Associations between postprandial gut hormones and markers of bone remodeling

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Dokumenter

  • Nina Wittorff Jensen
  • Kim Katrine Bjerring Clemmensen
  • Marie Møller Jensen
  • Hanne Pedersen
  • Kristine Færch
  • Lars Jorge Diaz
  • Jonas Salling Quist
  • Størling, Joachim

Gut‐derived hormones have been suggested to play a role in bone homeostasis following food intake, although the associations are highly complex and not fully understood. In a random-ized, two‐day cross‐over study on 14 healthy individuals, we performed postprandial time‐course studies to examine the associations of the bone remodeling markers carboxyl‐terminal collagen type I crosslinks (CTX) and procollagen type 1 N‐terminal propeptide (P1NP) with the gut hormones glucose‐dependent insulinotropic polypeptide (GIP), glucagon‐like peptide 1 (GLP‐1), and peptide YY (PYY) using two different meal types—a standardized mixed meal (498 kcal) or a granola bar (260 kcal). Plasma concentrations of total GIP, total GLP‐1, total PYY, CTX, and P1NP were measured up to 240 min after meal intake, and the incremental area under the curve (iAUC) for each marker was calculated. The iAUC of CTX and P1NP were used to assess associations with the iAUC of GIP, GLP‐1, and PYY in linear mixed effect models adjusted for meal type. CTX was positively associated with GIP and GLP‐1, and it was inversely associated with PYY (all p < 0.001). No associations of P1NP with GIP or GLP‐1 and PYY were found. In conclusion, the postprandial responses of the gut hormones GIP, GLP‐1, and PYY are associated with the bone resorption marker CTX, supporting a link between gut hormones and bone homeostasis following food intake.

OriginalsprogEngelsk
Artikelnummer3197
TidsskriftNutrients
Vol/bind13
Udgave nummer9
Antal sider9
ISSN2072-6643
DOI
StatusUdgivet - 2021

Bibliografisk note

Funding Information:
Funding: The study was funded by a grant from The Novo Nordisk Foundation (grant number: NNF17OC0027822).

Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.

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