title: Changes in glucose homeostasis after Roux-en-Y gastric bypass surgery for obesity at day three, two months, and one year after surgery: role of gut peptides.
abstract: BACKGROUND
  Endocrine effects of gastric bypass (GBP) surgery for obesity on glucose homeostasis are not fully understood.
  
  
  OBJECTIVE
  The main objective of the study was to assess the changes in plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), leptin, somatostatin, glucose-dependent insulinotropic peptide, enteroglucagon, and glucagon early after GBP.
  
  
  METHODS
  Twelve obese subjects (body mass index 45.3 ± 1.9 kg/m(2)) were subjected to a liquid meal without lipids before and 3 d, 2 months, and 1 yr after GBP. Plasma concentrations of glucose, insulin, leptin, and gut peptide hormones were assessed before and for 180 min after the meal. Satiety was measured with visual analog scales. The absorption rate of acetaminophen added to the liquid meal was measured. Insulin resistance was measured by the homeostasis model assessment of insulin resistance.
  
  
  RESULTS
  All subjects lost weight (body mass index 30.3 ± 1.8 kg/m(2) at 1 yr). Fasting glucose was significantly lower on d 3 (P < 0.05). There was a progressive decrease in the homeostasis model assessment of insulin resistance after 2 months postoperatively. Postprandially, there was a progressive rise of GLP-1 and enteroglucagon and a transient increase in pancreatic glucagon release over the study period. There was a leftward shift of the time course of plasma glucose and insulin. Somatostatin release was lower on d 3 (P < 0.05) but then unchanged. The absorption rate of acetaminophen was twice as fast after GBP compared with before surgery and did not change over time. Satiety scores increased markedly postoperatively.
  
  
  CONCLUSIONS
  Both enhanced insulin sensitivity and incretin hormones, such as GLP-1, contribute to the early control of glucose homeostasis. Progressively increasing postprandial levels of enteroglucagon (oxyntomodulin) and GLP-1 facilitate weight loss and enhance insulin effectiveness.
authors.affiliation: Division of Surgery, Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, SE-182 88 Stockholm, Sweden. ylva.falken@ds.se
authors.forename: Y
authors.initials: Y
authors.lastname: Falkén
authors.forename: P M
authors.initials: PM
authors.lastname: Hellström
authors.forename: J J
authors.initials: JJ
authors.lastname: Holst
authors.forename: E
authors.initials: E
authors.lastname: Näslund
mesh_terms: D000328:Adult; D001786:Blood Glucose; D005260:Female; D005500:Follow-Up Studies; D015390:Gastric Bypass; D052216:Glucagon-Like Peptide 1 / Q000097:blood; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood* / Q000601:surgery; D013004:Somatostatin / Q000097:blood; D016896:Treatment Outcome
chemical_list: D001786:Blood Glucose; D007328:Insulin; D020738:Leptin; D013004:Somatostatin; D052216:Glucagon-Like Peptide 1