地塞米松对护骨素基因敲除小鼠骨微结构的影响

目的探讨小剂量地塞米松对生长期小鼠骨密度及骨微结构的影响及其与OPG途径的关系。方法 20只4周龄OPG~(-/-)雌性小鼠及20只野生型小鼠随机分四组(n=10):野生型安慰剂组(WT+saline),野生型地塞米松干预组(WT+DEX,地塞米松1mg/kg体重,肌肉注射,每周3次),OPG~(-/-)敲除小鼠安慰剂组(OPG~(-/-)+saline),OPG~(-/-)敲除小鼠DEX干预组(OPG~(-/-)+DEX,地塞米松1 mg/kg体重,肌肉注射,每周3次)。6周后处死小鼠,一侧胫骨行显微CT扫描分析。结果OPG~(-/-)组的组织骨密度、骨小梁体积分数、骨小梁数量、骨小梁厚度均较其他三组降低(P0.05)。OPG~(-/-)+DEX组的组织骨密度、骨小梁体积分数、骨小梁数量、骨小梁厚度均较WT及WT+DEX组降低(P0.05)。OPG~(-/-)组的骨小梁模型因子及骨小梁分离度均较其他三组增加(P0.05);OPG~(-/-)+DEX组的骨小梁模型因子及骨小梁分离度均较WT及WT+DEX组增加(P0.05)。WT及WT+DEX组之间骨小梁微结构参数均无统计学差异。结论在生长期小鼠OPG基因功能缺失时,地塞米松有部分拮抗骨量丢失的作用,表明除了OPG/RANKL途径,地塞米松对骨代谢的影响是多途径的。     

高脂饮食诱导小鼠脂肪肝

目的 初步探索高脂饮食对小鼠肝脏的损伤情况.方法 40只小鼠随机分为2组,实验组给予高脂饮食,对照组正常饮食.1个月后,采用颈椎处死法,将取出的肝脏进行病理学观察以及肝脂的测定.结果 实验组和对照组相比,肝重、肝重/体重、肝脂、肝脏大体标本和肝脏病理组织学观察差异在统计学上均具有显著性意义.结论 高脂饮食可能在小鼠脂肪肝的发生中起到一定的作用,但有必要开展各种不同类饮食的混合喂养以及剂量反应关系的研究.     

高脂饮食对啮齿类动物卵巢功能影响的研究进展

随着现代生活水平的提高,肥胖的发病率急剧上升,成为影响当今人类生殖健康的一大问题。引起肥胖的一个重要原因是富含脂肪的高能量食品摄入增加,但是高脂饮食对女性生殖功能的影响机制尚不清楚。使用啮齿类动物模型进行研究时发现,高脂饮食会使其生殖系统出现卵巢周期紊乱,导致生育力下降、不孕、自发性流产等。本文就高脂饮食诱导的肥胖对啮齿类动物卵巢功能的影响及相关机制研究进行综述。     

高脂饮食通过抑制Wnt/β-catenin信号介导对骨质疏松大鼠骨密度和骨修复的负面影响

目的 评估高脂饮食（HFD）对骨质疏松大鼠骨密度（bone mineral density, BMD)及骨修复的影响并探讨可能的机制。方法 将雌性SD大鼠随机分为三组：假手术卵巢切除组（Sham）、手术卵巢切除模型组（OVX）、手术卵巢切除模型+HFD（OVX+HFD）;随后所有大鼠在双侧去卵巢手术或假手术后12周基础上制作双侧股骨干建立骨缺损模型,OVX+HFD组大鼠在股骨上接受HFD干预4周。随后使用影像学、血清学、骨生物力学以及基因水平检测来评估骨修复效果。结果 与Sham组相比,OVX和OVX+HFD组的血清E2、ALP水平均显著降低( P<0.05),而TRAP水平均显著升高(P<0.05);OVX和OVX+HFD组之间有显著差异(P<0.05)。Micro-CT检测显示OVX+HFD组骨修复效果较OVX和Sham组明显降低;定量检测结果显示OVX+HFD组的BMD、Tb.N和Tb.Th显著小于OVX组(P<0.01),而Tb.Sp(P<0.05)在OVX+HFD组中明显大于在OVX组。生物力学显示HFD干预后明显降低了去卵巢大鼠骨缺损部位的机械强度,包括大鼠股骨的极限载荷、刚度、能量吸收和弹性模量(P均<0.05);基因检测表明与OVX组相比,OVX + HFD组Smad2、Smad3和GSK-3βmRNA表达显著增加(P<0.01),而Wnt1和β-cateninmRNA表达均显著降低(P<0.01)。结论 HFD对骨质疏松状态下骨缺损愈合有负面影响,而这种影响可能是通过对Wnt/β-catenin信号传导抑制来实现的。     

