高胰岛素-血糖钳夹和运动对肥胖男性骨重塑标志物的影响。

BoneKEy reports Pub Date : 2015-08-26 eCollection Date: 2015-01-01 DOI:10.1038/bonekey.2015.100
Itamar Levinger, Tara C Brennan-Speranza, George Jerums, Nigel K Stepto, Fabio R Serpiello, Glenn K McConell, Mitchell Anderson, David L Hare, Elizabeth Byrnes, Peter R Ebeling, Ego Seeman
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引用次数: 12

摘要

骨重塑标志物(BRMs)在葡萄糖负荷和葡萄糖输注过程中被抑制。由于运动增加了骨骼健康指数并改善了葡萄糖处理,我们假设,在休息时,高胰岛素-血糖钳钳会抑制肥胖男性的brm,而在钳钳之前的运动可以防止这种抑制。11名肥胖非糖尿病男性(年龄58.1±2.2岁,体重指数=33.1±1.4 kg m(-2平均值±s.e.m))在休息时(对照组)和运动后60分钟(4次× 4分钟骑行,95%危险比)患有高胰岛素血症-血糖钳夹(HEC)。分析血液样本的血清胰岛素、葡萄糖、骨形成标志物、总骨钙素(tOC)和前胶原1型n端前肽(P1NP),以及骨吸收标志物β-异构c端端肽(β-CTx)。在对照试验(无运动)中,tOC、P1NP和β-CTx随HEC下降,与基线相比下降>10%
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The effect of hyperinsulinaemic-euglycaemic clamp and exercise on bone remodeling markers in obese men.

Bone remodelling markers (BRMs) are suppressed following a glucose load and during glucose infusion. As exercise increases indices of bone health and improves glucose handling, we hypothesised that, at rest, hyperinsulinaemic-euglycaemic clamp will suppress BRMs in obese men and that exercise prior to the clamp will prevent this suppression. Eleven obese nondiabetic men (age 58.1±2.2 years, body mass index=33.1±1.4 kg m(-2) mean±s.e.m.) had a hyperinsulinaemic-euglycaemic clamp (HEC) at rest (Control) and 60 min post exercise (four bouts × 4 min cycling at 95% of hazard ratiopeak). Blood samples were analysed for serum insulin, glucose, bone formation markers, total osteocalcin (tOC) and procollagen type 1 N-terminal propeptide (P1NP), and the bone resorption marker, β-isomerised C-terminal telopeptides (β-CTx). In the control trial (no exercise), tOC, P1NP and β-CTx decreased with HEC by >10% compared with baseline (P<0.05). Fasting serum glucose, but not insulin, tended to correlate negatively with the BRMs (β range -0.57 to -0.66, p range 0.051-0.087). β-CTx, but not OC or P1NP, increased within 60 min post exercise (∼16%, P<0.01). During the post-exercise HEC, the glucose infusion rate was ∼30% higher compared with the no exercise trial. Despite this, BRMs were only suppressed to a similar extent as in the control session (10%). HEC suppressed BRMs in obese men. Exercise did not prevent this suppression of BRMs by HEC but improved glucose handling during the trial. It remains to be tested whether an exercise intervention of longer duration may be able to prevent the effect of HEC on bone remodelling.

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