TY - JOUR
T1 - GIP and the gut-bone axis – Physiological, pathophysiological and potential therapeutic implications
AU - Stensen, Signe
AU - Gasbjerg, Lærke Smidt
AU - Helsted, Mads Marstrand
AU - Hartmann, Bolette
AU - Christensen, Mikkel Bring
AU - Knop, Filip Krag
PY - 2020
Y1 - 2020
N2 - The influence by gut-derived hormones on bone remodelling appears increasingly important as research on the enteroendocrine-osseous axis accelerates. Glucose-dependent insulinotropic polypeptide (GIP) is secreted from the gut and potentiates insulin secretion in a glucose-dependent manner. GIP has, like the two other gut-derived hormones, glucagon-like peptide 1 and glucagon-like peptide 2, been shown to affect bone remodelling as part of the enteroendocrine-osseous axis. Observational studies have shown that a mutation in the GIP receptor causing reduced receptor signalling leads to lower bone mineral density and increased fracture risk. Rodent as well as human studies have shown that GIP causes serum levels of the bone resorption marker carboxy-terminal type 1 collagen crosslinks to decline. GIP may also increase bone formation indicating a potential uncoupling of bone resorption and formation. Here, we review past and recent discoveries elucidating the enteroendocrine-osseous axis with a special focus on GIP.
AB - The influence by gut-derived hormones on bone remodelling appears increasingly important as research on the enteroendocrine-osseous axis accelerates. Glucose-dependent insulinotropic polypeptide (GIP) is secreted from the gut and potentiates insulin secretion in a glucose-dependent manner. GIP has, like the two other gut-derived hormones, glucagon-like peptide 1 and glucagon-like peptide 2, been shown to affect bone remodelling as part of the enteroendocrine-osseous axis. Observational studies have shown that a mutation in the GIP receptor causing reduced receptor signalling leads to lower bone mineral density and increased fracture risk. Rodent as well as human studies have shown that GIP causes serum levels of the bone resorption marker carboxy-terminal type 1 collagen crosslinks to decline. GIP may also increase bone formation indicating a potential uncoupling of bone resorption and formation. Here, we review past and recent discoveries elucidating the enteroendocrine-osseous axis with a special focus on GIP.
KW - Enteroendocrine-osseous axis
KW - GIP
KW - Gut-bone axis
U2 - 10.1016/j.peptides.2019.170197
DO - 10.1016/j.peptides.2019.170197
M3 - Review
C2 - 31715213
AN - SCOPUS:85075837309
VL - 125
JO - Peptides
JF - Peptides
SN - 0196-9781
M1 - 170197
ER -