Effects of Exogenous GIP and GLP-2 on Bone Turnover in Individuals With Type 2 Diabetes.
J Clin Endocrinol Metab
; 109(7): 1773-1780, 2024 Jun 17.
Article
in En
| MEDLINE
| ID: mdl-38217866
ABSTRACT
CONTEXT Individuals with type 2 diabetes (T2D) have an increased risk of bone fractures despite normal or increased bone mineral density. The underlying causes are not well understood but may include disturbances in the gut-bone axis, in which both glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-2 (GLP-2) are regulators of bone turnover. Thus, in healthy fasting participants, both exogenous GIP and GLP-2 acutely reduce bone resorption. OBJECTIVE:
The objective of this study was to investigate the acute effects of subcutaneously administered GIP and GLP-2 on bone turnover in individuals with T2D.METHODS:
We included 10 men with T2D. Participants met fasting in the morning on 3 separate test days and were injected subcutaneously with GIP, GLP-2, or placebo in a randomized crossover design. Blood samples were drawn at baseline and regularly after injections. Bone turnover was estimated by circulating levels of collagen type 1 C-terminal telopeptide (CTX), procollagen type 1 N-terminal propeptide (P1NP), sclerostin, and PTH.RESULTS:
GIP and GLP-2 significantly reduced CTX to (mean ± SEM) 66 ± 7.8% and 74 ± 5.9% of baseline, respectively, compared with after placebo (P = .001). In addition, P1NP and sclerostin increased acutely after GIP whereas a decrease in P1NP was seen after GLP-2. PTH levels decreased to 67 ± 2.5% of baseline after GLP-2 and to only 86 ± 3.4% after GIP.CONCLUSION:
Subcutaneous GIP and GLP-2 affect CTX and P1NP in individuals with T2D to the same extent as previously demonstrated in healthy individuals.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Gastric Inhibitory Polypeptide
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Bone Remodeling
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Cross-Over Studies
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Diabetes Mellitus, Type 2
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Glucagon-Like Peptide 2
Type of study:
Clinical_trials
Limits:
Adult
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Aged
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Humans
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Male
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Middle aged
Language:
En
Journal:
J Clin Endocrinol Metab
Year:
2024
Document type:
Article
Affiliation country: