2015年中国农村老年人维生素A营养状况及影响因素

目的了解中国农村老年人维生素A水平及影响因素。方法采用随机抽样方法选取2015年中国成人慢性病与营养监测生物样本库的农村老年人血清样本,共纳入3134名60岁以上农村老年人作为研究对象。采用问卷调查收集研究对象基本信息,利用高效液相色谱法分析仪测定调查对象血清中维生素A含量,依据WHO推荐的标准判定人群维生素A营养状况,应用多因素Logistic回归模型探讨中国农村老年人维生素A缺乏与影响因素的关联性。结果血清维生素A含量[M(P25,P75)]为1.92(1.50,2.45)μmoL/L。经加权后的维生素A缺乏率为0.99%,边缘缺乏率为4.38%。西部地区维生素A边缘缺乏率显著高于东部和中部地区,80岁及以上人群显著高于其他年龄,消瘦者显著高于其他,已婚者显著低于未婚/离婚/丧偶者。多因素Logistic回归模型分析显示,性别、年龄和体质指数对维生素A营养状况的影响具有统计学意义(P<0.05)。结论 2015年中国农村老年人维生素A营养状况较好,缺乏率较低。     

海南省琼中县中小学学生血清维生素A水平分析

目的了解海南省琼中县中小学学生血清维生素A水平,为该县相应人群维生素A缺乏的防治提供实验依据。方法采用分层整群随机抽样法,抽取琼中县2所小学和2所初中学校,每个学校各年级一个班的学生为研究对象,采用高效液相色谱法检测其血清视黄醇含量。结果 1)共检测561例,琼中县中小学学生血清视黄醇平均水平为(360.36±91.39)ng/mL,且血清视黄醇平均水平在男、女生间差异无统计学意义(P0.05),但其随年龄的增长而升高(P0.05)。2)维生素A缺乏率(≤200ng/mL)为2.0%,边缘缺乏率(200~300ng/mL)为22.3%,两者性别差异均无统计学意义(P0.05),但边缘缺乏率随着年龄的增长总体呈下降趋势(P0.05)。结论琼中县中小学学生维生素A缺乏率较低,但边缘缺乏率较高,应注意监测,且该地区维生素A缺乏重点防治对象为6~7岁的学生。     

锌与维生素A缺乏对小鼠免疫功能的影响

目的：通过建立动物模型，观察边缘性锌(Zn)与维生素A(VA)缺乏对小鼠免疫功能的影响，为在人群中科学而合理地实施Zn与VA的联合干预提供理论依据。方法：将BALB／C小鼠按体重随机分为Zn缺乏VA正常组(ZD)，VA缺乏Zn正常组(AD)，Zn缺乏VA缺乏组(zAD)，VA正常和Zn正常组(contr01)，饲养7周后，眼框取血测血清Zn和VA，无菌取脾制备脾单细胞悬液进行培养，测定脾抗体生成细胞(PFC)数、脾T淋巴细胞增值(MTT法)和NK细胞活性(LDH释放法)。结果：ZAD组小鼠脾脏重量和胸腺重量与control组比较有显著性降低，脾脏系数和胸腺系数各组差异无统计学意义；ZAD组小鼠血清Zn、VA、小鼠抗体生成细胞(PFC)数(体液免疫指标)，脾T淋巴细胞增殖与NK细胞活性(细胞免疫指标)均显著低于Control组和其它实验组。结论：边缘性Zn与VA缺乏对小鼠细胞免疫和体液免疫均有损伤，损伤程度较单一缺乏严重。     

儿童维生素A与铁营养状况的相关性研究

目的了解中国儿童维生素A(VA)的营养状况、VA缺乏率、VA边缘缺乏率,研究血浆VA与铁营养状况的相关性。方法由2002年“中国居民营养与健康状况调查”的大样本中随机抽取380名3~12岁儿童,检测血浆VA含量,同时测定血红蛋白(Hb)、总铁结合力(TIBC)、铁蛋白(SF)及转铁蛋白受体(sTfR)。了解儿童VA营养状况,计算VA缺乏率、VA边缘缺乏率,研究VA与铁营养状况评价指标的相关性。结果受试儿童VA平均含量为(1·03±0·24)μmol/L,其中8·4%儿童VA缺乏,44·7%儿童VA边缘缺乏。血浆VA与Hb呈正相关(r=0·16986,P<0·01),与sTfR呈负相关(r=-0·12863,P<0·05),与TIBC、SF不相关。结论铁缺乏伴随VA边缘缺乏在中国儿童中普遍存在,VA与铁营养状况存在相关性。     

