title: Patients with neuroglycopenia after gastric bypass surgery have exaggerated incretin and insulin secretory responses to a mixed meal.
abstract: OBJECTIVE
  Hyperinsulinemic hypoglycemia is newly recognized as a rare but important complication after Roux-en-Y gastric bypass (GB). The etiology of the syndrome and metabolic characteristics remain incompletely understood. Recent studies suggest that levels of incretin hormones are increased after GB and may promote excessive beta-cell function and/or growth.
  
  
  METHODS
  We performed a cross-sectional analysis of metabolic variables, in both the fasting state and after a liquid mixed-meal challenge, in four subject groups: 1) with clinically significant hypoglycemia [neuroglycopenia (NG)] after GB surgery, 2) with no symptoms of hypoglycemia at similar duration after GB surgery, 3) without GB similar to preoperative body mass index of the surgical cohorts, and 4) without GB similar to current body mass index of the surgical cohorts.
  
  
  RESULTS
  Insulin and C-peptide after the liquid mixed meal were both higher relative to the glucose level achieved in persons after GB with NG compared with asymptomatic individuals. Glucagon, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide levels were higher in both post-GB surgical groups compared with both overweight and morbidly obese persons, and glucagon-like peptide 1 was markedly higher in the group with NG. Insulin resistance, assessed by homeostasis model assessment of insulin resistance, the composite insulin sensitivity index, or adiponectin, was similar in both post-GB groups. Dumping score was also higher in both GB groups but did not discriminate between asymptomatic and symptomatic patients. Notably, the frequency of asymptomatic hypoglycemia after a liquid mixed meal was high in post-GB patients.
  
  
  CONCLUSIONS
  A robust insulin secretory response was associated with postprandial hypoglycemia in patients after GB presenting with NG. Increased incretin levels may contribute to the increased insulin secretory response.
authors: Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02215, USA. allison.goldfine@joslin.harvard.edu
authors: A B
authors: AB
authors: Goldfine
authors: E C
authors: EC
authors: Mun
authors: E
authors: E
authors: Devine
authors: R
authors: R
authors: Bernier
authors: M
authors: M
authors: Baz-Hecht
authors: D B
authors: DB
authors: Jones
authors: B E
authors: BE
authors: Schneider
authors: J J
authors: JJ
authors: Holst
authors: M E
authors: ME
authors: Patti
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis / Q000378:metabolism; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D004435:Eating / Q000502:physiology*; D005260:Female; D005502:Food; D015390:Gastric Bypass / Q000009:adverse effects*; D005749:Gastric Inhibitory Polypeptide / Q000378:metabolism; D005934:Glucagon / Q000097:blood; D052216:Glucagon-Like Peptide 1 / Q000378:metabolism; D006801:Humans; D007003:Hypoglycemia / Q000209:etiology*; D054795:Incretins / Q000097:blood*; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism; D009767:Obesity, Morbid / Q000378:metabolism; D011183:Postoperative Complications / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D002096:C-Peptide; D054795:Incretins; D007328:Insulin; D005749:Gastric Inhibitory Polypeptide; D052216:Glucagon-Like Peptide 1; D005934:Glucagon