title: Glucose turnover and insulin clearance after growth hormone treatment in girls with Turner's syndrome.
abstract: The study was performed to elucidate, by means of a euglycemic-hyperinsulinemic clamp, whether insulin sensitivity, lipid levels, posthepatic insulin delivery, and insulin clearance are impaired in girls with Turner's syndrome in the absence of previous treatment (T0) and after 6 (T6) and 12 (T12) months of growth hormone (GH) therapy (GHT). The study was performed in six girls with Turner's syndrome and eight healthy girls. We found that previously untreated girls with Turner's syndrome had a normal insulin activity on glucose metabolism. GHT progressively and significantly decreased hepatic insulin sensitivity. In fact, residual hepatic glucose release (HGR), which was 19.6 +/- 4.7 mg/m2. min at T0, doubled at T6 (39.3 +/- 5.1 mg/m2.min) and showed a threefold increase at T12 (68.7 +/- 10.8 mg/m2.min, P < .05 v T0). On the contrary, GHT did not show an appreciable influence on peripheral insulin sensitivity. Insulin clearance was higher in girls with Turner's syndrome than in control girls at T0 (30.0 +/- 2.8 v 20.2 +/- 1.1 mL.kg-1.min-1). It decreased to normal values at T6 (18.2 +/- 2.0 mL.kg-1.min-1, P < .05 v T0) and remained at normal levels at T12 (23.8 +/- 2.9 mL.kg-1. min-1). The posthepatic insulin delivery rate significantly increased at T6 and T12, suggesting increased insulin secretion. In conclusion, we found that insulin-stimulated glucose turnover was normal in girls with Turner's syndrome before therapy. One year of GHT was successful in stimulating the growth rate, but significantly decreased the insulin suppressibility on HGR with only slight changes in peripheral insulin sensitivity. In addition, an increase in the insulin posthepatic delivery rate and a normalization of insulin clearance were present, probably to counteract hepatic insulin resistance.
authors.affiliation: Istituto Scientifico H. San Raffaele, Cattedra di Clinica Medica, Milano, Italy.
authors.forename: L D
authors.initials: LD
authors.lastname: Monti
authors.forename: P
authors.initials: P
authors.lastname: Brambilla
authors.forename: A
authors.initials: A
authors.lastname: Caumo
authors.forename: F
authors.initials: F
authors.lastname: Magni
authors.forename: S
authors.initials: S
authors.lastname: Omati
authors.forename: G
authors.initials: G
authors.lastname: Nizzoli
authors.forename: B
authors.initials: B
authors.lastname: di Natale
authors.forename: M
authors.initials: M
authors.lastname: Galli-Kienle
authors.forename: C
authors.initials: C
authors.lastname: Cobelli
authors.forename: G
authors.initials: G
authors.lastname: Chiumello
authors.forename: G
authors.initials: G
authors.lastname: Pozza
mesh_terms: D000293:Adolescent; D002096:C-Peptide / Q000097:blood; D002648:Child; D005215:Fasting / Q000502:physiology; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006128:Growth / Q000187:drug effects / Q000502:physiology; D013006:Growth Hormone / Q000097:blood / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007328:Insulin / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology; D007333:Insulin Resistance / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000032:analysis / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008099:Liver / Q000378:metabolism; D011994:Recombinant Proteins / Q000097:blood / Q000494:pharmacology / Q000627:therapeutic use; D014424:Turner Syndrome / Q000188:drug therapy* / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D002096:C-Peptide; D007328:Insulin; D008055:Lipids; D011994:Recombinant Proteins; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D005947:Glucose