Xijie Yu, MD, PhD. Laboratory of Endocrinology and Metabolism, Department of Endocrinology, West China Hospital, Sichuan University, No. 37 Guoxue Xiang, 610041 Chengdu, P.R. China, E-mail:
J Nutr Health Aging. 2018;22(3):361-370. doi: 10.1007/s12603-017-0933-0.
To compare the effects of high-fat diet (HFD) and high-fructose diet (HFrD) on bone metabolism at different time points, dynamically observe the bone histology and femur trabecular micro-architecture, and analyze the underlying mechanisms.
Sixty -Five male 6- to 7-week-old C57BL/6J mice were given HFD, HFrD, or standard diets (SD) for 8, 16, and 24 weeks. Micro-computed tomography (μCT) and bone histology were used to measure bone mass and trabecular micro-structure. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of genes related to bone and lipid metabolisms.
Compared to SD mice, femoral trabecular bone mass was significantly increased in both HFrD mice and HFD mice at 8 weeks, it continued to be higher in HFrD mice at 16 and 24 weeks with the highest level at 16 weeks, but it was significantly decreased in HFD mice at 16 and 24 weeks. HFD mice showed more epididymal fat accumulation than HFrD mice. mRNA expression of Runx2 was up-regulated at 8 and 16 weeks, but down-regulated at 24 weeks similarly in both HFrD mice and HFD mice. mRNA expression of MMP9 and CTSK was up-regulated at 8 and 16 weeks in HFD mice, but down-regulated at 24 weeks in both HFrD mice and HFD mice.
Our data indicated that the HFrD and HFD had different modulating effects on bone mass. After short-term feeding, both HFrD and HFD showed positive effects on bone mass; however, after long-term feeding, bone mass was decreased in HFD mice. In contrast, the bone mass was first increased and then decreased in the HFrD mice. On the basis of these findings, we speculated that chronic consumption of fat and fructose would exert detrimental effects on bone mass which might a combination action of body mass, fat mass, and bone formation/bone resorption along with proinflammatory factor and bone marrow environment.
比较高脂肪饮食（HFD）和高果糖饮食（HFrD）在不同时间点对骨代谢的影响，动态观察骨组织学和股骨小梁微结构，并分析其潜在机制。
将 65 只 6 至 7 周龄雄性 C57BL/6J 小鼠分别给予 HFD、HFrD 或标准饮食（SD）8、16 和 24 周。采用微计算机断层扫描（μCT）和骨组织学方法测量骨量和小梁微结构。采用定量实时聚合酶链反应（qRT-PCR）测定与骨和脂代谢相关基因的表达。
与 SD 组小鼠相比，HFrD 组和 HFD 组小鼠的股骨小梁骨量在 8 周时均显著增加，HFrD 组在 16 周和 24 周时持续增加，在 16 周时达到最高水平，而 HFD 组在 16 周和 24 周时则显著减少。HFD 组小鼠附睾脂肪堆积较 HFrD 组明显。Runx2mRNA 表达在 8 周和 16 周时上调，但在 24 周时两组均下调。HFD 组小鼠 MMP9 和 CTSKmRNA 表达在 8 周和 16 周时上调，但在 24 周时两组均下调。
我们的数据表明，HFrD 和 HFD 对骨量有不同的调节作用。短期喂养后，HFrD 和 HFD 均对骨量有积极影响；但长期喂养后，HFD 组骨量减少。相比之下，HFrD 组的骨量先增加后减少。基于这些发现，我们推测长期摄入脂肪和果糖会对骨量产生不利影响，这可能是体重、脂肪量、骨形成/骨吸收以及促炎因子和骨髓环境共同作用的结果。
