Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Case Reports
. 2010 Feb;33(2):375-7.
doi: 10.2337/dc09-1374. Epub 2009 Nov 16.

Postprandial diabetic glucose tolerance is normalized by gastric bypass feeding as opposed to gastric feeding and is associated with exaggerated GLP-1 secretion: a case report

Affiliations
Case Reports

Postprandial diabetic glucose tolerance is normalized by gastric bypass feeding as opposed to gastric feeding and is associated with exaggerated GLP-1 secretion: a case report

Carsten Dirksen et al. Diabetes Care. 2010 Feb.

Abstract

Objective: To examine after gastric bypass the effect of peroral versus gastroduodenal feeding on glucose metabolism.

Research design and methods: A type 2 diabetic patient was examined on 2 consecutive days 5 weeks after gastric bypass. A standard liquid meal was given on the first day into the bypassed gastric remnant and on the second day perorally. Plasma glucose, insulin, C-peptide, glucagon, incretin hormones, peptide YY, and free fatty acids were measured.

Results: Peroral feeding reduced 2-h postprandial plasma glucose (7.8 vs. 11.1 mmol/l) and incremental area under the glucose curve (iAUC) (0.33 vs. 0.49 mmol . l(-1) . min(-1)) compared with gastroduodenal feeding. beta-Cell function (iAUC(Cpeptide/Glu)) was more than twofold improved during peroral feeding, and the glucagon-like peptide (GLP)-1 response increased nearly fivefold.

Conclusions: Improvement in postprandial glucose metabolism after gastric bypass is an immediate and direct consequence of the gastrointestinal rearrangement, associated with exaggerated GLP-1 release and independent of changes in insulin sensitivity, weight loss, and caloric restriction.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Plasma concentrations of glucose (A), insulin (B), C-peptide (C), glucagon (D), GLP-1 (E), intact GIP (F), PYY (G), and FFAs (H) after peroral or gastroduodenal feeding in a RYGB-operated patient. Figure includes iAUC estimations. Triangles and dotted lines, peroral feeding; circles and solid lines, gastroduodenal feeding.

References

    1. Buchwald H, Avidor Y, Braunwald E, Jensen MD, Pories W, Fahrbach K, Schoelles K. Bariatric surgery: a systematic review and meta-analysis. JAMA 2004; 292: 1724– 1737 - PubMed
    1. Bose M, Oliván B, Teixeira J, Pi-Sunyer FX, Laferrère B. Do incretins play a role in the remission of type 2 diabetes after gastric bypass surgery: what are the evidence? Obes Surg 2009; 19: 217– 229 - PMC - PubMed
    1. Højberg PV, Vilsbøll T, Rabøl R, Knop FK, Bache M, Krarup T, Holst JJ, Madsbad S. Four weeks of near-normalisation of blood glucose improves the insulin response to glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide in patients with type 2 diabetes. Diabetologia 2009; 52: 199– 207 - PubMed
    1. Nauck M, Stöckmann F, Ebert R, Creutzfeldt W. Reduced incretin effect in type 2 (non-insulin-dependent) diabetes. Diabetologia 1986; 29: 46– 52 - PubMed
    1. Borg CM, le Roux CW, Ghatei MA, Bloom SR, Patel AG, Aylwin SJ. Progressive rise in gut hormone levels after Roux-en-Y gastric bypass suggests gut adaptation and explains altered satiety. Br J Surg 2006; 93: 210– 215 - PubMed

Publication types

MeSH terms