Low vitamin a intake affects milk iron level and iron transporters in rat mammary gland and liver

Marginal vitamin A deficiency is common and can result in a secondary iron (Fe) deficiency. A positive correlation between maternal Fe status and milk Fe was observed in lactating women supplemented with both vitamin A and Fe but not with Fe alone, suggesting effects of vitamin A on mammary gland Fe transport. We hypothesized that low vitamin A intake during lactation elicits differential effects on mammary gland and liver Fe transport and storage proteins, thus affecting milk Fe concentration but not maternal Fe status. We fed rats a control (CON, 4 RE/g) or a marginal vitamin A diet (AD, 0.4 RE/g) through midlactation. Effects on plasma, milk, liver and mammary gland Fe and vitamin A concentrations, and divalent metal transporter-1 (DMT1), ferroportin (FPN), ferritin (Ft), and transferrin receptor (TfR) expression were determined. Dams fed AD were not vitamin A or Fe deficient. Milk and liver vitamin A and Fe and mammary gland Fe concentrations were lower in rats fed AD compared with rats fed CON. Liver TfR expression was higher, whereas mammary gland TfR expression was lower in rats fed AD compared with rats fed CON. Liver Ft was unaffected, whereas mammary gland Ft was lower in rats fed AD compared with rats fed CON. Liver and mammary gland DMT1 and FPN protein levels were lower in rats fed AD compared with rats fed CON. Our results indicate that the mammary gland and liver respond differently to marginal vitamin A intake during lactation and that milk Fe is significantly decreased due to effects on mammary gland Fe transporters, putting the nursing offspring at risk for Fe deficiency.     

维生素A缺乏对大鼠铁调节蛋白2影响

目的 探讨维生素A缺乏对大鼠铁调节蛋白2(IRP2)mRNA及铁蛋白(Fn) nRNA和转铁蛋白受体(TfR)mRNA表达影响.方法48只雄性SD大鼠按体重随机分为4组,每组12只,对照组、维生素A完全缺乏组;维生素A边缘缺乏组;铁及维生素A边缘缺乏组;喂养8周后,麻醉处死大鼠,取组织和血清,进行相关指标和基因表达检测.结果与对照组( 1.50 +0.41) μmol/L比较,维生素A完全缺乏大鼠血清维生素A(0.22±0.26) μmol/L水平明显降低(P＜0.05);与对照组比较,维生素A完全缺乏组大鼠血清铁(2.26 +0.72)lμg/mL明显降低;维生素A完全缺乏组大鼠肝脏IRP2、TfR表达水平分别为(1.53±0.18)、(0.62±0.06)与对照组相比明显升高,FnmRNA (0.52±0.08),明显低于对照组(P＜0.05).结论维生素A缺乏通过改变IRP2表达、IRP-RNA结合活性,在转录后水平改变TfR和Fn mRNA表达,影响铁稳态.     

Long-term marginal intakes of zinc and retinol affect retinol homeostasis without compromising circulating levels during lactation in rats.

