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  • Title: Growth hormone responses to growth hormone-releasing hormone and clonidine in patients with type I diabetes and in normal controls: effect of age, body mass index and sex.
    Author: Jacobs ML, Nathoe HM, Blankestijn PJ, Stijnen T, Weber RF.
    Journal: Clin Endocrinol (Oxf); 1996 May; 44(5):547-53. PubMed ID: 8762731.
    Abstract:
    OBJECTIVE: Increased plasma concentrations of GH and increased GH responses to provocative stimuli are reported in patients with poorly controlled type I diabetes and are suggested to be related to complications. Our aim was to investigate GH concentrations in moderately controlled patients. PATIENTS AND MEASUREMENTS: We have investigated IGF-I concentrations and fasting GH concentrations and the response to 1 microgram/kg body weight GH-releasing hormone (GHRH) intravenously and/or to 150 micrograms clonidine intravenously in 77 moderately controlled patients with type I diabetes and in 46 healthy controls. RESULTS: Median HbA1c in the patients was 8.5% (upper level of normal 6.3%). Fasting GH and GH concentrations after the administration of GHRH were not significantly different in patients with type I diabetes compared with normal controls. Fasting and stimulated GH concentrations after the administration of clonidine were significantly higher in the patients, but this could be explained by their lower age and body mass index compared with controls. In controls but not in patients there was a negative correlation between GH and glucose concentrations. IGF-I was significantly lower in patients with diabetes than in controls, even after correction for age, body mass index and sex. CONCLUSIONS: Patients with moderately controlled type I diabetes mellitus have normal baseline and stimulated GH concentrations after the administration of GHRH or clonidine compared with healthy controls, when corrected for age, body mass index and sex. However, these 'normal' GH concentrations must be considered inappropriately high in view of the hyperglycaemia in these patients. The low plasma IGF-I concentrations might be responsible for the GH over-production.
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