在小鼠中,卡路里限制会通过抑制骨重塑而损害皮质,但不是椎峰骨质量
Linyi Liu1, Phuong T Le1, J Patrizia Stohn1
1MaineHealth Institute for Research, Scarborough, ME 04074, United States.
概括
卡路里限制 (CR) 通过抑制骨形成和重塑来降低骨矿物质密度. 这种饮食引起的骨损失与大脑髓脂肪增加和Wnt信号受损有关,特别是影响皮质骨.
科学领域:
- 骨生物学 骨生物学 骨生物学
- 代谢性疾病 代谢性疾病
- 营养科学 营养科学
背景情况:
- 众所周知,卡路里限制 (CR) 会导致体重减轻,并影响骨健康.
- 人类饮食诱导的骨质损失的机制尚未完全理解.
- CR可能会损害峰值骨收益,并导致成年人的骨质损失.
研究的目的:
- 为了研究30%的CR对小鼠骨代谢的影响.
- 阐明CR诱导的骨损失背后的细胞和分子机制.
- 检查CR对骨微型架构,重塑和干细胞分化的影响.
主要方法:
- 8周大的雄性和雌性C57BL/6J小鼠在4周和8周内接受了30%的CR.
- 通过微型CT评估身体组成,面积骨矿物质密度 (aBMD) 和骨微型架构.
- 进行了组织形态测量,体外分化试验 (骨质母细胞和脂肪细胞),qRT-PCR和西式涂抹.
主要成果:
- 经过8周的时间,CR小鼠的体重减少,腿部下部和全身aBMD减少.
- 在CR小鼠中,皮层骨面积分数下降;雄性保留了状骨格参数,而雌性显示骨体积分数增加.
- 红细胞结核严重抑制骨形成和再吸收,增加骨髓脂肪组织,并有利于脂肪生成而不是骨质生成在体外,这与Wnt信号受损有关.
结论:
- 由于骨重塑被抑制,CR导致皮层骨质峰值受损.
- 在CR期间大脑髓脂肪增加与原始细胞招募和营养不足下的脂肪生成有关.
- 长期的CR可能会导致骨质减少,主要是在皮质外,可能是由于Wnt信号受损.
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