The effect of 3 months of recombinant human growth hormone (GH) therapy on insulin and glucose-mediated glucose disposal and insulin secretion in GH-deficient adults: a minimal model analysis
O’neal, DN, Kalfas, A, Dunning, Patricia L, Christopher, MJ, Sawyer, SD, Ward, GM and Alford, FP 1994, The effect of 3 months of recombinant human growth hormone (GH) therapy on insulin and glucose-mediated glucose disposal and insulin secretion in GH-deficient adults: a minimal model analysis, Journal of clinical endocrinology and metabolism, vol. 79, no. 4, pp. 975-983, doi: 10.1210/jcem.79.4.7962308.
Title
The effect of 3 months of recombinant human growth hormone (GH) therapy on insulin and glucose-mediated glucose disposal and insulin secretion in GH-deficient adults: a minimal model analysis
The effect of 3 months of low dose (120 μg/kg.week or 0.24 IU/kg.week) recombinant human GH (rhGH) treatment on glucose tolerance, insulin secretion, and insulin- and glucose-mediated glucose disposal was examined in 10 GH-deficient adults. The frequently sampled iv glucose tolerance test was performed at baseline and after 1 week and 3 months of rhGH therapy and analyzed by the minimal model method of Bergman to provide estimates of the glucose decay rate, first and second phase insulin secretion (phi 1 and phi 2), fractional clearance of insulin, and glucose-mediated and insulin-mediated glucose disposal. Fasting glucose, insulin, C-peptide, nonesterified fatty acids (NEFA), and serum cholesterol and triglycerides were also measured. When the 1 week data were compared to baseline, there was a small but significant rise in mean (± SE) fasting glucose (4.62 ± 0.17 vs. 5.1 ± 0.15 mmol/L; P < 0.01), NEFA (0.70 ± 0.09 vs. 1.1 ± 0.12 mmol/L; P < 0.005), insulin (93.6 ± 8.9 vs. 238.9 ± 9.2 pmol/L; P < 0.0001), C-peptide (0.32 ± 0.13 vs. 0.66 ± 0.13 nmol/L; P < 0.005), and phi 1 (11.9 ± 1.3 vs. 16.2 ± 1.8 pmol/L.min/mmol.L x 10(2)) and phi 2 (1.43 ± 0.17 vs. 3.15 ± 0.25 pmol/L.min/mmol.L x 10(3); P < 0.05). Conversely, there were associated decreases in glucose decay rate (1.83 ± 0.26 vs. 1.28 ± 0.12 min-1; P < 0.05) and insulin-mediated glucose disposal (0.36 ± 0.08 vs. 0.18 ± 0.06 min/pmol.L x 10(-4); P < 0.005). There was no change in glucose-mediated glucose disposal or the fractional clearance of insulin. By 3 months, fasting insulin and C-peptide levels remained significantly elevated, whereas other parameters had returned to baseline. There was a minor reduction in serum cholesterol at 1 week (5.1 ± 0.15 vs. 4.62 ± 0.17 mmol/L; P < 0.01), which was not maintained at 3 months. Serum triglycerides remained unchanged throughout the study. We conclude that short term low dose rhGH treatment of GH-deficient adults induces a temporary state of mild glucose intolerance, hyperinsulinemia, insulin resistance, and raised NEFA levels at 1 week. By 3 months, these metabolic disturbances had returned to baseline for a persisting modest hyperinsulinemia. Whether this hyperinsulinemia will last over the longer term and/or has distant detrimental metabolic consequences in the individual must await further studies.
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