title: Insulin-like growth factor binding protein 1 response to acute insulin induced hypoglycaemia in type 1 diabetes.
abstract: OBJECTIVE
  Insulin is believed to be the prime regulator of insulin-like growth factor binding protein 1 (IGFBP-1) secretion, and in normal subjects acute insulin induced hypoglycaemia exerts a rapid effect on concentrations of IGFBP-1, and may also influence insulin-like growth factor I (IGF-I) concentrations. The rise in IGFBP-1 concentrations in normal subjects following hypoglycaemia has been suggested to be due to suppression of endogenous insulin secretion. We have examined this further by studying diabetics with no endogenous insulin secretion.
  
  
  METHODS
  We have compared the IGFBP-1 response to acute insulin induced hypoglycaemia in normal subjects and patients with Type 1 (insulin dependent) diabetes mellitus.
  
  
  METHODS
  Insulin tolerance tests were performed using a bolus of insulin (0.15 U/kg), in six control subjects and six patients with Type 1 diabetes.
  
  
  METHODS
  Serum levels of IGFBP-1, insulin, glucose, and IGF-I were measured at regular intervals during the insulin tolerance test.
  
  
  RESULTS
  Blood glucose fell to a nadir which coincided with the onset of the acute autonomic reaction 'R' in both groups. The basal concentration of IGF-I was significantly lower in the diabetic group at 0.4 +/- 0.1 kU/l, compared to 0.9 +/- 0.1 kU/l in the control group, but there was no significant change in IGF-I concentrations in response to hypoglycaemia in either group. Hypoglycaemia provoked a fall in IGFBP-1 in patients with Type 1 diabetes, from 38 +/- 9 micrograms/l basally to 17 +/- 3 micrograms/l at R + 120 minutes, with a return to basal values of 45 +/- 11 micrograms/l at R + 180 minutes. In the control subjects there was no fall in IGFBP-1, but a significant increase to 71 +/- 14 micrograms/l at R + 180 minutes.
  
  
  CONCLUSIONS
  This difference in the IGFBP-1 response in the presence of a similar glucose response suggests that in Type 1 diabetes there may be different sensitivities to the actions of exogenous insulin on IGFBP-1 regulation.
authors.affiliation: Diabetes Centre, Royal Infirmary, Glasgow, UK.
authors.forename: J D
authors.initials: JD
authors.lastname: Quin
authors.forename: B M
authors.initials: BM
authors.lastname: Fisher
authors.forename: A C
authors.initials: AC
authors.lastname: MacCuish
authors.forename: G H
authors.initials: GH
authors.lastname: Beastall
authors.forename: M
authors.initials: M
authors.lastname: Small
authors.forename: J M
authors.initials: JM
authors.lastname: Holly
authors.forename: A M
authors.initials: AM
authors.lastname: Cotterill
mesh_terms: D000328:Adult; D002352:Carrier Proteins / Q000032:analysis / Q000378:metabolism*; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000503:physiopathology*; D006801:Humans; D007003:Hypoglycemia / Q000097:blood / Q000503:physiopathology*; D007328:Insulin / Q000097:blood; D018970:Insulin-Like Growth Factor Binding Protein 1; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D013002:Somatomedins / Q000378:metabolism*
chemical_list: D002352:Carrier Proteins; D007328:Insulin; D018970:Insulin-Like Growth Factor Binding Protein 1; D013002:Somatomedins; D007334:Insulin-Like Growth Factor I