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对幼鼠骨代谢的影响

目的探讨不同剂量的维生素Ｋ对幼鼠骨代谢的影响。方法选用４０只雄性断乳大鼠，分为４组：１组饲料中维生素Ｋ水平为５０μｇ／ｋｇ，并添加１％磺胺药阻断肠道菌群合成维生素Ｋ，其余３组饲料维生素Ｋ水平分别为５０、３００、２５５０μｇ／ｋｇ。实验进行３个月，通过钙代谢实验、骨代谢生化指标及骨密度的改变，综合评价维生素Ｋ对幼鼠骨代谢的影响。结果不同剂量水平的维生素Ｋ对大鼠胃肠道钙吸收无显著影响；维生素Ｋ缺乏组动物尿钙、尿羟脯氨酸排出增高，提示维生素Ｋ缺乏导致骨分解代谢增强；血清骨钙素及股骨骨密度随膳食维生素Ｋ摄入水平增加而提高，高剂量组显著高于维生素Ｋ缺乏组，而凝血酶原时间各组间差异无显著性。结论目前根据凝血功能制定的大鼠饲料维生素Ｋ的供给量不能满足幼鼠骨生长发育要求，幼鼠骨发育对维生素Ｋ的需求很可能高于５０μｇ／ｋｇ饲料。     

一种有机镓化合物对大鼠骨镓,钙及磷含量的影响

目的 探讨接触有机镓对动物骨镓、骨钙和骨磷含量的影响。方法 采用亚急性和慢笥动物染毒实验,将不同剂量的有机镓灌胃,分别偿同时间后大鼠的一般状况及及死后股骨中镓、钙、磷的含量及钙／磷比值。结果 亚急性染毒各剂量组动物股骨中镓及磷含量与对照组判别显著（Ｐ〈０．０１）,而骨钙值只有１２ｍｇ／ｋｇ剂量组与对照组有显著差异。慢性染毒各剂量组骨镓、钙、磷均与对照组差别显著（Ｐ〈０．０５）。而实验组与对照组的骨     

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。     

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     

补充钙、维生素D及镁、锌、铜对大鼠骨密度和骨强度的影响

目的观察在补充钙、维生素D的同时补充镁、锌、铜对大鼠骨密度和骨强度的影响。方法30只初始体重65～75g的清洁级断乳Wistar雄性大鼠,根据体重随机分为3组,即低钙饲料对照组、受试物低剂量实验组和高剂量实验组,每组10只。实验周期为12周。测定右侧股骨长度、重量、股骨骨密度及骨钙含量,左侧股骨最大载荷、最大挠度、弹性能量吸收、最大应力、弹性模量。结果低、高剂量实验组大鼠的股骨重量、股骨远心端和股骨中点的骨密度、股骨钙含量、股骨的最大载荷和弹性能量吸收均显著高于低钙对照组(P<0.05)。结论补充钙、维生素D及镁、锌、铜能明显增强大鼠股骨的骨密度、骨强度,提示对延缓骨骼的老化有一定的作用。     

乳酸钙防治实验性骨质疏松的研究

对１２月龄雌性Ｗｉｓｔａｒ大鼠行双侧卵巢切除术一个月后，每天灌胃给予乳酸钙连续三个月。结果发现，与手术对照组相比，乳酸钙中剂量［２５０ｍｇ／（ｋｇ．ｄ）］能明显增强大鼠股骨骨密度（ｐ＜０．０５），低剂量［１２５ｍｇ／（ｋｇ．ｄ）］能明显降低大鼠血清碱性磷酸酶的活性（Ｐ＜０．０５），高［７５０ｍｇ／（ｋｇ．ｄ）］、中、低剂量均明显增加血清钙的含量（Ｐ＜０．０１），明显降低２４小时尿羟脯氨酸／肌酐比值（Ｐ＜０．０５），中、高剂量能明显增加２４小时尿钙／肌酐比值（Ｐ＜０．０５）、股骨灰分重及灰分与干重的百分比，而对股骨湿重、干重、体积及血清骨钙素的含量无明显影响。结果提示，乳酸钙具有抑制骨吸收作用，其防治骨质疏松作用机理主要与适当增高体内钙水平有关     

