title: Insulin sensitivity and β-cell function in adults with lifetime, untreated isolated growth hormone deficiency.
abstract: BACKGROUND
  GH reduces insulin sensitivity (IS), whereas IGF-I increases it. IGF-I seems to be critical for the development of the β-cells, and impaired IS has been reported in GH deficiency (GHD).
  
  
  OBJECTIVE
  The aim of the study was to assess IS and β-cell function in adult patients with untreated isolated GHD (IGHD) due to a homozygous mutation in the GHRH receptor gene.
  
  
  METHODS
  We conducted a cross-sectional study in 24 GH-naive adult IGHD subjects and 25 controls.
  
  
  METHODS
  We performed an oral glucose tolerance test with glucose and insulin measurements at 0, 30, 60, 90, 120, and 180 min.
  
  
  METHODS
  IS was assessed by homeostasis model assessment index of insulin resistance (IR), quantitative IS check index, oral glucose IS in 2 h (OGIS2) and 3 h (OGIS3). β-Cell function was assayed by homeostasis model assessment index-β, insulinogenic index, and area under the curve of insulin-glucose ratio.
  
  
  RESULTS
  During the oral glucose tolerance test, glucose levels were higher in IGHD subjects (P<0.0001), whereas insulin response presented a trend toward reduction (P=0.08). The number of individuals with impaired glucose tolerance was higher in the IGHD group (P=0.001), whereas the frequency of diabetes was similar in the two groups. Homeostasis model assessment index of IR was lower (P=0.04), and quantitative IS check index and OGIS2 showed a nonsignificant trend toward elevation (P=0.066 and P=0.09, respectively) in IGHD. OGIS3 showed no difference between the groups. Homeostasis model assessment index-β, insulinogenic index, and ratio of the areas of the insulin and glucose curves were reduced in the IGDH group (P=0.015, P<0.0001, and P=0.02, respectively).
  
  
  CONCLUSIONS
  Adult subjects with lifetime congenital untreated IGHD present reduced β-cell function, no evidence of IR, and higher frequency of impaired glucose tolerance.
authors.affiliation: Federal University of Sergipe, Aracaju, SE, Brazil.
authors.forename: Carla R P
authors.initials: CR
authors.lastname: Oliveira
authors.forename: Roberto
authors.initials: R
authors.lastname: Salvatori
authors.forename: Jose A S
authors.initials: JA
authors.lastname: Barreto-Filho
authors.forename: Ivina E S
authors.initials: IE
authors.lastname: Rocha
authors.forename: Andrea
authors.initials: A
authors.lastname: Mari
authors.forename: Rossana M C
authors.initials: RM
authors.lastname: Pereira
authors.forename: Viviane C
authors.initials: VC
authors.lastname: Campos
authors.forename: Menilsson
authors.initials: M
authors.lastname: Menezes
authors.forename: Elenilde
authors.initials: E
authors.lastname: Gomes
authors.forename: Rafael A
authors.initials: RA
authors.lastname: Meneguz-Moreno
authors.forename: Vanessa P
authors.initials: VP
authors.lastname: Araújo
authors.forename: Natália T F
authors.initials: NT
authors.lastname: Leite
authors.forename: Adão C
authors.initials: AC
authors.lastname: Nascimento-Junior
authors.forename: Maria I T
authors.initials: MI
authors.lastname: Farias
authors.forename: Thaisa A R
authors.initials: TA
authors.lastname: Viscente
authors.forename: Raquel D C
authors.initials: RD
authors.lastname: Araújo
authors.forename: Enaldo V
authors.initials: EV
authors.lastname: Melo
authors.forename: Manuel H
authors.initials: MH
authors.lastname: Aguiar-Oliveira
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D003430:Cross-Sectional Studies; D004393:Dwarfism, Pituitary / Q000097:blood / Q000503:physiopathology*; D005260:Female; D018149:Glucose Intolerance / Q000097:blood / Q000503:physiopathology*; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D050417:Insulin-Secreting Cells / Q000502:physiology*; D008297:Male; D008875:Middle Aged
chemical_list: D001786:Blood Glucose; D007328:Insulin