title: Impaired beta-cell function in the presence of reduced insulin sensitivity determines glucose tolerance status in acromegalic patients.
abstract: OBJECTIVE
  Abnormal glucose tolerance is often demonstrated in acromegalic patients. Although insulin resistance is a common feature of acromegaly, it remains unclear whether the extent of insulin resistance per se determines the abnormal glucose tolerance. In order to elucidate this issue, we investigated insulin sensitivity and beta-cell function in acromegalic patients.
  
  
  METHODS
  Twenty-four acromegalic patients were studied in comparison with 24 healthy control subjects. To estimate insulin sensitivity and beta-cell function, we used correct homeostasis model assessment (HOMA) model, a computer-solved model. We also investigated the effects of surgical success on both parameters.
  
  
  RESULTS
  HOMA insulin sensitivity (HOMA-%S) in the acromegalic patients was 74 +/- 51 (SD)%, significantly lower than that in 24 healthy controls (144 +/- 49%). HOMA-%S in 12 normal glucose tolerance (NGT) patients was 54 +/- 31%, not significantly different from that in impaired glucose tolerance (IGT; n = 11) or diabetes mellitus (DM; n = 1) patients (93 +/- 60%). By contrast, HOMA beta-cell function (HOMA-%beta) in the NGT acromegalic patients was 163 +/- 67%, significantly higher than the IGT/DM acromegalic patients (89 +/- 34%) and the healthy controls (72 +/- 19%). In 11 patients who achieved complete normalization of GH excess after surgery, HOMA-%S significantly increased to control ranges (from 76 +/- 26 to 159 +/- 61%) within 2 weeks after the surgical success.
  
  
  CONCLUSIONS
  We conclude that insulin sensitivity is reduced to a similar extent in acromegalic patients with normal glucose tolerance and those with impaired glucose tolerance or diabetes. Compensatory hyperfunction of beta-cells appears to counterbalance the reduced insulin sensitivity in the acromegalic patients with normal glucose tolerance but not in those with impaired glucose tolerance or diabetes.
authors.affiliation: Department of Medicine III, Osaka University Medical School, Osaka, Japan. kasayama@imed3.med.osaka-u.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Kasayama
authors.forename: M
authors.initials: M
authors.lastname: Otsuki
authors.forename: M
authors.initials: M
authors.lastname: Takagi
authors.forename: H
authors.initials: H
authors.lastname: Saito
authors.forename: S
authors.initials: S
authors.lastname: Sumitani
authors.forename: H
authors.initials: H
authors.lastname: Kouhara
authors.forename: M
authors.initials: M
authors.lastname: Koga
authors.forename: Y
authors.initials: Y
authors.lastname: Saitoh
authors.forename: T
authors.initials: T
authors.lastname: Ohnishi
authors.forename: N
authors.initials: N
authors.lastname: Arita
mesh_terms: D000172:Acromegaly / Q000209:etiology / Q000378:metabolism* / Q000601:surgery; D000236:Adenoma / Q000150:complications / Q000378:metabolism / Q000601:surgery; D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D003198:Computer Simulation; D003920:Diabetes Mellitus / Q000378:metabolism; D005260:Female; D018149:Glucose Intolerance / Q000378:metabolism*; D013006:Growth Hormone / Q000097:blood; D006706:Homeostasis; D006801:Humans; D007333:Insulin Resistance; D007515:Islets of Langerhans / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D010911:Pituitary Neoplasms / Q000150:complications / Q000378:metabolism / Q000601:surgery
chemical_list: D013006:Growth Hormone