Horm Metab Res 1991; 23(12): 600-604
DOI: 10.1055/s-2007-1003764
Clinical

© Georg Thieme Verlag, Stuttgart · New York

Reduction of Baclofen-, but not Sodium Valproate-Induced Growth Hormone Release in Type I Diabetic Men

V. Coiro1 , L. Capretti3 , L. Bianconi2 , A. Castelli4 , L. Cerri5 , G. Roberti5 , A. Marcato1 , R. Volpi1 , P. Chiodera2
  • 1Cattedra di Clinica Medica Generale, Università di Parma, Parma
  • 2Cattedra di Endocrinologia, Università di Parma, Parma
  • 3Divisione di Medicina Generale, Ospedale di Codogno, Codogno
  • 4Divisione di Medicina Generale, Ospedale di Piacenza, Piacenza
  • 5Servizio di Medicina Nucleare, Ospedale di Piacenza, Piacenza, Italy
Further Information

Publication History

1990

1991

Publication Date:
14 March 2008 (online)

Summary

The effects of sodium valproate (a drug enhancing endogenous gamma aminobutyric acid (GABA)-ergic activity) and of the GABA analog baclofen (a GABA B receptor agonist) on serum GH levels was tested in 8 type I diabetic men and 8 normal controls. Sodium valproate (800 mg) or baclofen (10 mg) were given by mouth at 08.30 h on the experimental days. Control tests with a placebo were performed on different occasions. Basal GH levels were similar in controls and diabetic patients. Sodium valproate induced a 7 fold increase in serum GH concentrations in both groups. In contrast, baclofen-induced GH rise was significantly higher in normal controls (mean peak was 3.4 times higher than baseline) than in diabetic patients (mean peak was only 2.1 times higher than basal value). Serum GH levels did not change after placebo administration in any groups. These data suggest the presence of diabetes-induced alterations of a GABAergic pathway mediated by B receptors in the control of GH secretion. Alternatively, the data might indicate a change in diabetic men of other baclofen-sensitive neurotransmissions, different from GABA.