联合补充维生素Ｄ 胶原肽和钙对大鼠骨骼 发育影响的实验研究

摘要：目的　探讨补充维生素Ｄ、胶原肽和钙对大鼠骨骼发育的影响。方法　健康雄性初断乳ＳＤ 大鼠按 体质量随机分为５组,其中１组为低钙对照组,实验期间给予低钙饲料喂养,其余４组在低钙饲料的基础 上,分别给予含不同剂量的维生素Ｄ、胶原肽和钙的饲料喂养,１２ 周后测定大鼠骨骼生长发育相关指标、 血清骨代谢生化指标、钙表观吸收率,并对骨组织切片进行病理学观察。结果　各受试物剂量组大鼠股骨 中点骨密度为（１８８９±０．０１１０）ｇ／ｃｍ２、（２１８８±０．０２０４）ｇ／ｃｍ２、（１９０８±０．０１１４）ｇ／ｃｍ２、（１９１９± ０．００９７）ｇ／ｃｍ２,均显著高于低钙对照组,最大载荷分别为（９６．９５±１１．８５）、（１２２．８１±１３．６７）、（９７．４８± ８．９４）、（１００．４５±１９．５１）Ｎ,显著高于低钙对照组,维生素Ｄ 和碳酸钙联合干预组各指标优于其他各组; 碳酸钙、维生素Ｄ 和胶原肽三者联合干预组血清Ｉ型前胶原氨基端前肽（ＰＩＮＰ）水平显著低于对照组;各 组钙表观吸收率分别为（９３．８７±１．７０）％、（９３．７２±１．２０）％、（９２．４７±１．３３）％、（９０．４５±２．８１）％,其 中２、３组比对照组（９０．８６±４．１９）％高（犘＜０．０５）。结论　单独补充碳酸钙,或碳酸钙与维生素Ｄ 和／或 胶原肽联合补充均能够促进成长期雄性大鼠骨的发育,但碳酸钙、维生素Ｄ 和胶原肽三者联合的干预效果 未达预期,其机制有待进一步深入探讨。 关键词：维生素Ｄ;胶原肽;碳酸钙;骨密度 中图分类号：Ｒ１５１,Ｑ９８３＋．３　　文献标识码：Ａ　　文章编号：１００９ ６６３９ （２０１６）０７ ０５０９ ０５     

维生素K与钙对去卵巢大鼠骨代谢的影响

切除雌鼠双侧卵巢造成快速骨丢失,复制女性绝经后骨质疏松症的动物模型。以饲料添加方式补充维生素Ｋ（９０ｍｇ／ｋｇ） 和钙（５ｇ／ｋｇ） 。实验期６ 个月,通过测定尿钙、尿羟脯氨酸、血清钙、碱性磷酸酶、骨钙素等生化指标观察单纯补充维生素Ｋ、钙及两者联合作用对骨代谢的影响。结果发现：补充Ｖｋ 可减少尿钙、尿羟脯氨酸排泄,降低血清碱性磷酸酶水平,提高血清骨钙素及其羧化水平,表明维生素Ｋ 能抑制骨分解代谢,促进骨形成代谢,并且与钙的联合作用效果优于单纯补充维生素Ｋ 或钙。本实验结果提示：绝经后妇女作为骨质疏松危险人群,应注意膳食维生素Ｋ 与钙的摄入。大剂量的维生素Ｋ 有可能被用于骨质疏松症的药物防治     

维生素K和钙对去卵巢大鼠骨质疏松的影响

切除雌鼠双侧卵巢以造成骨快速丢失作为模拟女性绝经后骨质疏松症的动物模型,从骨计量学、骨生物力学等方面综合观察单纯补充维生素Ｋ（９０ｍ ｇ／ｋｇ）、钙（５ｇ／ｋｇ）及两者联合作用６个月对骨丢失的影响。结果发现：与正常对照组（Ａ）大鼠相比,模型对照组（Ｂ）大鼠骨量显著减少,骨脆性增加。与模型对照组相比,单纯补充维生素Ｋ组（Ｄ） 股骨中点骨密度值显著提高,股骨干骺端及腰椎骨密度、股骨近侧端矿物质含量都有增高趋势,表明补充维生素Ｋ 可在一定程度上减少骨丢失;同时补充维生素Ｋ及钙组（Ｅ）股骨的最大挠度与最大应变值,与模型对照组相比也有增高趋势,表明补充维生素Ｋ可提高骨的柔韧性,改善股骨的力学性能。综合骨计量学与骨力学观察结果,发现各种实验措施对密质骨的效果皆优于松质骨,并且维生素Ｋ与钙的联合作用效果优于单纯补充维生素Ｋ 或钙。本实验结果提示：绝经后妇女,作为骨质疏松危险人群,增加膳食维生素Ｋ 与钙的摄入是有帮助的     

