ICEECE2012 Oral Communications Pituitary Clinical I (6 abstracts)
Normal weight adult patients with Prader–Willi syndrome are not protected from insulin resistance during treatment with GH: results from a 12 month prospective study
A. Jørgensen 1 , T. Ueland 1 , R. Sode-Carlsen 2 , T. Schreiner 1 , K. Rabben 5 , S. Farholt 2 , C. Høybye 3 , J. Christiansen 4 & J. Bollerslev 1
1Oslo University Hospital, Rikshospitalet, Oslo, Norway; 2Aarhus University Hospital, Skejby, Aarhus, Denmark; 3Karolinska University Hospital, Stockholm, Sweden; 4Aarhus University Hospital, Aarhus, Denmark; 5Frambu, Siggerud, Norway.
Background: Diabetes mellitus is prevalent in adults with Prader–Willi syndrome (PWS), and GH therapy may deteriorate glucose balance.
Design: We prospectively investigated effects of 12 months of GH treatment on body composition and insulin resistance in relation to BMI in forty-two adults, mean(±S.D.) age 28.5±6.7 years with genetically verified PWS. Three patients with known diabetes were excluded. Data from baseline and 12 months of GH treatment in 35 patients, who completed the study are presented. The number of patients in each BMI-group (kg/cm2) were 14(<25), 10(25–30) and 11(>30). Fat mass (FM) and lean mass (LM) were assessed by DEXA. Fasting blood samples and 2 h p-glucose after oral glucose tolerance test (OGTT) were made at baseline and after 12 months. Insulin resistance was estimated by homeostasis model assessment (HOMA-IR).
Results: With a mean final GH dose of 0.6±0.25 mg we observed an increase in Insulin-like growth factor 1 (IGF1) from 115±35 to 171±52 μg/l, P<0.001, LM 39.9±8.1 to 42.2±8.8 kg, P<0.001, 2 h p-glucose 7.4±2.5 to 8.1±2.5, P<0.05, HOMA-IR 1.9±0.8 to 2.3±0.7, P<0.01 and a decrease in FM 29.4±12.5 to 27.5±13.4, P<0.02.
At baseline, IGF1 was lower with BMI (25–30) as compared to the other two groups, 95±27 vs 124±33 μg/l, P< 0.01 and HOMA-IR was higher with BMI >30, 1.7±0.7 vs 2.4±0.8. Age and LM did not differ between the groups and variations in BMI were due to different FM. Final mean GH dose and IGF1 level did not differ between the groups. A reduction in FM was seen only with BMI (25–30), 29.1±3.0 to 24.3±5.0 kg, P<0.01 and HOMA-IR increased in the lowest BMI-group only, 1.6±0.6 to 2.3±0.8, P<0.05.
Conclusions: GH treatment in PWS patients results in the expected increase in insulin resistance irrespective of fat mass.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This work was supported, however funding details are unavailable.
Volume 29
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