Differential effects of high fat diet and diet-induced obesity on skeletal acquisition in female C57BL/6J vs. FVB/NJ Mice.
Differential effects of high fat diet and diet-induced obesity on skeletal acquisition in female C57BL/6J vs. FVB/NJ Mice.
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DOI：
10.1016/j.bonr.2018.04.003
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发表时间：
2018-06
期刊：
影响因子：
2.5
通讯作者：
Bouxsein ML
中科院分区：
文献类型：
--
作者：
Devlin MJ;Robbins A;Cosman MN;Moursi CA;Cloutier AM;Louis L;Van Vliet M;Conlon C;Bouxsein ML
肥胖对骨代谢的影响是复杂的，可能是由高脂肪饮食和/或肥胖引起的代谢失调介导的。为了验证高脂肪饮食和饮食诱导的代谢疾病都能单独降低骨骼获得的假设，我们比较了高脂肪饮食对两种小鼠品系的骨量和微结构的影响：饮食诱导肥胖（DIO）易感的C57BL/6J （B6）和饮食诱导肥胖耐药的FVB/NJ （FVB）。在3周龄时，我们将120只雌性FVB和B6小鼠断奶，饲喂正常（N, 10% Kcal/fat）或高频（45% Kcal/fat）日粮，并在6、12和20 周龄时对它们实施安乐死（N = 10/grp）。结果包括体重；通过DXA测定脂肪百分比和全身骨密度（WBBMD, g/cm2）；μCT显示股骨中段和远端皮质骨和骨小梁骨结构；通过组织形态测定法测定骨髓脂肪。在FVB HF中，体质量、体脂率、WBBMD和骨髓脂肪与N相比没有差异，但HF与N相比，仅在6周龄时骨小梁骨量较低（p < 0.05），仅在12周龄时骨皮质几何特性较低，仅在20周龄时骨强度较低（p < 0.05）。相比之下，B6 HF的体质量、体脂率和瘦素高于N。B6 HF在9和12周龄时的WBBMD也高于N (p < 0.05)，但在12周龄时的股骨远端小梁骨量低于N (p < 0.05)，20周龄时的低体质量调节的皮质骨特性也低于N （p < 0.05）。B6 HF小鼠的骨髓脂肪也明显高于n。总体而言，HF饮食对两种品系的骨量均有负面影响，但对B6小鼠的骨小梁微结构和骨髓脂肪的损害比FVB小鼠更大。这些数据表明，除了脂肪消耗本身，对高脂肪饮食的代谢反应独立地改变了肥胖患者的骨骼获得。高脂肪饮食会导致肥胖易感小鼠的代谢功能障碍和骨质流失。高脂肪饮食的抗肥胖小鼠几乎没有代谢或骨骼变化。饮食引起的肥胖和代谢性疾病会减少小鼠的骨骼获得。
The effects of obesity on bone metabolism are complex, and may be mediated by consumption of a high fat diet and/or by obesity-induced metabolic dysregulation. To test the hypothesis that both high fat (HF) diet and diet-induced metabolic disease independently decrease skeletal acquisition, we compared effects of HF diet on bone mass and microarchitecture in two mouse strains: diet-induced obesity (DIO)-susceptible C57BL/6J (B6) and DIO-resistant FVB/NJ (FVB). At 3 wks of age we weaned 120 female FVB and B6 mice onto normal (N, 10% Kcal/fat) or HF diet (45% Kcal/fat) and euthanized them at 6, 12 and 20 weeks of age (N = 10/grp). Outcomes included body mass; percent fat and whole-body bone mineral density (WBBMD, g/cm2) via DXA; cortical and trabecular bone architecture at the midshaft and distal femur via μCT; and marrow adiposity via histomorphometry. In FVB HF, body mass, percent body fat, WBBMD and marrow adiposity did not differ vs. N, but trabecular bone mass was lower at 6 wks of age only (p < 0.05), cortical bone geometric properties were lower at 12 wks only, and bone strength was lower at 20 wks of age only in HF vs. N (p < 0.05). In contrast, B6 HF had higher body mass, percent body fat, and leptin vs. N. B6 HF also had higher WBBMD (p < 0.05) at 9 and 12 wks of age but lower distal femur trabecular bone mass at 12 wks of age, and lower body mass-adjusted cortical bone properties at 20 wks of age compared to N (p < 0.05). Marrow adiposity was also markedly higher in B6 HF vs. N. Overall, HF diet negatively affected bone mass in both strains, but was more deleterious to trabecular bone microarchitecture and marrow adiposity in B6 than in FVB mice. These data suggest that in addition to fat consumption itself, the metabolic response to high fat diet independently alters skeletal acquisition in obesity. High fat diet causes metabolic dysfunction and bone loss in obesity-prone mice. Obesity-resistant mice on high fat diet have few metabolic or skeletal changes. Diet-induced obesity and metabolic disease decrease skeletal acquisition in mice.