维生素B6对硒的生物利用率影响的研究：IV.对大鼠体内不同化学形式硒…

４周龄雄性大鼠饲缺维生素Ｂ６（ＶＢ６）缺硒酪蛋白蔗糖基础饲料，３周后按体重把动物分成１０组，即基础饲料组、基础饲料中补充含硒０．２５ｍｇ／ｋｇ饲料的硒酸钠组、亚硒酸钠组、ＤＬ－硒蛋氨酸组或硒胱氨酸组，在此基础上每种饲料又分成补充或不补充盐酸吡哆醇２．５０μｇ／ｇ饲料两组。实验期为４周。补ＶＢ６各组的红细胞、骨骼肌和心肌中硒水平和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性均显著高于相应缺ＶＢ６各组，ＶＢ     

维生素B6对硒的生物利用率影响的研究Ⅳ．对大鼠体内不同化学形式硒利用率及脂质过氧化物的影响

４周龄雄性大鼠饲缺维生素Ｂ６（ＶＢ６）缺硒酪蛋白蔗糖基础饲料，３周后按体重把动物分成１０组，即基础饲料组、基础饲料中补充含硒０．２５ｍｇ／ｋｇ饲料的硒酸钠组、亚硒酸钠组、ＤＬ－硒蛋氨酸组或硒胱氨酸组，在此基础上每种饲料又分成补充或不补充盐酸吡哆醇２．５０μｇ／ｇ饲料两组。实验期为４周。补ＶＢ６各组的红细胞、骨骼肌和心肌中硒水平和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性均显著高于相应缺ＶＢ６各组，ＶＢ６对饲硒酸钠、亚硒酸钠和硒胱氨酸大鼠肝硒和ＧＳＨ－Ｐｘ水平没有影响；但当补充硒蛋氨酸时，与补ＶＢ６大鼠相比缺ＶＢ６大鼠的肝硒水平较高而ＧＳＨ－Ｐｘ活性显著降低。本研究结果进一步证明，ＶＢ６与血浆硒的转运和利用有关，并且参与了硒蛋氨酸在肝脏中的代谢过程     

铅染毒对大鼠神经行为功能及神经化学的影响

作者研究了铅染毒对大鼠神经行为功能、海马中单胺类递质及脑组织脂质过氧化水平的影响。结果显示，１ ３３３．３ｍｇ／ｋｇ剂量组（Ｐｂ－Ｂ为６．２３μｍｏｌ／Ｌ）大鼠学习记忆能力受到影响，２６６．７ｍｇ／ｋｇ（Ｐｂ－Ｂ为４．２０μｍｏｌ／Ｌ）和１３３３．３ｍｇ／ｋｇ剂量组大鼠的运动改变，情绪状态不稳定；海马中多巴胺递质及其代谢产物含量有随染毒剂量增高而降低的趋势，而脑组织中脂质过氧化水平有随染毒剂量升高     

缺锌对大鼠生长发育及脂代谢的影响

本文观察缺锌饲料对雄性ＳＤ幼鼠的生长、血液学多数、血清锌、碱性磷酸酶及血脂的影响。实验分五组：１组为正常对照组（饲料含锌量３２．２μｇ／ｇ）；２组为严重缺锌组（饲料合锌量３．４μｇ／ｇ），两组均自由进食；３组为锌足量组（饲料含锌８４．９μｇ／ｇ）；４组为锌缺乏组（饲料含锌４．４μｇ／ｇ）；５组为锌边缘缺乏组（饲料含锌５．５μｇ／ｇ）。后三组动物均与２组对喂。实验期２６天。结果表明：（１）严重缺锌组体重和食物摄入量显著低于正常对照组，并且出现缺锌症状，最突出的是丧失食欲；（２）严重缺锌组红细胞数、血细胞容积、血红蛋白均明显高于正常对照组，而平均红细胞容积却显著低于正常对照组，但对喂组之间未见有意义的改变；（３）严重缺锌组血清锌：碱性磷酸酶均显著低于正常对照组，而血清锌结合能力却明显高；（４）严重缺锌组血清和脂蛋白中胆固醇、甘油三酯、磷脂浓度均显著低于正常对照组，但对喂组之间差别不明显。     

