GIP's effect on bone metabolism is reduced by the selective GIP receptor antagonist GIP(3-30)NH2

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GIP's effect on bone metabolism is reduced by the selective GIP receptor antagonist GIP(3-30)NH2. / Gasbjerg, Laerke S.; Hartmann, Bolette; Christensen, Mikkel B.; Lanng, Amalie R.; Vilsbøll, Tina; Jorgensen, Niklas R.; Holst, Jens J.; Rosenkilde, Mette M.; Knop, Filip K.

In: Bone, Vol. 130, 115079 , 2020.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Gasbjerg, LS, Hartmann, B, Christensen, MB, Lanng, AR, Vilsbøll, T, Jorgensen, NR, Holst, JJ, Rosenkilde, MM & Knop, FK 2020, 'GIP's effect on bone metabolism is reduced by the selective GIP receptor antagonist GIP(3-30)NH2', Bone, vol. 130, 115079 . https://doi.org/10.1016/j.bone.2019.115079

APA

Gasbjerg, L. S., Hartmann, B., Christensen, M. B., Lanng, A. R., Vilsbøll, T., Jorgensen, N. R., Holst, J. J., Rosenkilde, M. M., & Knop, F. K. (2020). GIP's effect on bone metabolism is reduced by the selective GIP receptor antagonist GIP(3-30)NH2. Bone, 130, [115079 ]. https://doi.org/10.1016/j.bone.2019.115079

Vancouver

Gasbjerg LS, Hartmann B, Christensen MB, Lanng AR, Vilsbøll T, Jorgensen NR et al. GIP's effect on bone metabolism is reduced by the selective GIP receptor antagonist GIP(3-30)NH2. Bone. 2020;130. 115079 . https://doi.org/10.1016/j.bone.2019.115079

Author

Gasbjerg, Laerke S. ; Hartmann, Bolette ; Christensen, Mikkel B. ; Lanng, Amalie R. ; Vilsbøll, Tina ; Jorgensen, Niklas R. ; Holst, Jens J. ; Rosenkilde, Mette M. ; Knop, Filip K. / GIP's effect on bone metabolism is reduced by the selective GIP receptor antagonist GIP(3-30)NH2. In: Bone. 2020 ; Vol. 130.

Bibtex

@article{b586ce6f95aa43d6bffacd73256638b7,
title = "GIP's effect on bone metabolism is reduced by the selective GIP receptor antagonist GIP(3-30)NH2",
abstract = "Infusion of the incretin hormone glucose-dependent insulinotropic polypeptide (GIP) suppresses the bone resorption marker carboxy-terminal type 1 collagen crosslinks (CTX). Using separate and combined infusions of the selective GIP receptor (GIPR) antagonist, GIP(3-30)NH2, and GIP, we investigated how GIPR inhibition affects bone turnover markers. Ten healthy men (median age 22.5 years (range 21-25), BMI 21.3 kg/m(2) (19.9-24.7)) participated in a randomized, doubled blinded, placebo-controlled, crossover study with four 1 h 12 mmol/l-hyperglycemic clamps on four separate study days with concomitant infusions of GIP, GIP + GIP(3-30)NH2, GIP(3-30)NH2, and placebo, respectively, separated by a period of at least one week. GIP was infused at 1.5 pmol/kg/min and GIP(3-30)NH2 at 800 pmol/kg/min. Plasma glucose was clamped at 12.0 +/- 1.2 mmol/l and plasma levels of GIP and GIP(3-30)NH2 amounted to similar to 80 pmol/l and similar to 50 nmol/l, respectively. GIP suppressed CTX more than placebo (baseline-subtracted AUC - 6,811 +/- 1,260 vs. - 3,012 +/- 3,018 ng/I x min, P = 0.002) and resulted in CTX values of 53 +/- 6.9% (GIP) versus 81 +/- 10% of baseline (placebo), respectively (P = 0.0006), at the end of the hyperglycemic clamp. Co-infusion of GIP and GIP(3-30)NH2 attenuated the GIP-induced CTX suppression by 51 +/- 33% (P = 0.01). The peak value of the bone formation marker N-terminal propeptide of type 1 procollagen (P1NP) peaked at higher levels during GIP (109 +/- 6.7% of baseline) than during GIP(3-30)NH2 infusion (101 +/- 8.9%) (P = 0.049) and GIP suppressed PTH levels compared to GIP(3-30)NH2 alone (P = 0.0158). In conclusion, blockade of the GIPR with GIP(3-30)NH2 diminished GIP-induced CTX and P1NP responses, showing that these effects are GIPR-mediated and that GIPR antagonism might interfere with bone resorption",
keywords = "Glucose-dependent insulinotropic polypeptide, Glucose-dependent insulinotropic polypeptide receptor antagonist, Gut-bone axis",
author = "Gasbjerg, {Laerke S.} and Bolette Hartmann and Christensen, {Mikkel B.} and Lanng, {Amalie R.} and Tina Vilsb{\o}ll and Jorgensen, {Niklas R.} and Holst, {Jens J.} and Rosenkilde, {Mette M.} and Knop, {Filip K.}",
year = "2020",
doi = "10.1016/j.bone.2019.115079",
language = "English",
volume = "130",
journal = "Bone",
issn = "8756-3282",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - GIP's effect on bone metabolism is reduced by the selective GIP receptor antagonist GIP(3-30)NH2

AU - Gasbjerg, Laerke S.

AU - Hartmann, Bolette

AU - Christensen, Mikkel B.

AU - Lanng, Amalie R.

AU - Vilsbøll, Tina

AU - Jorgensen, Niklas R.

AU - Holst, Jens J.

AU - Rosenkilde, Mette M.

AU - Knop, Filip K.

PY - 2020

Y1 - 2020

N2 - Infusion of the incretin hormone glucose-dependent insulinotropic polypeptide (GIP) suppresses the bone resorption marker carboxy-terminal type 1 collagen crosslinks (CTX). Using separate and combined infusions of the selective GIP receptor (GIPR) antagonist, GIP(3-30)NH2, and GIP, we investigated how GIPR inhibition affects bone turnover markers. Ten healthy men (median age 22.5 years (range 21-25), BMI 21.3 kg/m(2) (19.9-24.7)) participated in a randomized, doubled blinded, placebo-controlled, crossover study with four 1 h 12 mmol/l-hyperglycemic clamps on four separate study days with concomitant infusions of GIP, GIP + GIP(3-30)NH2, GIP(3-30)NH2, and placebo, respectively, separated by a period of at least one week. GIP was infused at 1.5 pmol/kg/min and GIP(3-30)NH2 at 800 pmol/kg/min. Plasma glucose was clamped at 12.0 +/- 1.2 mmol/l and plasma levels of GIP and GIP(3-30)NH2 amounted to similar to 80 pmol/l and similar to 50 nmol/l, respectively. GIP suppressed CTX more than placebo (baseline-subtracted AUC - 6,811 +/- 1,260 vs. - 3,012 +/- 3,018 ng/I x min, P = 0.002) and resulted in CTX values of 53 +/- 6.9% (GIP) versus 81 +/- 10% of baseline (placebo), respectively (P = 0.0006), at the end of the hyperglycemic clamp. Co-infusion of GIP and GIP(3-30)NH2 attenuated the GIP-induced CTX suppression by 51 +/- 33% (P = 0.01). The peak value of the bone formation marker N-terminal propeptide of type 1 procollagen (P1NP) peaked at higher levels during GIP (109 +/- 6.7% of baseline) than during GIP(3-30)NH2 infusion (101 +/- 8.9%) (P = 0.049) and GIP suppressed PTH levels compared to GIP(3-30)NH2 alone (P = 0.0158). In conclusion, blockade of the GIPR with GIP(3-30)NH2 diminished GIP-induced CTX and P1NP responses, showing that these effects are GIPR-mediated and that GIPR antagonism might interfere with bone resorption

AB - Infusion of the incretin hormone glucose-dependent insulinotropic polypeptide (GIP) suppresses the bone resorption marker carboxy-terminal type 1 collagen crosslinks (CTX). Using separate and combined infusions of the selective GIP receptor (GIPR) antagonist, GIP(3-30)NH2, and GIP, we investigated how GIPR inhibition affects bone turnover markers. Ten healthy men (median age 22.5 years (range 21-25), BMI 21.3 kg/m(2) (19.9-24.7)) participated in a randomized, doubled blinded, placebo-controlled, crossover study with four 1 h 12 mmol/l-hyperglycemic clamps on four separate study days with concomitant infusions of GIP, GIP + GIP(3-30)NH2, GIP(3-30)NH2, and placebo, respectively, separated by a period of at least one week. GIP was infused at 1.5 pmol/kg/min and GIP(3-30)NH2 at 800 pmol/kg/min. Plasma glucose was clamped at 12.0 +/- 1.2 mmol/l and plasma levels of GIP and GIP(3-30)NH2 amounted to similar to 80 pmol/l and similar to 50 nmol/l, respectively. GIP suppressed CTX more than placebo (baseline-subtracted AUC - 6,811 +/- 1,260 vs. - 3,012 +/- 3,018 ng/I x min, P = 0.002) and resulted in CTX values of 53 +/- 6.9% (GIP) versus 81 +/- 10% of baseline (placebo), respectively (P = 0.0006), at the end of the hyperglycemic clamp. Co-infusion of GIP and GIP(3-30)NH2 attenuated the GIP-induced CTX suppression by 51 +/- 33% (P = 0.01). The peak value of the bone formation marker N-terminal propeptide of type 1 procollagen (P1NP) peaked at higher levels during GIP (109 +/- 6.7% of baseline) than during GIP(3-30)NH2 infusion (101 +/- 8.9%) (P = 0.049) and GIP suppressed PTH levels compared to GIP(3-30)NH2 alone (P = 0.0158). In conclusion, blockade of the GIPR with GIP(3-30)NH2 diminished GIP-induced CTX and P1NP responses, showing that these effects are GIPR-mediated and that GIPR antagonism might interfere with bone resorption

KW - Glucose-dependent insulinotropic polypeptide

KW - Glucose-dependent insulinotropic polypeptide receptor antagonist

KW - Gut-bone axis

U2 - 10.1016/j.bone.2019.115079

DO - 10.1016/j.bone.2019.115079

M3 - Journal article

C2 - 31622777

VL - 130

JO - Bone

JF - Bone

SN - 8756-3282

M1 - 115079

ER -

ID: 233585648