黑芝麻油对环磷酰胺诱导大鼠股骨骨丢失的影响

目的应用骨生物力学和micro-CT技术,探讨黑芝麻油对环磷酰胺诱导的大鼠骨丢失模型中股骨的显微结构和生物力学的影响,并与阳性药物阿仑膦酸钠对比。方法 32只SPF级雄性SD大鼠,随机分为正常对照组(CON)、环磷酰胺模型组(CP)、阿仑膦酸钠治疗组(ALD)、黑芝麻油治疗组(BSO),连续干预15d。实验结束后,取右侧股骨进行生物力学检测,然后进行Micro-CT扫描及三维重建。结果与CON组比较,CP组大鼠股骨的骨微观参数:骨体积分数、骨小梁数量、骨小梁厚度和骨密度明显减少,骨小梁分离度和结构模型指数明显增高;而股骨的骨生物力学参数:最大强度、断裂强度、断裂应变及韧性系数明显减少,刚性系数明显增加。与CP组相比,ALD组大鼠股骨的骨微观参数均得到了良好地修复,但骨生物力学参数中仅断裂应变、韧性系数和刚性系数三个参数得到了明显修复。而BSO组大鼠股骨的微观参数和生物力学参数均得到了显著修复。结论 3ml/kg·d的黑芝麻油能良好的对抗CP诱导的大鼠骨丢失模型中股骨微观结构和骨质量的退化,提示黑芝麻油的良好抗骨质疏松作用前景。     

磁力活化水对骨钙、高脂血症和脂质过氧化的影响

探讨磁力活化水对实验小鼠和大民谢的影响。「方法」以磁化杯处理的结自来水为受试物,就其对骨钙,高脂血症和脂质过化的影响进行了动物实验。「结果」小鼠股骨含钙量（少年组３０１．６６ｍｇ／ｇ,且２５５．２５ｍｇ／ｇ）与对照组（分别为２９０．０８ｍｇ／ｇ和２５８．０１ｍｇ／ｇ）判别无显著性。     

低龄大鼠NaF与血清生化和元素含量慢性剂量效应研究

断乳２ 周雄性 Ｗｉｓｔａｒ大鼠５４ 只,饲氟浓度３２、８２、２３２、１５３、４０３ ｍ ｇ／ｋｇ。实验３ 个月。氟引起了体重、血液学、骨骼元素、肝铝、骨铝、血清钙等诸方面的剂量－ 效应的反应。约在８～２３ ｍ ｇ／ｋｇ 饲氟浓度范围内出现许多检测指标的“翻板”现象,呈现与正常对照为基准的相反的含量变化的显著差异。饲氟＞ ２３２ ｍ ｇ／ｋｇ ４ 个组的肝铝成倍增高。肝铝和骨铝与骨氟显著正相关。肝铝与血液学,血清钙,骨钙、铁、磷明显相关,此与铝中毒和铝氟病病人及其鸡模型的研究结果相吻合。认为＞ ２３ ｍ ｇ／ｋｇ 浓度的高氟促进了铝的吸收和蓄积,并主要由铝引起相关的生物效应。     

The Canadian Home Total Parenteral Nutrition (HTPN) Registry: vitamin K supplementation and bone mineral density