高钙饮食对老年雌性大鼠皮质骨的影响

目的研究高钙饮食对老年雌性大鼠皮质骨的保健作用。方法按照食料中钙含量不同,大鼠随机分为3组,分别喂饲低钙饲料(0.1?)、中钙饲料(0.6?)、高钙饲料(1.2?),持续12w。采用pQCT技术测定股骨中段皮质骨相关参数。结果高钙组大鼠股骨中段皮质骨的骨密度和骨矿含量都明显升高。高钙饮食显著提高皮质骨面积及皮质骨厚度,而对股骨中段外周面积和内周面积没有明显影响。结论高钙饮食能够提高老年雌性大鼠皮质骨的骨量、面积和厚度,从而维护皮质骨的骨骼健康。     

血流量改变和高脂饮食对动脉壁重构的影响

目的　对动脉移植于静脉后再饲高脂饮食发生的形态学改变进行探讨 ,以了解动脉移植于静脉是否发生硬化和重构。方法　兔 3 0只 (5组 ) ,将一侧颈总动脉移植于对侧颈外静脉 ,饲高脂饮食。测定血脂 ,在术后不同时间点取材。光、电镜观察。对管腔面积 ,管壁厚度和面积进行测量和统计分析。结果　动物均出现了明显的高脂血症。移植段管壁渐变薄 ,即术后 0、1、2周、1、2和 3个月时为 [(10 7.0± 16.6)、(94.0± 16.4)、(87.0± 7.4)、(4 0 .0± 8.2 )、(3 5 .0± 6.9)和(18.0± 3 .5 ) μm] ,管腔和管壁面积缩小 ,未见脂纹和斑块。对照动脉管腔面积渐增加 ,但厚度下降 ,可见内皮损伤、脂纹和粥样斑块。结论　动脉移植后 ,结构逐渐静脉化 ,对动脉硬化的易感性低于原位动脉 ,对照侧动脉产生适应性重构。     

小剂量地塞米松对生长期小鼠骨微结构及骨代谢的影响

目的 观察小剂量地塞米松对生长期小鼠骨微结构及骨代谢的影响。方法 24只4周龄雌性小鼠随机分两组（n=12）：地塞米松组（DEX,1mg/kg,肌肉注射,2次/周）,对照组。4w后处死小鼠,检测血清Ⅰ型前胶原N端肽(PINP)和骨Ⅰ型胶原交联C端肽（β-CTX）蛋白的表达水平;检测胫骨干骺端骨保护素（OPG）、核因子-κ B受体活化因子配体（RANKL）表达;抗酒石酸酸性磷酸酶（TRAP）染色方法检测破骨细胞;一侧胫骨行显微CT扫描分析。结果 DEX组小鼠胫表观骨密度和骨体积分数明显高于对照组（P<0.05）,骨小梁数量高于对照组,结构模型指数低于对照组,但无统计学意义。DEX组小鼠血清PINP及β-CTX浓度显著下降（P<0.05）。DEX组小鼠胫骨干骺端OPG表达明显增多,而RANKL表达无明显变化,相对于对照组,OPG/RANKL比值升高。TRAP染色示DEX组小鼠胫骨干骺端破骨细胞数量较对照组减少。结论 小剂量地塞米松间断给药可能通过上调OPG/RANKL比率维持生长期小鼠骨量。     

