Supplemental growth hormone increases the tumor cytotoxic activity of natural killer cells in healthy adults with normal growth hormone secretion

Abstract

Using double-blind, placebo-controlled procedures, the effects of methionyl-human growth hormone (met-hGH) on the tumor cytotoxic activity of natural killer (NK) cells were studied in seven healthy adults using a repeated measures experiment. Subjects were assigned at random to either a placebo (bacteriostatic water) treatment condition or a met-hGH (16.0 mg/wk of Protropin) treatment condition, then crossed-over to the alternative treatment. Treatments were delivered on alternate days (3 d/wk) for 6 weeks. Without bias from the met-hGH treatment, there was no evidence for GH hyposecretion as measured by the peak circulating GH response to exercise stimulation (14.1 ± 3.1 ng/mL) or insulin-like growth factor (IGF-I) levels (0.82 ± 0.09 U/mL). When compared with placebo, met-hGH induced a significant overall increase in the percent specific lysis (%SL) of K562 tumor target cells (placebo 22.2 ± 1.7 v met-hGH 28.5 ± 2.1 %SL; P = .008). NK activity was increased within the first week of treatment and this level was maintained throughout the remaining period of supplementation. There was a trend ( P = .057) for the met-hGH-induced percent change in NK activity (NK%) to be inversely related to placebo IGF-I levels ( r = −.761), while there were significant positive correlations between NK% and the met-hGH-induced percent changes in IGF-I ( r = .727; P = .035), the fat-free mass (FFM)/fat mass (FM) ratio derived by hydrodensitometry ( r = .792; P = .012), and the endogenous GH response to exercise ( r = .469; P = .034). We conclude that supplemental GH increases NK activity in healthy adults with normal GH secretion and that this effect is interrelated to the body composition and IGF-I responses to the hormone. Since these findings were observed in the absence of GH hyposecretion, exogenous GH might be of benefit in states in which the normal anabolic processes in vivo are insufficient to overcome the taxing influence of disease and/or disuse.