title: Hyperinsulinemic hypoglycemia after gastric bypass surgery is not accompanied by islet hyperplasia or increased beta-cell turnover.
abstract: OBJECTIVE
  The purpose of this study was to establish whether hypoglycemia after gastric bypass surgery (GBS) for morbid obesity is due to increased fractional beta-cell area or inappropriately increased insulin secretion.
  
  
  METHODS
  We examined pancreata obtained at partial pancreatectomy from 6 patients with post-GBS hypoglycemia and compared these with 31 pancreata from obese subjects and 16 pancreata from lean control subjects obtained at autopsy. We addressed the following questions. In patients with post-GBS hypoglycemia, is beta-cell area increased and is beta-cell formation increased or beta-cell apoptosis decreased?
  
  
  RESULTS
  We report that in patients with post-GBS hypoglycemia, beta-cell area was not increased compared with that in obese or even lean control subjects. Consistent with this finding, there was no evidence of increased beta-cell formation (islet neogenesis and beta-cell replication) or decreased beta-cell loss in patients with post-GBS hypoglycemia. In control subjects, mean beta-cell nuclear diameter correlated with BMI (r(2) = 0.79, P < 0.001). In patients with post-GBS hypoglycemia, beta-cell nuclear diameter was increased (P < 0.001) compared with that for BMI in matched control subjects but was appropriate for BMI before surgery.
  
  
  CONCLUSIONS
  We conclude that post-GBS hypoglycemia is not due to increases in beta-cell mass or formation. Rather, postprandial hypoglycemia after GBS is due to a combination of gastric dumping and inappropriately increased insulin secretion, either as a failure to adaptively decrease insulin secretion after GBS or as an acquired phenomenon.
authors.affiliation: Larry Hillblom Islet Research Center, UCLA David Geffen School of Medicine, 24-130 Warren Hall, 900 Veteran Ave., Los Angeles, CA 90095-7073, USA.
authors.forename: Juris J
authors.initials: JJ
authors.lastname: Meier
authors.forename: Alexandra E
authors.initials: AE
authors.lastname: Butler
authors.forename: Ryan
authors.initials: R
authors.lastname: Galasso
authors.forename: Peter C
authors.initials: PC
authors.lastname: Butler
mesh_terms: D000328:Adult; D015992:Body Mass Index; D002467:Cell Nucleus / Q000648:ultrastructure; D048429:Cell Size; D004377:Dumping Syndrome / Q000209:etiology; D005260:Female; D015390:Gastric Bypass / Q000009:adverse effects*; D006801:Humans; D006946:Hyperinsulinism / Q000209:etiology*; D006965:Hyperplasia; D007003:Hypoglycemia / Q000209:etiology*; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000166:cytology*; D007515:Islets of Langerhans / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009767:Obesity, Morbid / Q000601:surgery*
chemical_list: D007328:Insulin