自主运动对高脂饮食诱导的肥胖小鼠膝骨关节炎软骨形态学的影响

目的研究高脂饮食诱导的骨性关节炎发生过程中骨关节软骨病变以及自主运动对骨性关节炎软骨的影响机制,探讨自主运动对膝骨关节炎软骨的保护作用,为临床治疗膝骨关节炎提供有效的实验证据。方法将28只C57BL/6 J小鼠随机分为正常饮食组(C-Sed组,n=6)、正常饮食加运动组(C-Ex组,n=6)、高脂饮食组(HF-Sed组,n=8)及高脂饮食加运动组(HF-Ex组,n=8)。C-Sed组和C-Ex组喂养基础饲料(13.5%Kcal),HF-Sed组和HF-Ex组喂养高脂饲料(60%Kcal)。喂养8周后,C-Ex组和HF-Ex组小鼠采用自主转轮运动进行干预,记录运动数据,运动3周后行颈椎脱臼处死;C-Sed组和HF-Sed组小鼠不进行运动干预,继续喂养不同膳食4周后行颈椎脱臼处死,取膝关节软骨组织进行固定、脱钙,制成4μm厚石蜡切片,并进行HE及甲苯胺蓝染色,测量各组小鼠软骨层厚度,探究自主转轮运动对肥胖小鼠膝骨关节炎软骨形态学的影响。结果喂养12周结束后,与C-Sed组小鼠相比,HF-Sed组小鼠体重明显增加,高脂饮食成功诱导了高脂饮食组小鼠发生肥胖,且经HE及甲苯胺蓝染色后,可观察到与C-Sed组小鼠相比,HF-Sed组小鼠软骨表面粗糙、部分缺损,软骨层厚度降低(P0.001);而HF-Ex组较HF-Sed组小鼠关节软骨表面光滑,软骨层厚度增加,Mankin评分分值降低。结论 3周自主转轮运动可增加高脂组小鼠软骨层厚度,降低Mankin评分分值,延缓骨关节炎软骨退变,起到保护关节软骨的作用。     

高脂饲料对不同月龄小鼠骨质疏松的影响

目的 研究高脂饲料对不同月龄小鼠骨质疏松的影响。方法 将雄性C57BL/6J小鼠随机分为6月龄正常饲料组、6月龄高脂饲料组、12月龄正常饲料组、12月龄高脂饲料组。饲养16周后处死,取小鼠血清检测血脂（TC、TG、HDL-C、LDL-C）、氧化应激和炎症（SOD、MDA、IL-6、TNF-α）以及骨代谢标志物（CTX-1、PINP）等指标的水平;取小鼠股骨经Micro-CT和HE染色分析股骨远端微观结构和骨组织形态。结果 与正常饲料组相比,各月龄高脂饲料组小鼠的体重和体脂率增加（P＜0.05）,血清中TC、TG、LDL-C水平增高（P＜0.05）,且在12月龄高脂饲料组中最高。与正常饲料组相比,Micro-CT显示各月龄高脂饲料组小鼠BV/TV、BS/TV降低（P＜0.05）,骨微结构破坏明显;HE染色显示各月龄高脂饲料组小鼠骨小梁减少。饲料相同时,12月龄组小鼠的骨量和骨小梁数目也明显低于6月龄组,且在12月龄高脂饲料组中骨量丢失最为明显。各月龄高脂饲料组小鼠血清中IL-6、TNF-α、MDA水平均较正常饲料组增高（P＜0.05）;6月龄高脂饲料组的血清CTX-1水平高于正常饲料组（P＜0.05）。结论 高脂饮食和高龄可加重小鼠氧化应激和炎症水平,损害小鼠骨健康,且高脂饮食和高龄同时存在时对鼠骨健康的损害作用更为明显。     

高脂高糖饮食暴露诱导大鼠多囊卵巢综合征研究

目的通过高脂高糖饮食诱导雌性大鼠多囊卵巢综合征(PCOS),探讨其生殖和代谢特征。方法将23天断奶雌性大鼠随机分成两组:对照组接受正常饮食(对照组,n=18),实验组接受高脂高糖饮食(HFHS组,n=18),连续喂养14周。观察两组体重、动情周期和卵巢组织学变化,检测两组空腹血糖、空腹胰岛素、计算胰岛素抵抗指数(HOMA-IR)、血脂水平、性激素水平。结果 HFHS组大鼠体重至第3周起显著高于对照组(P0.001),但两组卵巢重量无显著差异[(0.041±0.006)g vs.(0.045±0.005)g,P0.05]。HFHS组动情周期失去规律变化,发情期持续时间占整个发情周期时间的比例显著长大对照组[(0.46±0.06)vs.(0.27±0.03),P0.001]。HFHS组卵巢组织学检查发现多个囊状扩张卵泡、黄体数量下降。HFHS组空腹胰岛素、HOMA-IR、总胆固醇水平显著高于对照组(P0.001);发情间期HFHS组LH和E2水平显著低于对照组(P0.05),睾酮(T)水平显著高于对照组(P0.001);发情前期HFHS组LH和P水平显著低于对照组(P0.05),T和E2水平显著高于对照组(P0.001)。结论高脂高糖饮食诱导雌性大鼠PCOS,并产生代谢紊乱和卵巢改变,与PCOS患者临床观察到的相似。     