Marginal zinc or vitamin A intake is more common than previously thought in industrialized and developing countries, with pregnant and lactating women believed to be particularly at risk. However, the lack of sensitive indicators of zinc and vitamin A status precludes accurate assessment of marginal nutriture. Concurrent deficiencies in zinc and vitamin A intake often coexist, and the interaction between zinc deficiency and vitamin A metabolism may confound results from epidemiologic or intervention studies. To investigate effects of a maternal diet chronically restricted in zinc or vitamin A intake on indices of vitamin A metabolism, we fed rats a control diet (C) or a diet marginal in zinc (ZD), marginal in vitamin A (AD), marginal in both (DD) or pair-fed to DD (PF), preconception through lactation. Plasma retinol (ROH) was greater and retinol binding protein (RBP) was lower in rats fed ZD, AD and DD compared with those fed C. Hepatic cellular retinol binding protein (CRBP) expression was greater than controls in rats fed ZD and AD and lower in those fed DD, whereas RBP expression was greater in the DD- and PF-fed groups compared with rats C. Mammary gland CRBP and RBP expression were not affected by the diets. Milk ROH was lower in rats fed AD, and milk RBP was lower in those fed ZD and DD compared with rats fed C. In summary, chronic, marginal intake of zinc or vitamin A resulted in alterations in tissue retinol metabolism and milk retinol levels without decreasing plasma zinc, retinol or ROH:RBP during lactation. These observations are of concern because these parameters, which are commonly used to assess zinc and vitamin A status, may lead to misassessment of marginal zinc or vitamin A nutriture in some human populations.     

维生素A营养状况对学龄前支气管哮喘患儿T淋巴细胞亚群、相关炎症介质及预后转归的影响

目的 研究维生素A营养状况对学龄前支气管哮喘患儿T淋巴细胞亚群、相关细胞因子及预后转归的影响,为支气管哮喘防治提供理论依据。方法 收集2017年6月-2019年6月鄂东医疗集团黄石市妇幼保健院收治的学龄前支气管哮喘患儿120例的临床资料(病例组),同期选择本院体检的健康的学龄期儿童80例对照组。将病例组按照住院期间维生素A营养状况分为维生素A正常组、维生素A边缘缺乏组、维生素A缺乏组。比较病例组和对照组维生素A营养状况,并记录不同维生素A状况组干预前后T淋巴细胞亚群、相关炎症介质及预后转归。结果 病例组维生素A水平[(0.73±0.32)μmol/L]显著低于对照组[(1.02±0.23)μmol/L](t=5.957,P＜0.05),且病例组维生素A营养状况显著差于对照组(Z=4.865,P＜0.05),维生素A缺乏组治疗后的CD4+、CD4+/CD8+均低于另外两组,CD8+高于另外两组,差异有统计学意义(P＜0.05)。维生素A缺乏组治疗后的hs-CRP、EOS、IL-6高于另外两组,差异有统计学意义(P＜0.05)。三组治疗临床疗效比较差异有统计学意义(χ²=13.165,P＜0.05),其中以维生素A缺乏组临床疗效最差(52.17%),维生素A正常组最高(94.74%)。结论 维生素A边缘缺乏或缺乏在学龄前支气管哮喘患儿中较为常见,对患儿细胞免疫功能、炎症反应的改善及疾病的预后转归造成不良影响,临床应当加强患儿维生素A的监测,适时酌情补充维生素A制剂以改善患儿预后。     

维生素A营养状况对学龄前支气管哮喘患儿T淋巴细胞亚群、相关炎症介质及预后转归的影响

目的 研究维生素A营养状况对学龄前支气管哮喘患儿T淋巴细胞亚群、相关细胞因子及预后转归的影响,为支气管哮喘防治提供理论依据。方法 收集2017年6月-2019年6月鄂东医疗集团黄石市妇幼保健院收治的学龄前支气管哮喘患儿120例的临床资料(病例组),同期选择本院体检的健康的学龄期儿童80例对照组。将病例组按照住院期间维生素A营养状况分为维生素A正常组、维生素A边缘缺乏组、维生素A缺乏组。比较病例组和对照组维生素A营养状况,并记录不同维生素A状况组干预前后T淋巴细胞亚群、相关炎症介质及预后转归。结果 病例组维生素A水平[(0.73±0.32)μmol/L]显著低于对照组[(1.02±0.23)μmol/L](t=5.957,P＜0.05),且病例组维生素A营养状况显著差于对照组(Z=4.865,P＜0.05),维生素A缺乏组治疗后的CD4+、CD4+/CD8+均低于另外两组,CD8+高于另外两组,差异有统计学意义(P＜0.05)。维生素A缺乏组治疗后的hs-CRP、EOS、IL-6高于另外两组,差异有统计学意义(P＜0.05)。三组治疗临床疗效比较差异有统计学意义(χ²=13.165,P＜0.05),其中以维生素A缺乏组临床疗效最差(52.17%),维生素A正常组最高(94.74%)。结论 维生素A边缘缺乏或缺乏在学龄前支气管哮喘患儿中较为常见,对患儿细胞免疫功能、炎症反应的改善及疾病的预后转归造成不良影响,临床应当加强患儿维生素A的监测,适时酌情补充维生素A制剂以改善患儿预后。     

