Objective: The reduction of spontaneous and stimulated growth hormone (GH) secretion in obesity could reflect an increase of the inhibitory effect of insulin growth factor I (IGF-I) on somatotroph secretion.
Design: In the present study we aimed to verify the effect of low dose recombinant human IGF-I (20 microg/kg subcutaneously (s.c.) at 0 min) on 3 h-spontaneous GH secretion (mGHc, 0-180 min) and on the GH response to growth hormone releasing hormone (GHRH) (1 microg/kg i.v. at+180 min) in obesity.
Subjects: Five obese women with abdominal adiposity (OB, age, mean+/-s.e.m.: 31+/-7.13 y; BMI: 32.04+/-3.69 kg/m(2)) and eight age-matched lean women (NW, 28.3+/-1.2 y; 20.1+/-0.5 kg/m(2)) were studied.
Results: The mGHc and GHRH-induced GH response in OB (1.0+/-0.7 microg/l; AUC(180-270 min): 688.6+/-202.4 microg/l min, respectively) were lower than in NW (2.6+/-0.8 microg/l, 1315.9+/-189.9 microg/l min, respectively, P<0.05). The administration of rhIGF-I increased circulating IGF-I levels in OB and NW to the same extent (339.0+/-50.39 and 420.3+/-30.5 microg/l, respectively). The rhIGF-I administration did not affect mGHc in OB or NW (1.1+/-0.9 and 3.2+/-1.0 microg/l, respectively) but inhibited (P<0.05) the GH response to GHRH in OB (324.2+/-153.1 microg/l) and NW (730.2+/-288.1 microg/l).
Conclusions: Our study shows that the administration of low dose rhIGF-I reduces the somatotroph responsiveness to GHRH in obesity as well as in normal subjects.