawn for 360 min from veins draining the anterior abdominal sc AD and from the radial artery. Blood flow was measured with ¹³³Xe. Lipoprotein lipase (LPL) was calculated as triglyceride flux across AD, and AD-lipolysis was calculated as glycerol flux minus LPL.

Results: Both groups displayed comparable postprandial glucose levels, with the HR having higher insulin levels than the EU. In AD of HR vs. EU: 1) blood flow was increased [area under curve 0–360 min (milliliters per 100 milliliters of tissue); 1746 ± 208 vs. 1344 ± 102, P = 0.001], but glucose uptake was normal [area under curve 0–360 min (micromoles per 100 milliliters of tissue); 501 ± 114 vs. 368 ± 48]; 2) fasting rates of lipolysis (nanomoles per minute per 100 milliliters of tissue; 329 ± 75 vs. 89 ± 22, P = 0.02) and nonesterified fatty acid (NEFA) release (nanomoles per minute per 100 milliliters of tissue; 841 ± 146 vs. 316 ± 97, P = 0.01), and plasma NEFA levels (micromoles per liter; 623 ± 50 vs. 454 ± 57, P = 0.03) were increased, but were all rapidly suppressed to levels similar to those in EU after the increase in plasma insulin levels after the meal; and 3) LPL was not stimulated by insulin.

Conclusions: In hyperthyroidism, AD lipolysis and glucose uptake are resistant to insulin. The defect in lipolysis is manifested in the fasting state, whereas postprandially this rate is rapidly suppressed to normal. This may relieve tissues from the burden of NEFAs after the meal, thus facilitating muscle glucose disposal by insulin.

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