2015年中国农村孕妇维生素A营养状况

目的评价中国农村孕妇维生素A的营养状况。方法数据来自2015年“中国成人慢性病与营养监测”,共调查了3273名孕妇,采用高效液相色谱法测定血清中视黄醇含量,采用免疫透射比浊法测定C反应蛋白和α-酸性糖蛋白。分析孕妇视黄醇含量在不同地域、年龄、民族、体质指数、文化程度、孕周、人均家庭收入及不同炎症状态下的分布情况,比较不同状况下孕妇维生素A缺乏率和边缘缺乏率。结果中国农村孕妇血清视黄醇含量[M(P25,P75)]为0.47(0.36,0.61)mg/L,且不同地区、年龄、文化程度、孕期分布及不同人均家庭收入间差异有统计学意义(P<0.01)。孕妇维生素A边缘缺乏率和缺乏率分别为10.5%和1.2%,且在不同年龄、孕期、是否存在炎症状态间差异具有统计学意义(P<0.01)。孕晚期人群的总体缺乏率为2.1%,边缘缺乏率为14.2%;30~44岁孕妇的总体缺乏率2.0%,边缘缺乏率12.2%。结论2015年中国农村孕妇维生素A营养状况得到明显改善,但仍需重点关注孕晚期和30~44岁孕妇。     

Iron deficiency and marginal vitamin A deficiency affect growth,hematological indices and the regulation of iron metabolism genes in rats

Iron deficiency and marginal vitamin A (VA) deficiency frequently coexist and affect billions of people, mostly children and women, worldwide. The effects of these micronutrient deficiencies alone and in combination on hematologic, biochemical and molecular indices of iron and VA status were investigated in a 2 x 2 randomized blocked study conducted in growing male Sprague-Dawley rats. From 3-8 wk of age, rats were fed one of four purified diets that were either adequate or restricted in iron (Fe) and adequate or marginal in VA: (+)Fe(+)VA, 20.3 and 0.367 micro g/g, respectively, denoted control diet; (-)Fe(+)VA, 3.34 and 0.405 micro g/g; (+)FeVA(m), 22.2 and 0.051 micro g/g; or (-)FeVA(m), 3.03 and 0.055 micro g/g. Weight-matched rats fed adequate micronutrients were included to control for possible confounding effects of Fe deficiency on growth and feed efficiency. Iron restriction reduced (P < 0.05) weight gain, feed efficiency, blood hemoglobin and hematocrit. Plasma and liver iron and plasma transferrin saturation were reduced by approximately 50%, whereas liver transferrin mRNA and protein and transferrin receptor mRNA were elevated, as was liver ferritin light-chain protein and light-chain mRNA. Liver heavy-chain ferritin mRNA, hemopexin, ceruloplasmin and cellular retinol-binding protein mRNA were not affected by iron or VA restriction. Although marginal VA deficiency did not exacerbate indices of poor iron status during iron deficiency, iron deficiency was associated with lower plasma retinol and elevated liver VA concentrations. These results are consistent with an impaired mobilization of liver retinol during iron deficiency as well as multiple alterations in iron metabolism.     

The interaction between vitamin A status and Newcastle disease virus infection in chickens

Newcastle disease virus (NDV) infection in chickens differing in vitamin A status has been selected as a model to examine the interrelationship between marginal vitamin A deficiency and the severity of consequences of measles infection in humans. Day-old chickens with limited vitamin A reserves, the progeny of marginally vitamin A-deficient hens, were fed purified diets containing either marginal (120 retinol equivalents/kg diet, ad libitum) or adequate (1200 retinol equivalents/kg diet, ad libitum or pair-fed) levels of vitamin A for a period of 10 wk. At 4 wk of age, half of the chickens in each group were infected intraocularly with the lentogenic, i.e., mildly pathogenic, La Sota strain of NDV. Within 1 wk of infection, plasma retinol levels in the infected, marginally vitamin A-deficient chickens showed a significant and persistent decrease compared to their noninfected counterparts fed the same diet. Moreover, infection with NDV resulted in increased rates of morbidity in the marginally vitamin A-deficient chickens compared with nondeficient chickens. The results of this study indicate that pre-existing marginal vitamin A status increases the severity of disease following NDV infection, and that infection with NDV reduces marginal plasma vitamin A levels to levels which can be regarded as deficient.     

