Background: Bone turnover markers (BTMs) are suppressed following a glucose load. Here we examined whether in vivo exercise can attenuate the suppressive effect of glucose on BTMs in pre and post-menopausal women. We also examined the direct effect of glucose and insulin on osteoblast apoptosis, viability and alkaline phosphatase (ALP) activity in vitro.
Methods: In vivo: Eight premenopausal women (age=36.1±2.7years, BMI=25.5±0.8, SEM) and 10 postmenopausal women (age=62.8±2.6 years, BMI=28.3±1.3 kg·m−2) had an oral glucose tolerance test (OGTT) at rest and 60 min post-exercise (30 min cycling at 7075% of the pre-determined VO2peak). Blood samples were analysed for serum insulin, glucose, total osteocalcin (tOC), undercarboxylated OC (ucOC), procollagen type I N-terminal propeptide (PINP) and β-isomerised C-terminal telopeptides (β-CTx). In vitro: Cultured human osteoblasts (HOBs) were treated for 2 hours with increasing glucose concentrations with or without insulin. HOBs apoptosis, viability and ALP activity were measured.
Results: In both rest and exercise trials, tOC, P1NP and β-CTx were significantly suppressed following OGTT, in both pre and post-menopausal women (8%-14%, p<0.05). In post-menopausal women, ucOC was significantly reduced following OGTT, with rest and exercise, compared with baseline despite a significant increase in ucOC post-exercise (~9%, p<0.05). In pre-menopausal women, OGTT did not suppress ucOC while exercise significantly increased ucOC (~14, p=0.039). Exercise had no significant effect on other BTMs. HOBs apoptosis was higher and viability and ALP activity were lower when cells were treated with 10 and 20 mmol/L D-glucose, compared with 5 mmol/L (all p<0.05). Importantly, insulin had a protective effect on all test parameters.
Conclusions: Glucose-load suppresses BTMs in pre and post-menopausal women and acute cycling exercise did not prevent the suppressive effect. BTMs are suppressed due to the higher glucose levels, and not insulin, perhaps due to increase osteoblast apoptosis and a reduction in osteoblast viability.
Disclosure: The authors declared no competing interests. Dr Levinger was supported by Future Leader Fellowship from the National Heart Foundation of Australia; Dr Brennan-Speranza was supported by an NHMRC Early Career Fellowship. This study was partly funded by the LEW Carty Charitable Foundation.