牛磺酸对低出生体质量仔鼠胰岛β细胞超微结构的影响

目的研究生后早期补充牛磺酸对低出生体质量（LBW）仔鼠体质量和胰岛β细胞超微结构的影响。方法给予孕期母鼠10％低蛋白饲料（R组）制造LBW仔鼠模型，并在哺乳期持续同饲料喂养21d；对照组（C组）母鼠给予20％正常蛋白饲料喂养。在哺乳期给予部分母鼠富含2．5％牛磺酸饮用水营养干预（RT组）；其他母鼠自由饮水。于生后d1、21取出胰腺备做电镜标本。结果生后21d时，RT组仔鼠体质量显著高于R组（P=0．003）。但仍明显低于C组（P=0．01）；RT组8细胞超微结构较R组也有明显改善。结论生后早期补充牛磺酸不仅可促使LBW仔鼠的完成部分生长追赶，且能改善其β细胞超微结构。     

叶酸缺乏的离乳大鼠空间学习记忆能力的检测及意义

探讨叶酸缺乏时离乳大鼠学习记忆能力的改变 ,应用 54只刚离乳的健康雄性SD大鼠 ,随机分成实验组、对饲组和对照组三组。实验组饲以去叶酸的RHAA配方饲料 ,另二组饲以添加了 8mg叶酸 /kg膳食的RHAA饲料 ,对饲组按实验组的进食量加以控制 ,但对照组不控制进食。每周记录体重和摄食量两次。分别于饲养第 2和第 6周末测定血清叶酸浓度和进行Morris水迷宫测试大鼠的学习记忆能力 ,记录平均逃避潜伏期和分析原平台象限游泳距离占游泳总距离的百分比 ;对血清叶酸浓度、逃避潜伏期及原平台象限游泳距离百分比做相关性分析。结果显示实验第 2周除实验组血清叶酸浓度降低外 ( p <0 0 1 ) ,其余各指标在三组间无明显差异 ( p >0 0 5)。实验组从第 3周、对饲组从第 4周开始摄食量减少 ,生长速度减慢 ( p <0 0 5) ;第 6周实验组的平均体重、血清叶酸浓度明显低于对照组和对饲组 ( p <0 0 1 ) ,平均逃避潜伏期明显延长 ,原平台象限游泳距离百分比明显下降。与对照组比较 ,对饲组上述指标的改变不明显 ( p >0 0 5)。相关分析结果表明 ,血清叶酸浓度与逃避潜伏期及原平台象限游泳距离百分比非常显著相关 (r =- 0 0 546 ,p <0 0 1 ;r =0 86 ,p <0 0 1 )。因此 ,可以结论 :叶酸缺乏可损害离乳大鼠的空间学习记忆     

孕前和孕期高脂饮食对新生仔鼠体格生长及胰岛素样生长因子-1的影响

目的 利用高脂饮食建立动物模型,观察孕前和孕期高脂饮食对新生仔鼠体格生长及胰岛素样生长因子1(IGF-1)的影响.方法 40只雌性SD大鼠采用简单随机抽样方法分为高脂组和对照组,分别喂养35％高脂饲料和普通饲料.喂养8周后,高脂组和对照组各取8只观察母鼠肝脏组织病理;其余与普通饲料喂养的雄性大鼠交配,孕期分别继续给予高脂饲料或普通饲料喂养.新生仔鼠出生24 h内检测各项指标:测量出生体质量和体长(鼻尾长度);酶联免疫吸附试验测定其血清IGF-1水平;生化分析仪检测血生化指标;光镜下观察肝脏组织病理;Western blot检测肝脏IGF-1蛋白的表达.结果 1.高脂组仔鼠的出生体质量和体长均较对照组显著降低(P均＜0.05).2.高脂组仔鼠血清IGF-1水平较对照组下降20.1％,但差异无统计学意义(P＞0.05).3.高脂组仔鼠的天冬氨酸转氨酶(AST)显著高于对照组(P＜0.05),其余各项血生化指标差异无统计学意义(P均＞0.05).4.高脂组母鼠及仔鼠肝组织可见脂肪变,而对照组肝脏病理形态正常.5.高脂组仔鼠肝脏IGF-1蛋白的表达高于对照组(P＜0.05).结论 母亲孕前和孕期高脂饮食会影响胎鼠在宫内的体格生长,可能与IGF-1的下降有关,但导致血清IGF-1下降的病因以及宫内体格生长迟缓的确切病理机制尚有待进一步阐明.     