水解牡蛎钙在大鼠体内的代谢和利用

为了解水解牡蛎钙的生物利用率，作者以含钙量相等（４５ｍｇ／ｄ）的水解牡蛎钙、碳酸钙、氯化钙喂饲缺钙动物模型大鼠４周，采用原子吸收法和ＥＤＴＡ络合滴定法测定了大鼠的血钙、尿钙、粪钙和骨钙，骨密度仪测定骨密度。结果表明，水解牡蛎钙组大鼠的钙吸收率和存留率分别为６７．３％±１６．７％和６４．６％±１７．５％，股骨骨钙含量为１３１．２±１．４８ｍｇ／ｇ，股骨骨密度（ＢＭＣ／ＢＷ）为０．３１８±０．０３４ｇ／ｃｍ２，均显著高于碳酸钙对照组。三组大鼠的血钙含量、体重增重和摄食量差异无显著性。提示水解牡蛎钙比常用钙剂碳酸钙更有利于机体的吸收和利用。     

多种钙剂不同钙含量对大鼠钙吸收及骨密度的影响

以断乳Wistar大鼠为模型 ,饲以用多种钙剂配制的不同钙含量的饲料 ,第 4周做 3天钙代谢实验 ,用原子吸收分光光度法测定粪便中的钙含量 ,计算表观吸收率。 12周时处死大鼠 ,剥出股骨 ,用SD10 0 0型单光子骨矿物仪测定股骨中点和干骺端骨密度。结果显示 ,钙摄入水平不同时表观吸收率可有很大差别 ,9种补钙产品在饲料钙水平相同时 ,吸收率除活性钙、奶粉和麦片组外 ,其余与同剂量碳酸钙组比较无显著差别。各样品的低、中、高剂量实验组大鼠股骨两点的骨密度均显著高于基础饲料组 (P <0 0 5 ) ,中、高剂量实验组的大鼠股骨中点和股骨干骺端骨密度与同剂量碳酸钙组比较均没有显著差异     

硫酸软骨素加钙对卵巢切除大鼠骨密度和骨钙含量的影响

目的探讨硫酸软骨素加钙对卵巢切除大鼠模型骨密度和骨钙含量的影响。方法选用卵巢切除大鼠所诱发的骨质疏松模型，给予硫酸软骨素加钙治疗，同时设假手术组及模型对照组。3个月后测定大鼠骨密度、骨钙含量。结果发现假手术组和高剂量组大鼠股骨骨密度和股骨钙含量显著高于阴性对照组（P〈0．05）。结论表明硫酸软骨素加钙能增加卵巢切除大鼠的骨密度，对雌激素缺乏所诱发的骨钙丢失具有抑制作用。     

Vitamin K and bone health

Vitamin K, originally recognised as a factor required for normal blood coagulation, is now receiving more attention in relation to its role in bone metabolism. Vitamin K is a coenzyme for glutamate carboxylase, which mediates the conversion of glutamate to gamma-carboxyglutamate (Gla). Gla residues attract Ca2+ and incorporate these ions into the hydroxyapatite crystals. There are at least three Gla proteins associated with bone tissue, of which osteocalcin is the most abundant and best known. Osteocalcin is the major non-collagenous protein incorporated in bone matrix during bone formation. However, approximately 30% of the newly-produced osteocalcin stays in the circulation where it may be used as an indicator of bone formation. Vitamin K deficiency results in an increase in undercarboxylated osteocalcin, a protein with low biological activity. Several studies have demonstrated that low dietary vitamin K intake is associated with low bone mineral density or increased fractures. Additionally, vitamin K supplementation has been shown to reduce undercarboxylated osteocalcin and improve the bone turnover profile. Some studies have indicated that high levels of undercarboxylated osteocalcin (as a result of low vitamin K intake?) are associated with low bone mineral density and increased hip fracture. The current dietary recommendation for vitamin K is 1 microg/kg body weight per d, based on saturation of the coagulation system. The daily dietary vitamin K intake is estimated to be in the range 124-375 microg/d in a European population. Thus, a deficiency based on the hepatic coagulation system would be unusual, but recent data suggest that the requirement in relation to bone health might be higher.     

