Glucose-dependent insulinotropic polypeptide receptor knockout mice have altered bone turnover

Ding Xie, Hua Cheng, Mark Hamrick, Qing Zhong, Ke Hong Ding, Daniel Correa, Sandra Williams, Anthony Mulloy, Wendy Bollag, Roni J. Bollag, Royce R. Runner, James C. McPherson, Karl Insogna, Carlos M. Isales

Research output: Contribution to journalArticle

117 Scopus citations

Abstract

Glucose-dependent insulinotropic polypeptide (GIP) is an incretin hormone, which is secreted from endocrine cells in the small intestine after meal ingestion. GIP has been shown to affect osteoblastic function in vitro; however, the in vivo effects of GIP on bone remodeling remain unclear. In the present study, we investigated the role of GIP in modulating bone turnover, by evaluating serum markers of bone turnover, bone density, bone morphology, and changes in biomechanical bone strength over time (one to five months) in GIP receptor knockout mice (GIPR-/- mice). The GIPR-/- mice showed a decreased bone size, lower bone mass, altered bone microarchitecture and biomechanical properties, and altered parameters for bone turnover, especially in bone formation. Moreover, the effects of GIP on bone mass were site-specific and compensatory mechanism developed over time and ameliorated the impact of the loss of GIP signaling on bone mass. Further, GIPR-/- mice had earlier age-related changes than wild-type mice in body composition, including bone mass, lean body mass, and fat percentage. In summary, our results indicate that GIP has an anabolic effect on bone mass and bone quality and suggests that GIP may be a hormonal link between nutrient ingestion and utilization.

Original languageEnglish (US)
Pages (from-to)759-769
Number of pages11
JournalBone
Volume37
Issue number6
DOIs
StatePublished - Dec 1 2005

Keywords

  • GIP
  • Gastric inhibitory peptide
  • Hormones
  • Incretin
  • Nutrition

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Histology

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