Background: Vitamin K supplementation improves bone health, and its absence might be associated with low bone mineral density (BMD). The authors aim to assess vitamin K supplementation practices in Canadian home parenteral nutrition (HPN) programs and their relationship with BMD. Methods: This is a cross‐sectional study of 189 patients from the Canadian HPN registry. Results: All 189 patients studied received M.V.I.‐12, which does not contain vitamin K. Of those, 41.3% were supplemented with 10 mg of intravenous vitamin K (VK+) weekly, whereas the others did not receive vitamin K except via lipid emulsion (VK?). Short bowel syndrome accounted for 69% of VK+ and 46% of VK? patients. On univariate analysis, VK+ patients had substantially lower body mass index (BMI) and received lower bisphosphonate infusion than did VK?patients. There were no statistically significant differences in HPN calcium or lipid content, liver function test results, age, sex, or reason for HPN between the 2 groups. Patients who were VK+ had higher lumbar spine T scores and hip T scores than did VK?patients. General linear modeling analysis, adjusted for BMI, age, PN magnesium, PN phosphate, PN calcium, and bisphosphonate as possible predictors of BMD, showed a trend toward better hip T scores (P = .063) for VK+ patients compared with VK? patients. Conclusion: In HPN patients supplemented with vitamin K, the trend toward a better hip BMD compared with no supplementation suggests a role for vitamin K in preserving BMD. This requires further study.     

膳食钙、磷以及奶制品对绝经后妇女骨密度的影响

目的探讨膳食中钙、磷以及奶制品的摄入量对骨密度及骨盐含量的影响,为研究骨质疏松的预防提供相关线索和依据。方法在广州市越秀区农林街社区发放传单招募调查对象,并采用自编的结构化标准问卷,对320名广州绝经后妇女的膳食习惯进行调查,并测量其全身、股骨全身、股骨颈、股骨干、大粗隆、Ward’s三角以及腰锥1～4的骨密度和骨量,采用多因素逐步回归分析探讨膳食钙、磷及奶制品对骨盐含量及骨密度的影响。结果 320名调查对象平均57.1岁,平均绝经年限7.3年,平均每天摄入钙、磷及奶制品分别为822 mg、949 mg和126 g,平均全身骨密度为1.054 g/cm2,磷与7个部位的骨密度及骨盐含量呈正相关关系（P〈0.05）。随着磷摄入量增加,全身及腰锥1～4骨密度增加,偏回归系数值分别为0.121和0.184 g.（cm2）-1.g-1.d-1。随着奶制品摄入量增加,股骨全身、股骨干骨密度也相应增加,骨密度偏回归系数值分别为0.686、0.841mg.（cm2）-1.g-1.d-1。钙与全身、股骨全身、股骨颈、大粗隆、股骨干和Ward’s三角的BMC具有正相关性,而在钙与BMD关系中,钙只与股骨全身、大粗隆和股骨干呈正相关性,且每日膳食中每增加100 g钙的摄入量,则股骨全身、大粗隆、股骨干的骨密度相应增加5.3、4.8和7.6 g/cm2。结论增加膳食中钙、磷以及奶制品的摄入量有利于绝经后妇女的骨盐含量及骨密度的提高。     

Vitamin D supplementation and bone mineral density in early postmenopausal women

BACKGROUND: Increased vitamin D intake may preserve or increase bone mineral density (BMD) in older persons. OBJECTIVE: A 2-y double-blind study was undertaken to determine whether weekly administration of 10 000 units of vitamin D(2) maintained or increased BMD in younger postmenopausal women more efficiently than did calcium supplements alone. DESIGN: One hundred eighty-seven women who were >or= 1 y postmenopausal were randomly assigned to take either 1000 mg Ca/d after the evening meal or 1000 mg Ca/d plus 10 000 U vitamin D(2)/wk in a double-blind, placebo-controlled format. The BMD of the proximal forearm, lumbar spine, femoral neck, Ward's triangle, and femoral trochanter was measured at 6-mo intervals by osteodensitometry. RESULTS: During the 2-y period, there was no significant difference in the change in BMD at any site between the subjects taking calcium supplements and those taking calcium plus vitamin D(2). Both groups significantly (P < 0.005) gained BMD in Ward's triangle and the femoral trochanter but significantly (P < 0.005) lost bone in the proximal radius. There was no significant change in the lumbar spine or femoral neck BMD. CONCLUSION: In younger postmenopausal women ( age: 56 y) whose average baseline serum 25-hydroxyvitamin D concentration was well within the normal range, the addition of 10 000 U vitamin D(2)/wk to calcium supplementation at 1000 mg/d did not confer benefits on BMD beyond those achieved with calcium supplementation alone.     

Vitamin K2 Therapy for Postmenopausal Osteoporosis

Vitamin K may play an important role in the prevention of fractures in postmenopausal women with osteoporosis. Menatetrenone is the brand name of a synthetic vitamin K₂ that is chemically identical to menaquinone-4. The present review study aimed to clarify the effect of menatetrenone on the skeleton in postmenopausal women with osteoporosis, by reviewing the results of randomized controlled trials (RCTs) in the literature. RCTs that investigated the effect of menatetrenone on bone mineral density (BMD), measured by dual-energy X-ray absorptiometry and fracture incidence in postmenopausal women with osteoporosis, were identified by a PubMed search for literature published in English. Eight studies met the criteria for RCTs. Small RCTs showed that menatetrenone monotherapy decreased serum undercarboxylated osteocalcin (ucOC) concentrations, modestly increased lumbar spine BMD, and reduced the incidence of fractures (mainly vertebral fracture), and that combined alendronate and menatetrenone therapy enhanced the decrease in serum ucOC concentrations and further increased femoral neck BMD. This review of the literature revealed positive evidence for the effects of menatetrenone monotherapy on fracture incidence in postmenopausal women with osteoporosis. Further studies are required to clarify the efficacy of menatetrenone in combination with bisphosphonates against fractures in postmenopausal women with osteoporosis.     

Tocotrienols are needed for normal bone calcification in growing female rats

In this study the effects of vitamin E deficiency and supplementation on bone calcification were determined using 4-month-old female Sprague-Dawley rats. The rats weighed between 180 and 200 g. The study was divided in three parts. In experiment I the rats were given normal rat chow (RC, control group), a vitamin E deficient (VED) diet or a 50% vitamin E deficient (50%VED) diet. In experiment 2 the rats were given VED supplemented with 30 mg/kg palm vitamin E (PVE30), 60 mg/kg palm vitamin E (PVE60) or 30 mg/kg pure alpha-tocopherol (ATF). In experiment 3 the rats were fed RC and given the same supplements as in experiment 2. The treatment lasted 8 months. Vitamin E derived from palm oil contained a mixture of ATF and tocotrienols. Rats on the VED and 50%VED diets had lower bone calcium content in the left femur compared to the RC group (91.6 +/- 13.3 mg and 118.3 +/- 26.0 mg cf 165.7 +/- 15.2 mg; P < 0.05) and L5 vertebra (28.3 +/- 4.0 mg and 39.5 +/- 6.2 mg compared with 51.4 +/- 5.8 mg; P < 0.05). Supplementing the VED group with PVE60 improved bone calcification in the left femur (133.6 +/- 5.0 mg compared with 91.6 +/- 13.3 mg; P < 0.05) and L5 vertebra (41.3 +/- 3.3 mg compared with 28.3 +/- 4.0 mg; P < 0.05) while supplementation with PVE30 improved bone calcium content in the L5 vertebra (35.6 +/- 3.1 mg compared with 28.3 +/- 4.0 mg; P < 0.05). However, supplementation with ATF did not change the lumbar and femoral bone calcium content compared to the VED group. Supplementing the RC group with PVE30, PVE60 or ATF did not cause any significant changes in bone calcium content. In conclusion, vitamin E deficiency impaired bone calcification. Supplementation with the higher dose of palm vitamin E improved bone calcium content, but supplementation with pure ATF alone did not. This effect may be attributed to the tocotrienol content of palm vitamin E. Therefore, tocotrienols play an important role in bone calcification.     

