Insulin action in adipose tissue and muscle in hypothyroidism.

BACKGROUND: Although insulin resistance in thyroid hormone excess is well documented, information on insulin action in hypothyroidism is limited. METHODS: To investigate this, a meal was given to 11 hypothyroid (HO; aged 45 +/- 3 yr) and 10 euthyroid subjects (EU; aged 42 +/- 4 yr). Blood was withdrawn for 360 min from veins (V) draining the anterior abdominal sc adipose tissue and the forearm and from the radial artery (A). Blood flow (BF) in adipose tissue was measured with 133Xe and in forearm with strain-gauge plethysmography. Tissue glucose uptake was calculated as (A-V)glucose(BF), lipoprotein lipase as (A-V)Triglycerides(BF), and lipolysis as [(V-A)glycerol(BF)]-lipoprotein lipase. RESULTS: The HO group had higher glucose and insulin levels than the EU group (P < 0.05). In HO vs. EU after meal ingestion (area under curve 0-360 min): 1) BF (1290 +/- 79 vs. 1579 +/- 106 ml per 100 ml tissue in forearm and 706 +/- 105 vs. 1340 +/- 144 ml per 100 ml tissue in adipose tissue) and glucose uptake (464 +/- 74 vs. 850 +/- 155 micromol per 100 ml tissue in forearm and 208 +/- 42 vs. 406 +/- 47 micromol per 100 ml tissue in adipose tissue) were decreased (P < 0.05), but fractional glucose uptake was similar (28 +/- 6 vs. 33 +/- 6% per minute in forearm and 17 +/- 4 vs. 14 +/- 3% per minute in adipose tissue); 2) suppression of lipolysis by insulin was similar; and 3) plasma triglycerides were elevated (489 +/- 91 vs. 264 +/- 36 nmol/liter.min, P < 0.05), whereas adipose tissue lipoprotein lipase (42 +/- 11 vs. 80 +/- 21 micromol per 100 ml tissue) and triglyceride clearance (45 +/- 10 vs. 109 +/- 21 ml per 100 ml tissue) were decreased in HO (P < 0.05). CONCLUSIONS: In hypothyroidism: 1) glucose uptake in muscle and adipose tissue is resistant to insulin; 2) suppression of lipolysis by insulin is not impaired; and 3) hypertriglyceridemia is due to decreased clearance by the adipose tissue.

Glucose and lipid fluxes in the adipose tissue after meal ingestion in hyperthyroidism.

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 Blood was withdrawn for 360 min from veins draining the anterior abdominal sc AD and from the radial artery.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.