Pleiotropic effects of GIP on islet function involve osteopontin

Research output: Contribution to journalJournal articleResearchpeer-review

  • Valeriya Lyssenko
  • Lena Eliasson
  • Olga Kotova
  • Kasper Pilgaard
  • Nils Wierup
  • Albert Salehi
  • Anna Wendt
  • Yang Z De Marinis
  • Lisa M Berglund
  • Jalal Taneera
  • Alexander Balhuizen
  • Ola Hansson
  • Peter Osmark
  • Pontus Dunér
  • Charlotte Brøns
  • Alena Stancáková
  • Johanna Kuusisto
  • Marco Bugliani
  • Richa Saxena
  • Emma Ahlqvist
  • Timothy J Kieffer
  • Tiinamaija Tuomi
  • Bo Isomaa
  • Olle Melander
  • Emily Sonestedt
  • Marju Orho-Melander
  • Peter Nilsson
  • Sara Bonetti
  • Riccardo Bonadonna
  • Roberto Miccoli
  • Stefano Delprato
  • Piero Marchetti
  • Pernille Poulsen
  • Markku Laakso
  • Maria F Gomez
  • Leif Groop
The incretin hormone GIP (glucose-dependent insulinotropic polypeptide) promotes pancreatic β-cell function by potentiating insulin secretion and β-cell proliferation. Recently, a combined analysis of several genome-wide association studies (Meta-analysis of Glucose and Insulin-Related Traits Consortium [MAGIC]) showed association to postprandial insulin at the GIP receptor (GIPR) locus. Here we explored mechanisms that could explain the protective effects of GIP on islet function.
Original languageEnglish
JournalDiabetes
Volume60
Issue number9
Pages (from-to)2424-33
Number of pages10
ISSN0012-1797
DOIs
Publication statusPublished - Sep 2011

    Research areas

  • Alleles, Diabetes Mellitus, Type 2, Gastric Inhibitory Polypeptide, Genome-Wide Association Study, Glucagon-Like Peptide 1, Humans, Insulin, Insulin-Secreting Cells, Islets of Langerhans, Male, Osteopontin

ID: 40176782