Bone and gastric bypass surgery: effects of dietary calcium and vitamin D

OBJECTIVE: To examine bone mass and metabolism in women who had previously undergone Roux-en-Y gastric bypass (RYGB) and determine the effect of supplementation with calcium (Ca) and vitamin D. RESEARCH METHODS AND PROCEDURES: Bone mineral density and bone mineral content (BMC) were examined in 44 RYGB women (> or = 3 years post-surgery; 31% weight loss; BMI, 34 kg/m(2)) and compared with age- and weight-matched control (CNT) women (n = 65). In a separate analysis, RYGB women who presented with low bone mass (n = 13) were supplemented to a total 1.2 g Ca/d and 8 microg vitamin D/d over 6 months and compared with an unsupplemented CNT group (n = 13). Bone mass and turnover and serum parathyroid hormone (PTH) and 25-hydroxyvitamin D were measured. RESULTS: Bone mass did not differ between premenopausal RYGB and CNT women (42 +/- 5 years), whereas postmenopausal RYGB women (55 +/- 7 years) had higher bone mineral density and BMC at the lumbar spine and lower BMC at the femoral neck. Before and after dietary supplementation, bone mass was similar, and serum PTH and markers of bone resorption were higher (p < 0.001) in RYGB compared with CNT women and did not change significantly after supplementation. DISCUSSION: Postmenopausal RYGB women show evidence of secondary hyperparathyroidism, elevated bone resorption, and patterns of bone loss (reduced femoral neck and higher lumbar spine) similar to other subjects with hyperparathyroidism. Although a modest increase in Ca or vitamin D does not suppress PTH or bone resorption, it is possible that greater dietary supplementation may be beneficial.     

Glucocorticoid-induced osteoporosis

Chronic glucocorticoid treatment is the most frequent cause of secondary osteoporosis. The direct inhibitory effect of glucocorticoids on osteoblasts results in decreased bone formation. Increased osteoclastic bone resorption due to low concentrations of gonadal steroid hormones and glucocorticoid-induced direct suppression of intestinal calcium absorption also contribute to the decrease of bone mass in these patients. Bone loss is rapid, particularly in the first months of glucocorticoid therapy. Bone mineral density of the lumbar spine and proximal femur should be measured in patients who are starting chronic therapy with glucocorticoids. Although glucocorticoid-induced osteoporosis is a severe and nowadays partially preventable disorder, osteoporosis prophylaxis is only rarely prescribed to these patients. Recent randomized, controlled trials proved the therapeutic effects of hormone replacement therapy, as well as of bisphosphonates and active vitamin D analogs in primary and secondary prevention of glucocorticoid-induced osteoporosis.     

Nutrition, mild hyperparathyroidism, and bone mineral density in young Japanese women

BACKGROUND: The adverse effects of poor nutrition on the bones of young Asian women have not been fully elucidated. OBJECTIVE: The purpose of this study was to investigate possible associations of vitamin D nutrition, calcium intake, and other nutrients with bone metabolism and bone mass in young Japanese women. DESIGN: The subjects were 108 female college students aged 19-25 y. Dietary nutrients were measured by using the duplicate sampling method on 3 weekdays. Serum 25-hydroxyvitamin D [25(OH)D], intact parathyroid hormone, and bone turnover markers were also measured. Bone mineral density (BMD) of the spine and femur was measured by dual-energy X-ray absorptiometry. RESULTS: The proportions of the subjects with low 25(OH)D (< 30 nmol/L) and high intact parathyroid hormone (> or = 6.9 pmol/L) concentrations were 32.4% and 15.7%, respectively. Serum 25(OH)D concentrations (P = 0.0265) and calcium intake (P = 0.0103) were inversely associated with serum intact parathyroid hormone. In addition to weight and physical activity, the presence of mild hyperparathyroidism was associated with a low BMD of the lumbar spine (P = 0.0062) and the femoral neck (P = 0.0250), and a low calcium intake was associated with a low BMD of the femoral neck (P = 0.0044). CONCLUSIONS: Low calcium intake (based on low BMD of the femoral neck only) and mild hyperparathyroidism (based on low BMD of both the femoral neck and lumbar spine), partly explained by low vitamin D nutrition and a low calcium intake, are important predictors of low BMD in young Japanese women. Effects of poor nutrition and mild hyperparathyroidism on bone peak bone mass in young women should be further investigated in longitudinal studies.     

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。