Fructose consumption does not worsen bone deficits resulting from high-fat feeding in young male rats.
Fructose consumption does not worsen bone deficits resulting from high-fat feeding in young male rats.
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DOI：
10.1016/j.bone.2016.02.004
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发表时间：
2016-04
期刊：
影响因子：
4.1
通讯作者：
Scarpace PJ
中科院分区：
文献类型：
--
作者：
Yarrow JF;Toklu HZ;Balaez A;Phillips EG;Otzel DM;Chen C;Wronski TJ;Aguirre JI;Sakarya Y;Tümer N;Scarpace PJ
高脂肪 (HF) 或高糖饮食导致的膳食诱发肥胖 (DIO) 会产生一系列有害的代谢后果，包括不利的骨骼发育。我们比较了标准啮齿动物饲料（对照）、30% 中度 HF（淀粉/无糖）饮食或 30%/40% HF/高果糖 (HF/F) 联合饮食 12 周对 8 周龄雄性 Sprague-Dawley 大鼠松质骨/皮质骨发育的影响。与对照组相比，两种高频喂养方案均降低了瘦肉/脂肪质量比，升高了循环瘦素，并降低了血清总抗氧化能力（tAOC）。两个 HF 组的股骨远端松质骨密度 (BMD) 均降低 23-34%（p<0.001），其特点是松质骨体积较低（BV/TV，p<0.01）、小梁数量较低（Tb.N，p<0.001），且与对照组相比，小梁分离增加（p<0.001）。股骨远端松质骨 BMD、BV/TV 和 Tb.N 与瘦素呈负相关，与 tAOC 呈正相关。在近端胫骨处观察到类似的松质骨缺陷，同时骨髓脂肪细胞密度增加（p<0.05），这与 BV/TV 和 Tb.N 呈负相关。 HF/F 动物还表现出较低的成骨细胞表面和减少的循环骨钙素（p<0.05）。与对照组相比，高频喂养组的皮质厚度（p<0.01）和组织矿物质密度（p<0.05）均较高，而全骨生物力学特征在各组之间没有差异。这些结果表明，“西化”的高频饮食会使骨骼未成熟的雄性大鼠的松质骨参数恶化，但不会恶化皮质骨参数，并且在高频饮食中加入果糖不会加剧骨质流失。此外，他们认为瘦素和/或氧化应激可能会影响 DIO 诱导的青少年骨骼发育的改变。
Dietary-induced obesity (DIO) resulting from high-fat (HF) or high-sugar diets produces a host of deleterious metabolic consequences including adverse bone development. We compared the effects of feeding standard rodent chow (Control), a 30% moderately HF (starch-based/sugar-free) diet, or a combined 30%/40% HF/high-fructose (HF/F) diet for 12 weeks on cancellous/cortical bone development in male Sprague-Dawley rats aged 8 weeks. Both HF feeding regimens reduced the lean/fat mass ratio, elevated circulating leptin, and reduced serum total antioxidant capacity (tAOC) when compared with Controls. Distal femur cancellous bone mineral density (BMD) was 23–34% lower in both HF groups (p<0.001) and was characterized by lower cancellous bone volume (BV/TV, p<0.01), lower trabecular number (Tb.N, p<0.001), and increased trabecular separation versus Controls (p<0.001). Cancellous BMD, BV/TV, and Tb.N were negatively associated with leptin and positively associated with tAOC at the distal femur. Similar cancellous bone deficits were observed at the proximal tibia, along with increased bone marrow adipocyte density (p<0.05), which was negatively associated with BV/TV and Tb.N. HF/F animals also exhibited lower osteoblast surface and reduced circulating osteocalcin (p<0.05). Cortical thickness (p<0.01) and tissue mineral density (p<0.05) were higher in both HF-fed groups versus Controls, while whole bone biomechanical characteristics were not different among groups. These results demonstrate that “westernized” HF diets worsen cancellous, but not cortical, bone parameters in skeletally-immature male rats and that fructose incorporation into HF diets does not exacerbate bone loss. In addition, they suggest that leptin and/or oxidative stress may influence DIO-induced alterations in adolescent bone development.