Marginal vitamin A deficiency in pigs experimentally infected with Trichuris suis: a model for vitamin A inadequacy in children.

The development of an experimental model for marginal vitamin A deficiency in humans is of major interest, enabling the elucidation of possible interactions with helminth infections. We established a useful experimental model for human vitamin A deficiency in young pigs; deficiency was induced through a depletion method encompassing both sow and offspring. We report on a 2 x 2 study in which 18-week-old vitamin A deficient pigs and vitamin A sufficient littermates were infected with both of the intestinal nematodes Trichuris suis and Ascaris suum and followed for 14 weeks through 32 weeks of age. Forty-nine pigs were followed with respect to bodyweight, liver biopsies and blood samples for retinol concentration and faecal samples for parasite eggs and worms. Liver and serum concentrations of vitamin A were significantly diminished in the vitamin A deficient (VAD) group as compared to the vitamin A sufficient (VAS) group both before (P < 0.001) and after inoculation with T. suis and A. suum (P < 0.02). A significant correlation between retinol content in micro-biopsy needle samples and gross liver content was found (r = 0.457, n = 48, P = 0.001). The adult T. suis worms in the VAD group were marginally smaller (36.7 vs 40.2 mm; P = 0.08), more orally located (section 2.9 vs 3.9; P = 0.08) and had a higher proportion of males (0.58 vs 0.50; P = 0.08) whereas there were no effects of diet treatment on fecundity. The proportion of pigs with faecal T. suis egg excretion 12 weeks post inoculation (p.i.) was significantly lower in the VAD group compared with the VAS infected group (21 vs 78%; P = 0.036). In addition, faecal T. suis egg excretion was significantly lower in the VAD group at both week 11 (P = 0.040) and week 12 p.i. (P = 0.021). Vitamin A deficiency may have altered the functional integrity of the mucosal intestinal epithelium, disrupting the normally delicate attachment of T. suis and leading to the premature termination of infection. However, a possible antagonistic interaction, if verified, should not preclude interventions to improve vitamin A status, i.e., treatment should accompany anthelmintic treatment.     

6月龄婴儿维生素A缺乏症的影响因素研究

目的调查深圳市龙岗区6月龄婴儿维生素A水平,分析维生素A缺乏症的影响因素,为维生素A缺乏症的防控提供依据。方法以2019年1—12月在龙岗区妇幼保健院儿保门诊接受健康体检的1638例6月龄婴儿为研究对象,检测婴儿血清维生素A水平,并分析维生素A缺乏症可能的影响因素。1638例婴儿根据喂养方式分为母乳喂养组(n=1005)、混合喂养组(n=228)和配方奶喂养组(n=405);根据维生素AD补充情况分为持续补充组(n=183)、交替补充组(n=420)及单独补充组(n=1035)。结果6月龄婴儿血清维生素A平均水平为(0.30±0.07)mg/L。维生素A缺乏的婴儿882例(53.84%),维生素A平均水平为(0.24±0.03)mg/L,其中边缘型维生素A缺乏795例(48.53%),亚临床型维生素A缺乏87例(5.31%);维生素A正常的婴儿756例,维生素A平均水平为(0.36±0.06)mg/L。持续补充组维生素A缺乏症检出率明显低于交替补充组及单独补充组,差异均有统计学意义(χ²值分别为26.818、36.050,均P<0.05)。母乳喂养组及混合喂养组维生素A缺乏症检出率均高于配方奶喂养组,差异均有统计学意义(χ²值分别为113.482、47.534,均P<0.05)。早产的婴儿维生素A缺乏症检出率高于足月的(χ²=16.957,P<0.05)。多因素二分类Logistic回归分析显示母乳喂养(OR=4.196)、混合喂养(OR=3.466)增加了婴儿维生素A缺乏症的发生风险(均P<0.05);持续补充维生素AD(OR=0.361)、足月(OR=0.326)、6月龄时未患营养不良(OR=0.257)、6月龄内未患呼吸道感染(OR=0.675)降低了维生素A缺乏症的发生风险(均P<0.05)。结论深圳市龙岗区6月龄婴儿维生素A缺乏症检出率较高,母乳喂养儿、混合喂养儿及早产儿出生后6月龄内应及时、合理地补充推荐摄入量的维生素AD。     