High fat diet accelerates cartilage repair in DBA/1 mice

Obesity is a well‐known risk factor for osteoarthritis, but it is unknown what it does on cartilage repair. Here we investigated whether a high fat diet (HFD) influences cartilage repair in a mouse model of cartilage repair. We fed DBA/1 mice control or HFD (60% energy from fat). After 2 weeks, a full thickness cartilage defect was made in the trochlear groove. Mice were sacrificed, 1, 8, and 24 weeks after operation. Cartilage repair was evaluated on histology. Serum glucose, insulin and amyloid A were measured 24 h before operation and at endpoints. Immunohistochemical staining was performed on synovium and adipose tissue to evaluate macrophage infiltration and phenotype. One week after operation, mice on HFD had defect filling with fibroblast‐like cells and more cartilage repair as indicated by a lower Pineda score. After 8 weeks, mice on a HFD still had a lower Pineda score. After 24 weeks, no mice had complete cartilage repair and we did not detect a significant difference in cartilage repair between diets. Bodyweight was increased by HFD, whereas serum glucose, amyloid A and insulin were not influenced. Macrophage infiltration and phenotype in adipose tissue and synovium were not influenced by HFD. In contrast to common wisdom, HFD accelerated intrinsic cartilage repair in DBA/1 mice on the short term. Resistance to HFD induced inflammatory and metabolic changes could be associated with accelerated cartilage repair. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1258–1264, 2017.

     

大黄丹参对高脂饮食诱发的胰腺纤维化大鼠影响的研究

目的:研究大黄丹参对高脂饮食诱导的胰腺纤维化大鼠氧化应激、内质网应激相关因子的影响。方法:将40只雄性清洁级SD大鼠,采用随机数表法均分成对照组、模型组、大黄丹参低、中、高剂量组,每组8只;对照组喂以普通饲料,其余4组均喂以高脂饲料连续10周建立胰腺纤维化模型。造模同时,各组以相应药物灌胃,对照组与模型组生理盐水灌胃,...     

The effect of a low-carbohydrate diet on bone turnover

Introduction Low-carbohydrate diets have become popular as weight loss techniques. These diets are high in protein, saturated fats, and omega-6 fatty acids. They also lead to a ketogenic state. These factors could lead to increased bone turnover. This study was designed to see whether a low-carbohydrate diet would lead to increased bone turnover in humans.Methods Thirty patients (15 study subjects and 15 controls) were recruited for this 3-month study. The 15 patients on the diet were instructed to consume less than 20 g of carbohydrates per day for the 1st month and then less than 40 g per day for months 2 and 3. Control subjects had no restrictions on their diet. The primary end point was urinary N-telopeptide (UNTx) at 3 months. Secondary end points included UNTx at 1 month, bone-specific alkaline phosphatase (BSAP) at 1 month, bone turnover ratio (BSAP/UNTx) at 1 month, and weight loss.Results The mean UNTx in the study subjects increased by 1.6 [95% confidence interval (CI) ±22.8] compared with an increase of 1.9 (95% CI ±17.6) in the controls at 3 months (p=0.86). The mean UNTx decreased by 2.2 (95% CI ±27.2) and 3.1 (95% CI ±17.6) at 1 month in the dieters and controls, respectively (p=0.36). The mean BSAP decreased by 0.53 (95% CI ±2.96) in the dieters and increased by 0.34 (95% CI ±2.92) in the controls at 1 month (p=0.27). The bone turnover ratio increased by 0.08 (95% CI ±0.81) in the dieters and by 0.05 (95% CI ± 0.27) in the controls at 1 month (p=0.78). The dieters lost 6.39 kg versus 1.05 kg for the controls at 3 months (p=0.0008).Conclusions Although the patients on the low-carbohydrate diet did lose significantly more weight than the controls did, the diet did not increase bone turnover markers compared with controls at any time point. Further, there was no significant change in the bone turnover ratio compared with controls.     

