Journal of clinical & translational endocrinology · 2025
Effect of GIP and GLP-1 infusion on bone resorption in glucose intolerant, pancreatic insufficient cystic fibrosis.
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Lei Wang Shin, Chen XianYan, Zhao Lingyu, Daley Tanicia, Phillips Bradley, Rickels Michael R, Kelly Andrea, Kindler Joseph M
Аннотация
CONTEXT: Diabetes and bone disease are common in cystic fibrosis (CF) and primarily occur alongside exocrine pancreatic insufficiency (PI). "Incretins," glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), augment insulin secretion and regulate bone metabolism. In CF, PI dampens the incretin response. Loss of the insulinotropic effect of GIP in CF was recently identified, but effects on bone are unknown.
OBJECTIVE: Determine effects of incretins on bone resorption markers in adults with PI-CF.
DESIGN: Secondary analysis of a mechanistic double-blinded randomized placebo-controlled crossover trial including adults ages 18-40 years with PI-CF (n = 25).
INTERVENTION: Adults with PI-CF received either GIP (4 pmol/kg/min) or GLP-1 (1.5 pmol/kg/min) infusion, followed by double-blind randomization to either incretin or placebo infusion. Non-CF healthy controls received double-blind GIP (4 pmol/kg/min) or placebo. Serum C-terminal telopeptide (CTX), a bone resorption marker, was assessed during the infusion over 80 (GIP) or 60 (GLP-1) minutes.
MAIN OUTCOME MEASURES: CTX (mg/dL) concentrations.
RESULTS: In PI-CF, CTX decreased during GIP infusion, but not during placebo (time-by-treatment interaction P < 0.01). GLP-1 did not affect CTX. In non-CF healthy controls, time-by-treatment interaction was not significant (P = 0.23), but CTX decreased during GIP (P = 0.02) but not placebo (P = 0.47).
CONCLUSIONS: GIP evokes a bone anti-resorptive effect in people with PI-CF. Since the incretin response is perturbed in PI-CF, and an infusion of GIP lowers bone resorption, the "gut-bone axis" in CF-related bone disease requires attention.
OBJECTIVE: Determine effects of incretins on bone resorption markers in adults with PI-CF.
DESIGN: Secondary analysis of a mechanistic double-blinded randomized placebo-controlled crossover trial including adults ages 18-40 years with PI-CF (n = 25).
INTERVENTION: Adults with PI-CF received either GIP (4 pmol/kg/min) or GLP-1 (1.5 pmol/kg/min) infusion, followed by double-blind randomization to either incretin or placebo infusion. Non-CF healthy controls received double-blind GIP (4 pmol/kg/min) or placebo. Serum C-terminal telopeptide (CTX), a bone resorption marker, was assessed during the infusion over 80 (GIP) or 60 (GLP-1) minutes.
MAIN OUTCOME MEASURES: CTX (mg/dL) concentrations.
RESULTS: In PI-CF, CTX decreased during GIP infusion, but not during placebo (time-by-treatment interaction P < 0.01). GLP-1 did not affect CTX. In non-CF healthy controls, time-by-treatment interaction was not significant (P = 0.23), but CTX decreased during GIP (P = 0.02) but not placebo (P = 0.47).
CONCLUSIONS: GIP evokes a bone anti-resorptive effect in people with PI-CF. Since the incretin response is perturbed in PI-CF, and an infusion of GIP lowers bone resorption, the "gut-bone axis" in CF-related bone disease requires attention.