Insulin‐like growth factor I administration induces fluid and sodium retention in healthy adults: possible involvement of renin and atrial natriuretic factor

OBJECTIVE: Growth hormone induces fluid and sodium retention. The underlying mechanism is, however, incompletely understood. A possible mediator could be IGF-I. To investigate the impact of IGF-I administration on body fluid distribution and sodium homeostasis in healthy subjects, we examined normal subjects during six days IGF-I treatment and during a six-day control period. DESIGN AND MEASUREMENTS: Eight normal male subjects aged 23-30 years were randomised to receive IGF-I 50 microg/kg subcutaneously thrice daily during a six day study period, and to a six day control period. After each study period, extracellular volume and plasma volume (ECV, PV) were determined using 82Br and 125I-albumin. Blood samples, urinary sodium excretion, and bioimpedance were measured every second day of each study period. RESULTS: Serum IGF-I (microg/l) increased during active treatment (control, 293 +/- 9; IGF-I, 628 +/- 42; P < 0.01). ECV (l) was expanded by IGF-I (control, 18.42 +/- 0.28; IGF-I, 19.72 +/- 0.50; P < 0.05) whereas PV (l) remained unaffected (control, 3.76 +/- 0.11; IGF-I, 3.80 +/- 0.16; n.s.). Likewise, bioimpedance and body weight were unchanged by IGF-I. Plasma renin (mU/l) increased but not significantly during IGF-I (control, 28.7 +/- 2.7; IGF-I, 39.9 +/- 4.3; P = 0.08), and plasma aldosterone was unaffected by IGF-I. N-Terminal proANF (pmol/l) was suppressed during IGF-I administration (control, 422 +/- 32; IGF-I, 330 +/- 20; P < 0.05). Diurnal sodium excretion (mmol) was reduced during IGF-I administration (control, 151 +/- 8; IGF-I, 124 +/- 7; P < 0.05). CONCLUSION: IGF-I treatment causes fluid and sodium retention. This may be mediated by increased renin release and suppression of atrial natriuretic factor. The present data suggest that the fluid and sodium retaining effect of GH is at least partly mediated through IGF-I.