Effects of metformin, rosiglitazone and insulin on bone metabolism in patients with type 2 diabetes
Bone Apr 19, 2018
Stage TB, et al. - Researchers evaluated if different insulin regimens, metformin and rosiglitazone influenced bone metabolism. They also sought to ascertain whether the concentration of metformin and rosiglitazone in blood or improved glycaemic control altered bone turnover. Findings suggested that the choice of insulin treatment was not influencing bone turnover markers (BTM), BTMs could be decreased with metformin treatment, and the bone resorption activity could be influenced by the improvement of glycaemic control.
Methods
- Authors conducted a 2-year clinical trial designed to investigate impacts of antidiabetic treatment in 371 T2D patients.
- They randomized the participants to short or long-acting human insulin (non-blinded) and then further randomized to metformin + placebo, rosiglitazone + placebo, metformin + rosiglitazone or placebo + placebo (blinded).
- At baseline and after 3, 12 and 24-months, fasting bone turnover markers (BTM) representing bone resorption (CTX) and formation (PINP) including HbA1c were measured.
- After 3, 6 and 9-months of treatment, experts measured the trough steady-state plasma concentrations of metformin and rosiglitazone.
- During the follow-up of the trial, relationships between treatments and BTMs were analysed in mixed-effects models that included adjustments for age, gender, BMI, renal function and repeated measures of HbA1c.
Results
- Findings suggested that BTMs increased from baseline to month 12 and remained higher at month 24, with CTX and PINP increasing 28.5% and 23.0% (all: p < 0.001), respectively.
- Results demonstrated no association of the allocation of insulin regimens with different levels of BTMs.
- An association of metformin and metformin + rosiglitazone but not rosiglitazone alone with lower bone formation (PINP) was noted.
- Authors found neither metformin nor rosiglitazone plasma concentrations to be associated with BTMs.
- They noted an inverse association of HbA1c with CTX but not with P1NP.
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