Bone health and osteoporosis: the role of vitamin K and potential antagonism by anticoagulants.

BACKGROUND: Vitamin K's effects extend beyond blood clotting to include a role in bone metabolism and potential protection against osteoporosis. Vitamin K is required for the gamma-carboxylation of osteocalcin. Likewise, this gamma-carboxylation also occurs in the liver for several coagulation proteins. This mechanism is interrupted by coumarin-based anticoagulants in both the liver and bone. METHODS: A thorough review of the literature on vitamin K, osteocalcin and their role in bone metabolism and osteoporosis, as well as the potential bone effects of anticoagulant therapy was conducted. CONCLUSIONS: Epidemiological studies and clinical trials consistently indicate that vitamin K has a positive effect on bone mineral density and decreases fracture risk. Typical dietary intakes of vitamin K are below the levels associated with better BMD and reduced fracture risk; thus issues of increasing dietary intakes, supplementation, and/or fortification arise. To effectively address these issues, large-scale, intervention trials of vitamin K are needed. The effects of coumarin-based anticoagulants on bone health are more ambiguous, with retrospective studies suggesting that long-term therapy adversely affects vertebral BMD and fracture risk. Anticoagulants that do not affect vitamin K metabolism are now available and make clinical trials feasible to answer the question of whether coumarins adversely affect bone. The research suggests that at a minimum, clinicians should carefully assess anticoagulated patients for osteoporosis risk, monitor BMD, and refer them to dietitians for dietary and supplement advice on bone health. Further research is needed to make more efficacious decisions about vitamin K intake, anticoagulant therapy, and bone health.     

钙、维生素D缺乏对幼鼠骨生长和成骨细胞功能的影响

目的：探讨钙与维生素D营养缺乏对幼鼠骨骼生长和矿化的影响及机制。方法：建立单纯钙缺乏、维生素D缺乏和钙与维生素D同时缺乏的幼鼠动物模型，追踪其长骨的生长发育，并监测血清Ca,P,25-ODH3,骨碱性磷酸酶（B－ALP）水平及骨矿含量的构成的改变；观察反映骨形成和成骨细胞功能的生化标志－血清骨钙素水平。结果：钙缺乏、维生素D缺乏和两者同时缺乏大鼠的长骨生长发育明显落后于正常大鼠；其胫骨重、骨灰重均显著降低；对骨矿成分的分析显示，除K以外Ca,P,Mg,Na均有不同程度减少；实验组大鼠的血清骨钙素水平随实验期延长呈进行性下降。结论：钙和维生素D缺乏影响成骨细胞的功能，使骨形成和矿化过程受阻，从而导致骨骼生长发育质和量的异常。     

对长期低钙摄入幼鼠的骨骼的研究——Ⅲ 低钙时幼鼠的骨钙素水平

本文研究低钙摄入、维生素D供给正常时幼鼠血中骨钙素水平,以了解低钙时成骨细胞活性。实验采用60只21～23日Wistar断乳幼鼠,随机分为四组:A组,正常钙与VitD摄X组;B组,中度低钙组;C组,重度低钙组;D组,VitD缺乏组。定期监测血25-(OH)D_3水平。于实验中期(3周),末期(6周)分别处死1/2幼鼠,取血与左股骨标本。测血骨钙素水平,以股骨钙与股骨长计算股骨含钙指数。实验建立低钙与低VitD动物模型。结果发现严重低钙幼鼠股骨生长显著落后,VitD缺乏幼鼠股骨生长与正常组相似。低钙与VitD缺乏幼鼠股骨含钙指数均明显低于正常组,低钙组更严重。低钙组幼鼠血骨钙素水平略高于正常组,VitD缺乏幼鼠血骨钙素有增高趋势;提示低钙时股骨增生的成骨细胞活性低下,VitD缺乏幼鼠骨生长受阻程度不如低钙组明显,推测VitD缺乏与低钙时对成骨细胞的作用机理不同。本文研究证实低钙对生长期骨骼的影响远远超过临床估计。     

