HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Hyperinsulinemic hypoglycemia after gastric bypass surgery is not accompanied by islet hyperplasia or increased beta-cell turnover.

AbstractOBJECTIVE:
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.
RESEARCH DESIGN AND 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.
AuthorsJuris J Meier, Alexandra E Butler, Ryan Galasso, Peter C Butler
JournalDiabetes care (Diabetes Care) Vol. 29 Issue 7 Pg. 1554-9 (Jul 2006) ISSN: 0149-5992 [Print] United States
PMID16801578 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References
  • Insulin
Topics
  • Adult
  • Body Mass Index
  • Cell Nucleus (ultrastructure)
  • Cell Size
  • Dumping Syndrome (etiology)
  • Female
  • Gastric Bypass (adverse effects)
  • Humans
  • Hyperinsulinism (etiology)
  • Hyperplasia
  • Hypoglycemia (etiology)
  • Insulin (metabolism)
  • Insulin Secretion
  • Insulin-Secreting Cells (cytology)
  • Islets of Langerhans (pathology)
  • Male
  • Middle Aged
  • Obesity, Morbid (surgery)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: