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Glucose-dependent Insulinotropic Polypeptide (GIP) reduces bone resorption in patients with type 2 diabetes

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@article{2e037dbaa36f43999f31b8812cad3f62,
title = "Glucose-dependent Insulinotropic Polypeptide (GIP) reduces bone resorption in patients with type 2 diabetes",
abstract = "Context: In healthy individuals, glucose-dependent insulinotropic polypeptide (GIP) enhances insulin secretion and reduces bone resorption by up to 25% estimated by absolute placebo-corrected changes in carboxy-terminal type 1 collagen crosslinks (CTX) during GIP and glucose administration. In patients with type 2 diabetes (T2D), GIP's insulinotropic effect is impaired and effects on bone may be reduced. Objective: To investigate GIP's effect on bone biomarkers in patients with T2D. Design: Randomized, double-blinded, crossover study investigating 6 interventions. Patients: Twelve male patients with T2D. Interventions: A primed continuous 90-minute GIP infusion (2 pmol/kg/min) or matching placebo (saline) administered at 3 plasma glucose (PG) levels (i.e., paired days with “insulin-induced hypoglycemia” (PG lowered to 3 mmol/L), “fasting hyperglycemia” (mean PG ~8 mmol/L), or “aggravated hyperglycemia” (mean PG ~12 mmol/L). Main Outcome Measures: Bone biomarkers: CTX, procollagen type 1 N-terminal propeptide (P1NP) and PTH. Results: On days with insulin-induced hypoglycemia, CTX was suppressed by up to 40 ± 15% during GIP administration compared with 12 ± 11% during placebo infusion (P < 0.0001). On days with fasting hyperglycemia, CTX was suppressed by up to 36 ± 15% during GIP administration, compared with 0 ± 9% during placebo infusion (P < 0.0001). On days with aggravated hyperglycemia, CTX was suppressed by up to 47 ± 23% during GIP administration compared with 10 ± 9% during placebo infusion (P = 0.0005). At all glycemic levels, P1NP and PTH concentrations were similar between paired days after 90 minutes. Conclusions: Short-term GIP infusions reduce bone resorption by more than one-third (estimated by absolute placebo-corrected CTX reductions) in patients with T2DM, suggesting preserved bone effects of GIP in these patients. Pr{\'e}cis: Short-term GIP infusions reduce the bone resorption marker CTX by one-third in patients with type 2 diabetes independent of glycemic levels.",
keywords = "Bone markers, Carboxy-terminal collagen type 1 crosslinks (CTX), Gastric inhibitory polypeptide, Glucose-dependent insulinotropic polypeptide (GIP), Procollagen type 1 N-terminal propeptide (P1NP)",
author = "Christensen, {Mikkel B} and Lund, {Asger B} and J{\o}rgensen, {Niklas R} and Holst, {Jens J} and Tina Vilsb{\o}ll and Knop, {Filip K}",
note = "{\textcopyright} Endocrine Society 2020.",
year = "2020",
month = sep,
day = "1",
doi = "10.1210/jendso/bvaa097",
language = "English",
volume = "4",
pages = "bvaa097",
journal = "Journal of the Endocrine Society",
issn = "2472-1972",
publisher = "Endocrine Society",
number = "9",

}

RIS

TY - JOUR

T1 - Glucose-dependent Insulinotropic Polypeptide (GIP) reduces bone resorption in patients with type 2 diabetes

AU - Christensen, Mikkel B

AU - Lund, Asger B

AU - Jørgensen, Niklas R

AU - Holst, Jens J

AU - Vilsbøll, Tina

AU - Knop, Filip K

N1 - © Endocrine Society 2020.

PY - 2020/9/1

Y1 - 2020/9/1

N2 - Context: In healthy individuals, glucose-dependent insulinotropic polypeptide (GIP) enhances insulin secretion and reduces bone resorption by up to 25% estimated by absolute placebo-corrected changes in carboxy-terminal type 1 collagen crosslinks (CTX) during GIP and glucose administration. In patients with type 2 diabetes (T2D), GIP's insulinotropic effect is impaired and effects on bone may be reduced. Objective: To investigate GIP's effect on bone biomarkers in patients with T2D. Design: Randomized, double-blinded, crossover study investigating 6 interventions. Patients: Twelve male patients with T2D. Interventions: A primed continuous 90-minute GIP infusion (2 pmol/kg/min) or matching placebo (saline) administered at 3 plasma glucose (PG) levels (i.e., paired days with “insulin-induced hypoglycemia” (PG lowered to 3 mmol/L), “fasting hyperglycemia” (mean PG ~8 mmol/L), or “aggravated hyperglycemia” (mean PG ~12 mmol/L). Main Outcome Measures: Bone biomarkers: CTX, procollagen type 1 N-terminal propeptide (P1NP) and PTH. Results: On days with insulin-induced hypoglycemia, CTX was suppressed by up to 40 ± 15% during GIP administration compared with 12 ± 11% during placebo infusion (P < 0.0001). On days with fasting hyperglycemia, CTX was suppressed by up to 36 ± 15% during GIP administration, compared with 0 ± 9% during placebo infusion (P < 0.0001). On days with aggravated hyperglycemia, CTX was suppressed by up to 47 ± 23% during GIP administration compared with 10 ± 9% during placebo infusion (P = 0.0005). At all glycemic levels, P1NP and PTH concentrations were similar between paired days after 90 minutes. Conclusions: Short-term GIP infusions reduce bone resorption by more than one-third (estimated by absolute placebo-corrected CTX reductions) in patients with T2DM, suggesting preserved bone effects of GIP in these patients. Précis: Short-term GIP infusions reduce the bone resorption marker CTX by one-third in patients with type 2 diabetes independent of glycemic levels.

AB - Context: In healthy individuals, glucose-dependent insulinotropic polypeptide (GIP) enhances insulin secretion and reduces bone resorption by up to 25% estimated by absolute placebo-corrected changes in carboxy-terminal type 1 collagen crosslinks (CTX) during GIP and glucose administration. In patients with type 2 diabetes (T2D), GIP's insulinotropic effect is impaired and effects on bone may be reduced. Objective: To investigate GIP's effect on bone biomarkers in patients with T2D. Design: Randomized, double-blinded, crossover study investigating 6 interventions. Patients: Twelve male patients with T2D. Interventions: A primed continuous 90-minute GIP infusion (2 pmol/kg/min) or matching placebo (saline) administered at 3 plasma glucose (PG) levels (i.e., paired days with “insulin-induced hypoglycemia” (PG lowered to 3 mmol/L), “fasting hyperglycemia” (mean PG ~8 mmol/L), or “aggravated hyperglycemia” (mean PG ~12 mmol/L). Main Outcome Measures: Bone biomarkers: CTX, procollagen type 1 N-terminal propeptide (P1NP) and PTH. Results: On days with insulin-induced hypoglycemia, CTX was suppressed by up to 40 ± 15% during GIP administration compared with 12 ± 11% during placebo infusion (P < 0.0001). On days with fasting hyperglycemia, CTX was suppressed by up to 36 ± 15% during GIP administration, compared with 0 ± 9% during placebo infusion (P < 0.0001). On days with aggravated hyperglycemia, CTX was suppressed by up to 47 ± 23% during GIP administration compared with 10 ± 9% during placebo infusion (P = 0.0005). At all glycemic levels, P1NP and PTH concentrations were similar between paired days after 90 minutes. Conclusions: Short-term GIP infusions reduce bone resorption by more than one-third (estimated by absolute placebo-corrected CTX reductions) in patients with T2DM, suggesting preserved bone effects of GIP in these patients. Précis: Short-term GIP infusions reduce the bone resorption marker CTX by one-third in patients with type 2 diabetes independent of glycemic levels.

KW - Bone markers

KW - Carboxy-terminal collagen type 1 crosslinks (CTX)

KW - Gastric inhibitory polypeptide

KW - Glucose-dependent insulinotropic polypeptide (GIP)

KW - Procollagen type 1 N-terminal propeptide (P1NP)

UR - http://www.scopus.com/inward/record.url?scp=85096490416&partnerID=8YFLogxK

U2 - 10.1210/jendso/bvaa097

DO - 10.1210/jendso/bvaa097

M3 - Journal article

C2 - 32904711

VL - 4

SP - bvaa097

JO - Journal of the Endocrine Society

JF - Journal of the Endocrine Society

SN - 2472-1972

IS - 9

M1 - bvaa097

ER -

ID: 60904969