Morphological changes in the tracheal epithelium of guinea pigs in conditions of "marginal" vitamin A deficiency. A light, scanning- and transmission-electron microscopic study under special breeding conditions appropriate to early vitamin A deficiency.

The aim of the study was to find out the influence of marginal vitamin A deficiency on morphological structures in the tracheobronchial epithelium in guinea pigs. The tracheobronchial epithelium of animals with vitamin A deficiency (n = 15) and control animals (n = 7), kept under optimal laboratory conditions, was evaluated by light and electron microscopy. The cellular ultrastructure was morphometrically analyzed. The height of the respiratory epithelium was slightly increased. The basal cells were arranged in a loose cell band of three to four layers. The quantity of cytofilaments in their cytoplasm was enhanced. Goblet cells were significantly reduced in vitamin A deficiency. There was also a significant decrease in their secretory granules. The number of ciliated cells was almost unchanged. They showed a significant reduction in mitochondria. The kinocilia often contained an atypical structure of the microtubules. Our findings confirm multiple ultrastructural dysplasias in early vitamin A deficiency which may lead to a disturbance of mucociliary clearance.     

维生素A缺乏对大鼠细胞免疫功能的影响

方法：初断乳ＳＤ大鼠２４只，均分为严重ＶＡ缺乏（Ａ）、轻度ＶＡ缺乏（Ｂ）和正常对照（Ｃ）三组，饲含ＶＡ０、４００、６００ＩＵ／ｋｇ饲料８周，测定大鼠外周血淋巴细胞转化、Ｔ细胞亚群及单个核细胞ＩＬ－２，ＴＮＦ－α变化。结果：重度ＶＡ缺乏会导致大鼠胸腺和脾脏的萎缩，ＣＤ３、ＣＤ４亚群减少，ＣＤ４／ＣＤ８下降，淋巴细胞转化受抑，单个核细胞分泌ＩＬ－２、ＴＮＦ－α明显减少；轻度ＶＡ缺乏时，虽无明显临床表现，但ＣＤ４、ＣＤ４／ＣＤ８有所降低，ＩＬ－２及ＴＮＦ－α亦分泌减少。结论：轻度ＶＡ缺乏和严重ＶＡ缺乏均会使细胞免疫功能受损，需引起重视     

孕期亚临床维生素A缺乏对胎鼠肺形态发育的影响

【目的】 探讨孕期亚临床维生素A(vitamin A,VA)缺乏对胎鼠肺形态发育的影响。 【方法】 建立孕期VA正常(vitamin A normal,VAN)和亚临床缺乏(marginal vitamin A deficiency,MVAD)动物模型,每组均于孕19 d剖宫取胎鼠,比较其体重、肺重、肝重和肺组织VA含量及其肺视黄酸受体(retinoic acid receptor,RAR)mRNAs的表达,HE染色光镜观察胎鼠肺的形态结构。 【结果】 1)胎鼠基本情况的比较 体重、肺重和肝重三个指标VAN组均显著高于MVAD组(P<0.05);2)胎肺大体形态比较 低倍镜(×200)与高倍镜(×400)下观察结果显示,VAN组肺泡样结构分布较规则,肺泡间隔较薄,肺实质发育较好,肺间质毛细血管较丰富,肺泡2型细胞较明显,大多处于小管期;而MVAD组上述指标均相对较差,发育幼稚,局部为小管期,大多为假腺体期;3)胎鼠肺单位组织VA水平 VAN组>MVAD组,差异均有统计学意义(P<0.05);4)胎鼠肺RAR-α、RAR-γ和RAR-β mRNAs表达水平VAN组P<0.05)。 【结论】 孕期VA水平不同能影响胎鼠基本发育、胎肺形态结构、肺单位组织VA水平及其RAR mRNAs的表达;孕期MVAD时其胎肺发育相对较差。     