防己诺林碱对去卵巢小鼠骨代谢及骨微结构的影响

目的探讨防己诺林碱对去卵巢小鼠骨质疏松的保护作用。方法将40只C57BL/6小鼠随机分为空白(假手术)对照组、模型(去卵巢)组、阳性(雌二醇,E2)对照组、防己诺林碱组共4组,每组10只。连续腹腔给药7周后处死小鼠,取股骨及外周血清,通过ELISA法检测骨代谢相关血清学指标:抗酒石酸酸性磷酸酶(TRAc P)、I型胶原羧基末端肽(CTX)及I型胶原氨基末端肽(NTX);通过Micro-CT评估各组小鼠骨组织微结构相关指标:骨小梁百分比(BV/TV)、骨小梁数量(Tb.N)、骨小梁分离度(Tb.Sp)和骨小梁厚度(Tb.Th);通过实时荧光定量PCR检测小鼠骨质疏松骨吸收相关基因的表达情况,包括TRAc P、组织蛋白酶K(Cathepsin K)、活化T细胞核因子1(NFATc1)以及降钙素受体(CTR)。结果与去卵巢模型组比较,防己诺林碱治疗组小鼠BV/TV、Tb.N、Tb.Th显著升高,Tb.Sp明显降低,骨代谢相关指标(TRAc P、CTX、NTX)显著降低,破骨细胞标志基因(TRAc P、Cathepsin K、NFATc1以及CTR)表达水平明显下降。结论防己诺林碱对去卵巢小鼠骨质疏松有保护作用,有望为骨质疏松的临床用药提供新思路。     

D-半乳糖对不同月龄雌性小鼠骨代谢的影响

目的比较D-半乳糖对1月龄及3月龄雌性小鼠骨干重、骨羟脯氨酸、骨钙及微量元素的影响.方法 1月龄及3月龄昆明种雌性小鼠每日颈背部皮下注射D-半乳糖1O00mg·mg·d-1,连续42d,取右侧股骨测定骨干重、骨羟脯氨酸、骨钙、骨微量元素.结果 D-半乳糖对1月龄小鼠骨干重、骨羟脯氨酸、骨钙和微量元素无明显影响;可使3月龄小鼠骨干重、骨羟脯氨酸和骨钙减少,骨干重与体重比值,骨镁与骨干重比值降低.结论 D-半乳糖不能导致1月龄小鼠骨质丢失,但可导致3月龄小鼠骨质丢失,提示D-半乳糖对处于骨生长期及已进入骨维持期的雌性小鼠具有不同的骨药理作用.D-半乳糖导致3月龄小鼠骨质丢失可能与骨镁减少有关.     

High-fat diet decreases cancellous bone mass but has no effect on cortical bone mass in the tibia in mice

Body mass has a positive effect on bone health. Whether mass derived from an obesity condition or excessive fat accumulation is beneficial to bone has not been established; neither have the mechanisms by which obesity affects bone metabolism. The aim of this study was to examine the effects of obesity on bone structure and osteoblastic expression of key markers involved in bone formation and resorption in a diet-induced obesity mouse model. Six-wk-old male C57BL/6 mice (n = 21) were assigned to two groups and fed either a control (10 kcal% energy as fat) or high-fat diet (HFD, 45 kcal% energy as fat) for 14 weeks. Bone marrow stromal/osteoblastic cells (BMSC) were cultured. Osteoprogenitor activity [alkaline phosphatase (ALP) positive colonies] and mineralization (calcium nodule formation) were determined. Gene expression was measured using quantitative real-time PCR. Bone structure of proximal and midshaft tibia was evaluated by micro-computed tomography. Mice fed the HFD were 31% heavier (P < 0.01) than those fed the control diet. There were more ALP positive colony forming units at d 14 and calcium nodules at d 28 of culture by BMSC from HFD mice than from control mice (P < 0.01). Receptor activator of NF-κB ligand (RANKL) mRNA levels and the ratio of RANKL to osteoprotegerin expression in HFD animals was higher (P < 0.01) than in control diet animals. Serum tartrate-resistant acid phosphatase levels were higher in HFD fed mice when compared to control diet fed mice (P < 0.05). There were no significant differences in tibial fat-free weight, length, and cortical parameters of midshaft between the two groups. Compared with control mice, tibial trabecular bone volume was reduced, and trabecular separation was increased in HFD mice. Trabecular number was lower (P < 0.05) and connectivity density tended to be less (P = 0.07) in HFD mice than in control mice. In conclusion, our data indicate that obesity induced by a high-fat diet decreases cancellous bone mass but has no effect on cortical bone mass in the tibia in mice.     

