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Submitted on May 3, 2005
Accepted on December 19, 2005
2nd Department of Internal Medicine, Research Institute and Diabetes Center, Athens University Medical School, Athens, Greece, Hellenic National Diabetes Center, Athens, Greece, and Departments of Endocrinology "Elena Venizelou" and "Evangelismos" Hospitals, Athens, Greece
* To whom correspondence should be addressed. 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 Blood was withdrawn for 360min from veins (V) draining the anterior abdominal sc AD and from the radial artery (A). Blood flow (BF) was measured with 133Xe. Lipoprotein lipase (LPL) was calculated as triglyceride flux across AD, and AD-lipolysis 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: (a) BF was increased (AreaUnderCurve0-360min [ml/100ml tissue]; 1746 ± 208 vs. 1344 ± 102, P = 0.001), but glucose uptake was normal (AreaUnderCurve0-360min [µmol/100ml tissue]; 501 ± 114 vs. 368 ± 48); (b) fasting rates of lipolysis (nmol/min/100ml tissue; 329 ± 75 vs. 89 ± 22, P = 0.02) and NEFA release (nmol/min/100ml tissue; 841 ± 146 vs. 316 ± 97, P = 0.01), and plasma NEFA levels (µmol/l; 623 ± 50 vs. 454 ± 57, P = 0.03) were increased, but were all rapidly suppressed to levels similar to those in EU following the increase in plasma insulin levels after the meal; (c) LPL was not stimulated by insulin.
Conclusions: In hyperthyroidism, adipose tissue lipolysis and glucose uptake are resistant to insulin. The defect in lipolysis is manifested in the fasting state, while 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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