Key result
Individually titrated GH therapy for 6 months in adult hypopituitary patients did not alter peripheral or hepatic insulin sensitivity (P=0.6), but significantly increased fasting plasma glucose and HbA1c.
Why the study?
Does individually titrated recombinant human GH therapy alter insulin action in adult hypopituitary patients?
Does individually titrated recombinant human GH therapy alter insulin action in adult hypopituitary patients?
Individually titrated GH therapy for 6 months in adult hypopituitary patients increases fasting glucose and HbA1c without altering peripheral or hepatic insulin sensitivity, highlighting the need for long-term glucose monitoring.
Answers are grounded in this paper and cite their sources.
GH may raise fasting glucose/HbA1c independently of insulin sensitivity; leaves open long-term glycemic monitoring needs in hypopituitarism.
There is controversy about the effect of replacement GH on insulin action in adult hypopituitary patients. GH replacement calculated from weight leads to unacceptable side effects in some patients. Recent studies suggest it should be individually titrated in adults using serum IGF-I levels. We have assessed the effect of titrated GH replacement on peripheral and hepatic insulin action in 13 adult-onset hypopituitary patients (8 males and 5 females; ages 47 +/- 10 yr, mean duration of hypopituitarism 6 yr) with confirmed GH deficiency (GHD; maximum GH <5 mU/liter during insulin induced hypoglycemia), ACTH deficiency, and normal glucose tolerance. All patients were on stable hydrocortisone replacement (15 mg with breakfast, 5 mg with evening meal) for at least 2 months before the trial. Insulin action was assessed by the euglycemic hyperinsulinemic glucose clamp technique (1 mU/kg x min) before and after 6 months of GH therapy. GH was started at 0.8 IU sc daily and titrated monthly until the serum IGF-I increased to within 1-2 SD of the mean of normal age-matched controls. Body mass index did not change significantly during the 6 months of GH therapy. Fasting plasma glucose and HbA1c increased significantly after 6 months (5.2 +/- 0.0 vs. 5.5 +/- 0.0 mmol/liter, P < 0.0001, and 4.5 +/- 0.1 vs. 4.7 +/- 0.1%, P < 0.0005, respectively). There was no increase in fasting serum insulin (51.6 +/- 10.2 vs. 60.0 +/- 10.2 pmol/liter, P = 0.12). Exogenous glucose infusion rates required to maintain euglycemia were similar after GH (23.0 +/- 0.4 vs. 21.1 +/- 0.3 micromol/kg x min, P = 0.6). Endogenous glucose production in the fasting state was also unchanged following GH (11.8 +/- 0.7 vs.12.3 +/- 0.9 micromol/kg x min, P = 0.5) and suppressed to a similar extent following insulin (4.4 +/- 0.8 vs. 5.5 +/- 0.8 micromol/kg x min, P = 0.3). In summary, GH therapy for 6 months, with serum IGF-I maintained in the upper physiological range, increased fasting plasma glucose and HbA1c. There was no effect on peripheral or hepatic insulin sensitivity. Patients receiving GH therapy require long-term monitoring of glucose tolerance.
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McConnell et al. (2001) studied Adult hypopituitarism with GH deficiency (n=13). Recombinant Human GH therapy vs. Baseline (before therapy) was evaluated on Exogenous glucose infusion rates required to maintain euglycemia (p=0.6). Individually titrated GH therapy for 6 months in adult hypopituitary patients did not alter peripheral or hepatic insulin sensitivity (P=0.6), but significantly increased fasting plasma glucose and HbA1c.
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