Maternal high-fat high-sugar diet impairs bone quality and strength but not cartilage in aging mice.

IF 2.1 3区 医学 Q2 ORTHOPEDICS
Arin K Oestreich, Natalia S Harasymowicz, Alireza Savadipour, Zainab Harissa, Neda Rashidi, Meredith K Luhmann, Mohammed Kuziez, Kelle H Moley, Farshid Guilak
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引用次数: 0

Abstract

Osteoarthritis (OA) is a prevalent aging disorder of synovial joints and recent work suggests that a parental high-fat diet increases OA severity following joint injury in offspring. We hypothesized that a maternal high-fat high-sugar (HFHS) diet would promote spontaneous osteoarthritis-related cartilage and bone changes in 1-year-old offspring. Female C57BL/6 J mice were placed on either a chow control or HFHS diet for 6 weeks before mating to a chow-fed C57BL/6 J male and maintained on their assigned diets throughout pregnancy and lactation. Male and female offspring were weaned onto a chow diet, raised to 1 year of age, and evaluated for cartilage and bone changes indicative of OA. However, offspring did not show early signs of OA as measured by histological Mankin scoring, mechanical testing of the pericellular matrix, histological synovitis scoring, or subchondral bone thickening as measured by microcomputed Tomography. On the other hand, male offspring from HFHS-fed dams had reduced trabecular bone quality in the tibial metaphysis and decreased cortical thickness. Although maternal HFHS diet did not impact trabecular or cortical bone quality in tibias of female offspring, the radii of these animals had decreased cortical thickness, increased medullary area, and impaired breaking strength compared to those of control-fed dams. Finally, we evaluated bone quality and strength in male and female F2 offspring and found that the grandmaternal diet modestly impacted radial bone geometry but not strength. Together these results suggest that maternal HFHS diet impairs F1 offspring skeletal integrity in a sex and bone site-specific manner.

母体高脂高糖饮食会损害衰老小鼠的骨骼质量和强度,但不会损害软骨。
骨关节炎(OA)是滑膜关节的一种常见老化疾病,最近的研究表明,父母的高脂肪饮食会增加后代关节损伤后骨关节炎的严重程度。我们假设,母体高脂高糖(HFHS)饮食会促进1岁后代自发性骨关节炎相关软骨和骨骼变化。雌性 C57BL/6 J 小鼠在与饲料喂养的 C57BL/6 J 雄性小鼠交配前 6 周食用对照组饲料或 HFHS 饲料,并在整个妊娠期和哺乳期食用指定的饲料。雄性和雌性后代断奶后改用饲料喂养,养育至一岁,并对其软骨和骨骼变化进行评估,以确定是否出现 OA。然而,通过组织学曼金评分、细胞外基质机械测试、组织学滑膜炎评分以及微计算机断层扫描测量软骨下骨增厚,后代并没有表现出OA的早期症状。另一方面,以 HFHS 为食的母体的雄性后代胫骨干骺端骨小梁质量下降,皮质厚度减少。虽然母体喂食 HFHS 不会影响雌性后代胫骨的骨小梁或皮质骨质量,但与喂食对照组母体的后代相比,这些动物的桡骨皮质厚度减少,髓质面积增加,断裂强度受损。最后,我们评估了雄性和雌性 F2 后代的骨质和强度,发现祖母饮食对桡骨几何形状影响不大,但对强度影响不大。这些结果表明,母体高氟高含氢膳食会以性别和骨骼部位特异性的方式损害F1后代的骨骼完整性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Orthopaedic Research®
Journal of Orthopaedic Research® 医学-整形外科
CiteScore
6.10
自引率
3.60%
发文量
261
审稿时长
3-6 weeks
期刊介绍: The Journal of Orthopaedic Research is the forum for the rapid publication of high quality reports of new information on the full spectrum of orthopaedic research, including life sciences, engineering, translational, and clinical studies.
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