Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. IL-6 release from muscles during exercise is stimulated by lactate-dependent protease activity

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Effect of bariatric surgery on plasma GDF15 in humans

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Growth hormone signaling and action in obese versus lean human subjects

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Glucose and Amino Acid Metabolism in Mice Depend Mutually on Glucagon and Insulin Receptor Signaling

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  5. Paracrine Crosstalk between Intestinal L- and D-cells Controls Secretion of Glucagon-Like Peptide-1 in mice

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

Exaggerated secretion of glucagon-like peptide 1 (GLP-1) is important for postprandial glucose tolerance after Roux-en-Y gastric bypass (RYGB), whereas the role of glucose-dependent insulinotropic polypeptide (GIP) remains to be resolved. We aimed to explore the relative importance of endogenously secreted GLP-1 and GIP on glucose tolerance and beta-cell function after RYGB. We used DPP-4 inhibition to enhance concentrations of intact GIP and GLP-1 and the GLP-1 receptor antagonist exendin 9-39 (Ex-9) for specific blockage of GLP-1 actions. Twelve glucose tolerant patients were studied after RYGB in a randomized, placebo-controlled, four-day, cross-over study with standard mixed meal tests and concurrent administration of: placebo, oral sitagliptin, Ex-9 infusion or combined Ex-9/sitagliptin. GLP-1 receptor antagonism increased glucose excursions, clearly attenuated beta-cell function and aggravated postprandial hyperglucagonaemia compared with placebo, whereas sitagliptin had no effect despite 2-3-fold increased concentrations of intact GLP-1 and GIP. Similarly, sitagliptin did not affect glucose tolerance or beta-cell function during GLP-1R blockage. This study confirms the importance of GLP-1 for glucose tolerance after RYGB via increased insulin and attenuated glucagon secretion in the postprandial state, whereas amplification of the GIP signal (or other DPP-4 sensitive glucose lowering mechanisms) did not appear to contribute to the improved glucose tolerance seen after RYGB.

OriginalsprogEngelsk
TidsskriftAmerican Journal of Physiology: Endocrinology and Metabolism
Vol/bind310
Udgave nummer7
Sider (fra-til)E505-E514
ISSN0193-1849
DOI
StatusUdgivet - apr. 2016

ID: 46016504