Growth hormone favorably affects bone turnover and bone mineral density in patients with short bowel syndrome undergoing intestinal rehabilitation

BACKGROUND: Patients with short bowel syndrome (SBS) have a high prevalence of metabolic bone disease due to nutrient malabsorption and potential effects of parenteral nutrition (PN). Human growth hormone (hGH) has been shown in some studies to have anabolic effects on bone, but hGH effects on bone in patients with SBS are unknown. METHODS: Adults with PN-dependent SBS underwent a 7-day period of baseline studies while receiving usual oral diet and PN and then began receiving modified diets designed to improve nutrient absorption and daily oral calcium/vitamin D supplements (1500 mg elemental calcium and 600 IU vitamin D, respectively). Subjects were randomized to receive in a double-blind manner either subcutaneous (sc) saline placebo as the control or hGH (0.1 mg/kg/d for 3 weeks, then 0.1 mg/kg 3 days a week for 8 subsequent weeks). Open-label hGH was given from week 13 to week 24 in subjects who required PN after completion of the 12-week double-blind phase. Markers of bone turnover (serum osteocalcin and urinary N-telopeptide [NTX]), vitamin D nutriture (serum calcium, 25-hydroxyvitamin D [25-OH D] and parathyroid hormone [PTH] concentrations), and intestinal calcium absorption were measured at baseline and at weeks 4 and 12. Dual x-ray absorptiometry (DXA) of the hip and spine was performed to determine bone mineral density (BMD) at baseline and weeks 12 and 24. RESULTS: The majority of subjects in each group exhibited evidence of vitamin D deficiency at baseline (25-OH D levels<30 ng/mL; 78% and 79% of control and hGH-treated subjects, respectively). Subjects treated with hGH demonstrated a significant increase from baseline in serum osteocalcin levels at 12 weeks (+62%; p<.05). The levels of NTX were increased over time in the hGH-treated group; however, this did not reach statistical significance. Both NTX and osteocalcin remained unchanged in control subjects. BMD of the spine and total hip was unchanged in subjects treated with placebo or hGH at 24 weeks. However, femoral neck BMD was slightly but significantly decreased in the placebo group at this time point but remained unchanged from baseline in the hGH-treated subjects. CONCLUSIONS: hGH therapy significantly increased markers of bone turnover during the initial 3 months of therapy and stabilized femoral neck bone mass over a 6-month period in patients with severe SBS undergoing intestinal rehabilitation.     

Comparative effects of vitamin K and vitamin D supplementation on calcium balance in young rats fed normal or low calcium diets

We examined the effect of vitamin K and vitamin D supplementation on calcium balance in young rats fed a normal or low calcium diet. Eighty female Sprague-Dawley rats, 6 wk of age, were randomized by the stratified weight method into eight groups with 10 rats in each group: 0.5% (normal) or 0.1% (low) calcium diet, 0.5% or 0.1% calcium diet+vitamin K (vitamin K2, menatetrenone, 30 mg/100 g, food intake), 0.5% or 0.1% calcium diet+vitamin D (25 microg/100 g, food intake), and 0.5% or 0.1% calcium diet+vitamin K+vitamin D. The duration of the study was 10 wk. Vitamin K supplementation promoted the reduction in urinary calcium excretion and retarded the abnormal elevation of serum PTH level in rats fed a low calcium diet, and stimulated intestinal calcium absorption in rats fed a normal calcium diet. Vitamin D supplementation stimulated intestinal calcium absorption with prevention of the abnormal elevation of serum PTH levels and prevented hypocalcemia in rats fed a low calcium diet, and stimulated intestinal calcium absorption in rats fed a normal calcium diet. The stimulation of intestinal calcium absorption was associated with increased serum 1,25-dihydroxyvitamin D levels. An additive effect of vitamin K and vitamin D on intestinal calcium absorption was found only in rats fed a normal calcium diet. This study shows the differential effects of vitamin K and vitamin D supplementation on calcium balance in young rats fed a normal or low calcium diet.     