Comparative effects of 17β-estradiol,raloxifene and genistein on bone 3D microarchitecture and volumetric bone mineral density in the ovariectomized mice

Summary This study assessed the effect of estradiol, raloxifene and genistein on the preservation of bone 3D-microarchitecture and volumetric bone mineral density (vBMD) in the ovariectomized mouse model. Our results indicated that raloxifene was more effective in preserving bone ovariectomized-induced changes, the advantage being concentrated in both bone microarchitecture and vBMD. Introduction This study assessed the effect of different estrogen receptor (ER) agonists on the preservation of bone 3D-microarchitecture and volumetric bone mineral density (vBMD) in the ovariectomized (OVX) mouse model. Methods Twelve-week-old female C57BL/6 mice were randomly assigned to one of five groups: (1) SHAM-operated + vehicle; (2) OVX + vehicle; (3) OVX + 17β-estradiol (5 μg/kg); (4) OVX + raloxifene (1 mg/kg); (5) OVX + genistein (25 mg/kg), during 4-weeks. Bone microarchitecture and trabecular, cortical and total vBMD of distal femur were imaged by ex vivo microcomputed tomography (micro-CT). Results Ovariectomy produced a global deterioration involving both trabecular and cortical 3D-microarchitecture and vBMD. Raloxifene maintained both microarchitecture and vBMD, whereas estradiol prevented deterioration of some microstructural parameters, such as trabecular thickness (Tb.Th), trabecular bone pattern factor (Tb.Pf), and cortical periosteal perimeter (Ct.Pe.Pm), but did not completely block the loss in vBMD. Mice treated with genistein exhibited the less favourable profile in both vBMD and microstructural parameters preserving only cross-sectional bone area (B.Ar) and Ct.Pe.Pm in cortical bone. Conclusion Our data indicate that, at the selected doses, raloxifene was more effective in preserving bone OVX-induced changes than either estradiol or genistein, the advantage being concentrated in both bone microarchitecture and vBMD.     

低磷食物对模拟失重小鼠后肢骨骨质丢失防治作用的探讨

目的 初步探讨低磷食物对模拟失重下小鼠骨丢失防治的可能性及防治效果,为后期可能的临床应用提供实验依据.方法 利用尾部悬吊法模拟失重.将24只C57BL/6雌性小鼠随机分为四组,即对照(CON)组、对照低磷(CON-LP)组、悬尾(SUS)组及悬尾低磷(SUS-LP)组,每组6只.4周实验期满后取小鼠后肢骨标本,通过Micro-CT扫描分析比较各组小鼠股骨的骨体积分数(bone volume frac-tion,BV/TV)、骨小梁密度(trabecular density,Tb.Density)等骨密度参数,骨小梁厚度(trabecular thickness,Tb.Th)、平均骨小梁数(trabecular number,Tb.N)等骨形态学参数.通过抗酒石酸酸性磷酸酶(tartrate-resistant acid phosphatase,TRAP)染色、碱性磷酸酶(alkaline phosphatase,ALP)染色和丽春红三色(Ponceau S)染色对各组小鼠胫骨生长发育和改建情况进行组织形态学观察.结果 Micro-CT结果显示,CON-LP组与CON组比较:骨密度参数BV/TV和Tb.Density减小(P<0.05),形态学参数Tb.Th增高和Tb.N减少(P<0.05).SUS-LP组与SUS组比较:骨密度参数BV/TV和Tb.Density减小(P<0.05),形态学参数Tb.Th和Tb.N减少(P<0.05).染色结果显示:悬尾的小鼠(SUS组、SUS-LP组)与地面的小鼠(CON组、CON-LP组)比较,骨小梁出现明显的骨吸收,Tb.N减少、骨小梁间距变大.CON-LP组与CON组比较,Tb.Density减低、Tb.N减少.SUS-LP组与SUS组比较,骨小梁变细、Tb.N减少.结论 低磷食物对模拟失重下小鼠后肢骨骨丢失防治效果不明显,甚至可能产生不利的后果.