Effects of chronic slow release-lanreotide treatment on insulin-like growth factor system and metabolic parameters in acromegalic patients
V. Gasco1, G. Beccuti1, F. Marotta1, N. Prencipe1, M. Maccario1, J. Janssen2, A.J. van der Lely2, E. Ghigo1, and S. Grottoli1
1Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Turin, Turin, Italy; 2Department of Internal Medicine, Erasmus University of Rotterdam, Rotterdam, The Netherlands

Insulin and IGF binding protein (IGFBP)-1 are linked by negative association. Somatostatin (SS) reduces insulin secretion by acting on pancreatic β-cell and also by decreasing GH secretion. SS analogues in acromegaly reduce total IGF-I levels inhibiting GH hypersecretion, but they also reduce free IGF-I bioactivity increasing IGFBP-1 levels by inducing insulin decrease. In 13 acromegalic patients we studied GH, IGF system, insulin, and glucagon levels at baseline and at 7 days, 1 and 6 months under treatment with slow release (SR)-lanreotide (LAN) (60 mg im monthly). The hormonal and metabolic response to arginine (ARG) (0.5 g/kg iv in 30 min) was also studied at each time point. LAN decreased GH, total IGF-I, and IGFBP-3 levels at each time point. Insulin and glucagon levels were reduced, while IGFBP-1 and free IGF-I levels were increased by LAN at day 7 and after 1 month only. LAN did not modify the GH, insulin, glucagon, glucose, and IGFBP-1 responses to ARG. At each time point ARG-induced insulin increase was coupled to increase in glucagon and IGFBP-1 levels. This study shows that acromegalic patients under chronic treatment with LAN display: a) inhibition of GH and total IGF-I levels, not coupled to persistent decrease in free IGF-I levels; b) persistent decrease in IGFBP-3 but transient decrease and increase in insulin and IGFBP-1, respectively; c) unchanged hormonal and metabolic response to ARG. Our findings also show that ARG stimulates IGFBP-1 despite marked increase in insulin secretion; this escape from the negative relationship linking insulin and IGFBP-1 would likely reflect the ARG-induced glucagon increase. (J. Endocrinol. Invest. 35: 372-377, 2012) ©2012, Editrice Kurtis

[« Torna indietro] [Full text non abbonati] [Full text abbonati] [Acquista PDF]