Vitamin D status and concentrations of serum vitamin D metabolites and osteocalcin in elderly patients with femoral neck fracture: a follow-up study

Vitamin D status and the serum osteocalcin concentration in patients with femoral neck fractures were studied as follows. Thirty-seven elderly patients (P) with fracture of the femoral neck were studied, whereas 24 age-matched persons (C) seen at the out-patient department for non-orthopaedic reasons served as controls. The dietary intake of vitamin D, estimated using a vitamin D score based on food items known to be the main sources of vitamin D, was significantly lower in the patients than in the controls. There was no difference in the serum 25-hydroxy-vitamin D (25-OH-D) (P: 22.3 +/- 7.5 nmol/l; C: 27.5 +/- 13.5) or the serum 1,25-dihydroxy-vitamin D3 concentration (P: 86 +/- 43 pmol/l; 31) C: 85 +/- 31) between the groups. The 25-OH-D concentration was, however, low as compared to reference values, suggesting vitamin D deficiency in both groups. There was no difference in the serum osteocalcin concentration between the groups (P: 3.1 +/- 1.7 micrograms/l; C: 3.4 +/- 1.5). One year later the serum osteocalcin concentrations (5.9 +/- 2.2 micrograms/l, n = 11) was significantly higher (P less than 0.005) in the patients than at the time of the fracture (3.2 +/- 2.2 micrograms/l), indicating an active bone turnover in the patients still present 1 year after the fracture.     

Subclinical vitamin D deficiency is increased in adolescent girls who wear concealing clothing

Vitamin D deficiency continues to be a worldwide problem, especially in developing countries. The aim of this study was to investigate potential risk factors for vitamin D deficiency. Girls (n = 89) aged 13 to 17 y were enrolled in the study. Study subjects were stratified into 3 groups: Group I included girls living in a suburban area; Group II girls lived in an urban area, and Group III girls lived in an urban area and wore concealing clothes for religious reasons. At the end of winter (in April) serum 25-hydroxyvitamin D [25(OH)D] levels were measured and dietary data were collected using questionnaires. Vitamin D deficiency was defined as a serum 25(OH)D concentration < 25 nmol/L, and insufficiency as a 25(OH)D concentration between 25 and 50 nmol/L. The lumbar and femur neck bone mineral densities (BMD) were measured using dual X-ray absorptiometry (DEXA). Overall, 39 girls (43.8%) had vitamin D insufficiency and 19 (21.3%) had vitamin D deficiency. In group III (wearing covered dress) the serum 25(OH)D concentrations (28.13 +/- 12.53 nmol/L) were significantly lower than in the other 2 groups, and within this group, 50% of girls were vitamin D deficient. The lumbar and femur neck BMD of girls with lower 25(OH)D levels did not differ from those with adequate vitamin D levels. We conclude that vitamin D deficiency is an important problem in Turkish adolescent girls, especially in those who follow a religious dress code; therefore, vitamin D supplementation appears to be necessary for adolescent girls.     

Iron deficiency negatively affects vertebrae and femurs of rats independently of energy intake and body weight

The question of whether iron deficiency has direct adverse effects on vertebral trabecular bone and long bones was answered by this study. Four groups of female weanling rats were fed for 5 wk diets that were 1) control; 2) calcium restricted, 1.0 g Ca/kg diet; 3) iron deficient, <8 mg Fe/kg diet; or 4) control, pair-fed to the iron-deficient group. Whole body and femur DEXA analysis revealed that calcium-restricted and iron-deficient rats had lower bone mineral density (BMD) and content (BMC) than pair-fed and control rats. However, pair-fed rats also had decreased BMD and BMC compared to control rats. The third lumbar trabecular bone microarchitecture in both diet-restricted groups had decreased bone volume fraction (BV/TV) and trabecular number and thickness, a less favorable structural model index, and increased trabecular separation compared with the controls and the pair-fed groups as determined by microcomputer tomography. The control and pair-fed groups did not differ from one another, suggesting that iron deficiency and calcium restriction affected vertebrae independently of food intake and body weight. Finite element analysis revealed lower force to compress the vertebrae and lower stiffness but greater von Mises stress in calcium-restricted and iron-deficient groups compared to the control and pair-fed groups. Urinary deoxypyridinium crosslinks, serum osteocalcin, and cholcalciferol were increased in calcium-restricted rats compared to the other 3 groups. Using micro-CT imaging technology, this study demonstrated microarchitectural pathology due to iron deficiency upon vertebral trabecular bone compared to the control and pair-fed rats, although not to the same extent as severe calcium restriction.