Key result
Standard GH replacement doses reduced insulin sensitivity (P=0.01), whereas intermediate doses increased insulin sensitivity (P<0.005) and low doses reduced fasting glucose (P<0.0001).
Why the study?
Do lower physiological doses of GH improve insulin sensitivity and fasting glucose compared to standard replacement doses in healthy adults?
Do lower physiological doses of GH improve insulin sensitivity and fasting glucose compared to standard replacement doses in healthy adults?
Lower physiological doses of GH improve insulin sensitivity and fasting glucose levels, contrasting with the insulin resistance induced by standard replacement doses.
May favor lower GH doses for insulin sensitivity; leaves open clinical adoption pending randomized trials.
GH has both diabetogenic and insulin-like actions. Supraphysiological GH doses are known to reduce insulin sensitivity (S(I)), but lower doses are less well studied. We therefore compared the effects of two physiological GH doses (intermediate, 0.0033 mg/kg x d; low, 0.0017 mg/kg x d) with the standard adult GH deficiency replacement dose (standard, 0.008 mg/kg x d) on S(I), beta-cell function, IGF-I, and IGF binding proteins (IGFBPs)-1 and -3 in healthy adults. Eleven healthy nonobese volunteers (4 males and 7 females, aged 21-38 yr) received 7 daily injections of the standard and intermediate GH doses, and 10 (5 males and 5 females, aged 21-38 yr) received the low dose. Fasting blood samples were collected daily (days 1-8). S(I) and beta-cell function were calculated using the Homeostasis model assessment. All GH doses increased IGF-I and IGFBP-3 levels, with the standard dose inducing the greatest rise (P < 0.001). At day 2 vs. baseline, all three doses increased the IGF-I/IGFBP-3 ratio, but only the standard dose lowered IGFBP-1 levels (P = 0.03). The standard dose reduced S(I) (P = 0.01), whereas the intermediate dose increased S(I) (P < 0.005) and lowered fasting insulin levels (P < 0.01). The low dose did not modify S(I), but reduced fasting glucose levels (P < 0.0001) and increased beta-cell function (P = 0.001). Males demonstrated higher IGF-I and IGFBP-3 responsiveness to the standard dose than females. Males also showed greater increase in S(I) and decrease in fasting glucose levels on both intermediate and low doses. In conclusion, the metabolic effects of GH are dose- and gender-dependent. The standard adult GH deficiency replacement dose induced insulin resistance, whereas lower doses improved S(I), especially in males. The low GH dose lowered fasting glucose levels and could represent the optimal dose to stimulate beta-cell function without compromising S(I) in insulin-resistant GH-deficient adults.
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Yuen et al. (2002) studied Healthy adults (n=21). Growth Hormone (GH) vs. Standard adult GH deficiency replacement dose (0.008 mg/kg x d) was evaluated on Insulin sensitivity (S(I)) (p=0.01). Standard GH replacement doses reduced insulin sensitivity (P=0.01), whereas intermediate doses increased insulin sensitivity (P<0.005) and low doses reduced fasting glucose (P<0.0001).
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