Clinical Department of Orthopedics and Traumatology of the Musculoskeletal System, Antoni Jurasz University Hospital in Bydgoszcz, M. Curie-Skłodowskiej 9, 85-094 Bydgoszcz, Poland.
Department of Laboratory Diagnostics, Collegium Medicum, Nicolaus Copernicus University, M. Curie-Skłodowskiej 9, 85-094 Bydgoszcz, Poland.
Int J Mol Sci. 2023 Jul 19;24(14):11629. doi: 10.3390/ijms241411629.
Oxidative stress, which promotes bone catabolism, also affects the quality of bone tissue. We aimed to assess the impact of metabolic disorders and oxidant-antioxidant imbalance associated with primary obesity on bone resorption and formation processes. Anthropometric parameters, metabolic variables, oxidative stress indicators (malondialdehyde, vitamins A and E, uric acid, superoxide dismutase, catalase, glutathione peroxidase, type 1 paraoxonase, iron-reducing plasma antioxidant power) and markers of bone turnover (type I procollagen N-terminal propeptide and the type I collagen C-terminal cross-linked telopeptide; P1NP and CTX) were assessed in 108 Polish participants. Under the influence of oxidative stress, both enzymatic and non-enzymatic defense mechanisms were stimulated in obese subjects, especially in women, who had increased lipid peroxidation and activity of catalase (particularly in first-degree obesity) and decreased vitamin E concentration. The process of lipid peroxidation, as well as the weakening of the bone formation, was strongly manifested in women at a BMI range of 35.0-39.9 kg/m but not at BMI > 40.0 kg/m, but it had a comprehensive negative impact on bone turnover in obese men. Obesity and its degree of advancement significantly affected the decrease in the concentration of the marker of bone formation-P1NP-only in the plasma of women. Excessive body weight had no effect on the value of the bone resorption marker in plasma, regardless of gender. Our results confirm the existence of the "obesity paradox" in the aspect of bone tissue metabolism and suggest that a specific body weight threshold changed the molecular response of the tissue.
氧化应激会促进骨分解代谢，也会影响骨组织质量。我们旨在评估与原发性肥胖相关的代谢紊乱和氧化还原失衡对骨吸收和形成过程的影响。在 108 名波兰参与者中评估了人体测量参数、代谢变量、氧化应激指标（丙二醛、维生素 A 和 E、尿酸、超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、1 型对氧磷酶、还原型血浆抗氧化能力）和骨转换标志物（I 型前胶原 N 端前肽和 I 型胶原 C 端交联肽；P1NP 和 CTX）。在肥胖人群中，氧化应激的影响下，酶和非酶防御机制均被激活，尤其是女性，其脂质过氧化和过氧化氢酶活性增加（尤其是在一度肥胖中），维生素 E 浓度降低。脂质过氧化过程以及骨形成的减弱在 BMI 范围为 35.0-39.9kg/m2 的女性中表现得尤为明显，但在 BMI>40.0kg/m2 的女性中则不然，但它对肥胖男性的骨转换有全面的负面影响。肥胖及其严重程度显著影响女性血浆中骨形成标志物 P1NP 的浓度下降。无论性别如何，超重对血浆中骨吸收标志物的价值均没有影响。我们的结果证实了在骨组织代谢方面存在“肥胖悖论”，表明特定的体重阈值改变了组织的分子反应。