Effects of vitamin A deficiency on mitochondrial function in rat liver and heart

The aim of this study was to investigate comparative effects of vitamin A deficiency on respiratory activity and structural integrity in liver and heart mitochondria. Male rats were fed a liquid control diet (control rats) or a liquid vitamin A-deficient diet (vitamin A-deficient rats) for 50 days. One group of vitamin-A deficient rats was refed a control diet for 15 days (vitamin A-recovered rats). To assess the respiratory function of mitochondria the contents of coenzyme Q (ubiquinone, CoQ), cytochrome c and the activities of the whole electron transport chain and of each of its respiratory complexes were evaluated. Chronic vitamin A deficiency promoted a significant increase in the endogenous coenzyme Q content in liver and heart mitochondria when compared with control values. Vitamin A deficiency induced a decrease in the activity of complex I (NADH-CoQ reductase) and complex II (succinate-CoQ reductase) and in the levels of complex I and cytochrome c in heart mitochondria. However, NADH and succinate oxidation rates were maintained at the control levels due to an increase in the CoQ content in accordance with the kinetic behaviour of CoQ as an homogeneous pool. On the contrary, the high CoQ content did not affect the electron-transfer rate in liver mitochondria, whose integrity was preserved from the deleterious effects of the vitamin A deficiency. Ultrastructural assessment of liver and heart showed that vitamin A deficiency did not induce appreciable alterations in the morphology of their mitochondria. After refeeding the control diet, serum retinol, liver and heart CoQ content and the activity of complex I and complex II in heart mitochondria returned to normality. However, the activities of both whole electron transfer chain and complex I in liver were increased over the control values. The interrelationships between physiological antioxidants in biological membranes and the beneficial effects of their administration in mitochondrial diseases are discussed.     

Vitamin A deficiency impairs fetal islet development and causes subsequent glucose intolerance in adult rats

To determine the role of vitamin A in fetal islet development, beta- and alpha-cell mass, apoptosis, and alpha- and beta-cell replication were measured in rats using a model of marginal vitamin A deficiency. Female rats before and during pregnancy and their offspring postweaning were fed a diet containing retinol as retinyl palmitate at a low marginal (LM, 0.25 mg/kg diet) or a sufficient (SUFF, 4.0 mg/kg diet) level. Fetal islet size, replication, apoptosis, and offspring glucose tolerance were examined. Both beta-cell area and number per islet were reduced approximately 50% in fetuses from dams fed an LM vitamin A diet compared with those from dams fed the SUFF vitamin A diet. The alpha-cell area and number per fetal islet were not affected by vitamin A deficiency. Apoptosis was not increased. The percentage of newly replicated beta-cells in the LM fetal pancreas was 42% less than that of SUFF offspring, but alpha-cell replication was not affected. To determine whether this decrease in beta-cell area affected adult glucose tolerance and insulin secretion, 65-d-old offspring were subject to glucose tolerance tests. LM rats had a 55% lower plasma insulin level and a 76% higher serum glucose than SUFF rats. The same pattern could be seen in 35-d-old rats. These findings show that vitamin A deficiency decreases beta-cell mass and this reduction can be attributed to a reduced rate of fetal beta-cell replication in LM offspring. This may contribute to impaired glucose tolerance later in adult life.     

2013年中国2岁以下儿童母亲维生素B12营养状况及其影响因素

目的 了解中国2岁以下儿童母亲维生素Bl2营养状况的现状,并分析其影响因素.方法 利用2013年中国居民营养与健康状况监测中2岁以下儿童母亲的调查数据,采用多阶段分层抽样方法抽取中国30个省(自治区、直辖市)的55个县(市/区)2岁以下儿童母亲.最终采集2岁以下儿童母亲血液样本10331份,问卷调查收集其基本情况,通过...