The increased insulin sensitivity in growth hormone-deficient adults is reduced by growth hormone replacement therapy.

作者: Riedl , Ludvik , Pacini , Clodi , Kotzmann

DOI: 10.1046/J.1365-2362.2000.00695.X

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摘要: Background Growth hormone deficiency is associated with increa~ed morbidity and mortality from cardiovascular diseases, which might be related to changes in glucose lipid metabolism. Design To assess the infiuence oflong-term growth replacement therapy (GHRT) on metabolism we examined eight hormone-deficient (GHD) adults (seven female/one male; age, 46 ± 3 years; body mass index, 31 2 kg m -2) over aperiod of 18 months comparison an adequate control group consisting obese subjects matched for sex, index. We performed frequently sampled intravenous tolerance tests (FSIGT) minimal model analysis before study, after 12 months. Results FoHowing GHRT, insulin-like factor-1 (IGF-1) increased significantly a basal level of75·9 18·9 200·8 31·0 JLgL-1 oftherapy remained stable, thereafter. GHRT did not affect fasting blood glucose, insulin, cholesterol, pressure weight. However, at 12months, HbA1c (6·0 0·1 vs. 5·6 % b~sal, P< 0·05) triglyceride (2·3 0·4 1·4 0·3 mmol L-1) but returned pretreatment values Insulin sensitivity was higher GHD (8·2 3·1) compared controls (3·6 0·53 x 10- 4 min-l/(JLU mL-1), P= 0·06) decreased 5·1 2·6, 0·05. Basal insulin secretion similar that months, total only SG (glucose effectiveness)was lower patients (0·0095 0·001 min- 1 ) (0·020 0·003 min-l, P<0·05) (0·016 0·002, 0·015 min-1 , 0·05), respectively. Hepatic extraction rate both groups unchanged foHowing GHRT. Conclusion conclude long-term induces significant decrease levels observed index-matched subjects. This accompanied by increase as weH effectiveness possible compensatory mechanism.

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