L-精氨酸对宫内发育迟缓大鼠肾脏Pax2表达的影响

目的：研究L-精氨酸（L-Arg）对宫内发育迟缓(IUGR)大鼠肾脏 Pax2表达的影响。方法：孕鼠随机分为 3 组：正常对照组、IUGR 组和干预组。正常对照组母鼠全程以普通饲料（含 21％ 蛋白）喂养。IUGR 组和干预组大鼠孕期均采用低蛋白饲料（含 10% 蛋白）喂养。仔鼠出生后,IUGR 组母鼠常规饲料喂养;干预组母鼠在常规饲料喂养的基础上,于部分饮水中每日添加 L-Arg 200 mg/kg。取 7 d、21 d、2月和 3月龄仔鼠肾脏组织,用免疫组化和 Western blot 法检测 Pax2 表达。结果：免疫组化显示正常对照组仔鼠在各时间点均未见明显 Pax2 表达。IUGR 组、干预组仔鼠2月龄和 3月龄时,两组大鼠在肾小球和肾小管区可见 Pax2 阳性细胞,且 3月龄鼠的 Pax2 表达比 2月龄的更显著（P<0.05）;干预组的 Pax2 表达低于同龄IUGR组（P<0.05）。Western blot 检测发现,3 组仔鼠肾脏在 7 d 和 21 d 均未见 Pax2 蛋白明显表达。到 2月龄和 3月龄时,干预组和 IUGR 组仔鼠肾组织 Pax2 蛋白表达均较正常对照组显著增多,但干预组的表达低于 IUGR 组（P＜0.01）。结论：IUGR 大鼠成年后肾脏 Pax2 基因有再表达现象;用L-Arg 干预后Pax2 表达明显减少。     

哺乳期营养对雌鼠阴门开启时间及卵巢功能的影响

目的通过建立哺乳期不同营养状态大鼠模型,观察哺乳期营养对雌鼠阴门开启时间及卵巢功能的影响。方法利用同系新生雌性SD大鼠制作哺乳期营养适中（1只母鼠喂养10只仔鼠,共30只）、营养过剩（1只母鼠喂养2只仔鼠,共30只）及营养不良（1只母鼠喂养20只仔鼠,共60只）模型,观察各组雌鼠阴门开启时间、体重、卵巢组织学变化。结果营养过剩组雌鼠阴门开启时间明显先于营养适中组（P〈0.05）,而营养适中组明显先于营养不良组（P〈0.05）;卵巢组织学显示不同营养状态雌鼠卵巢发育成熟度不同,营养越好卵巢发育越早、越趋于成熟。结论营养过剩即肥胖的雌鼠性发育明显提前,营养不良雌鼠性发育明显延迟,哺乳期营养是调节雌鼠性发育的重要因素。     

叶酸缺乏的离乳大鼠学习记忆能力与海马突触体膜流动性改变的相关性研究(二)

为初步探索叶酸缺乏的离乳大鼠学习记忆能力的改变与海马突触体膜流动性之间的关系 ,从膜功能的角度为叶酸缺乏影响学习记忆能力提供动物学方面的依据。挑选 5 4只刚离乳的健康雄性SD大鼠 ,随机分成实验组 (FD)、对饲组 (PF)和对照组 (AL)三组。实验组饲以去叶酸的RHAA配方饲料 ,另二组饲以添加了叶酸 8mg/kg膳食的RHAA饲料 ,对饲组按实验组的进食量加以控制 ,对照组不控制进食。每周记录体重和摄食量两次。分别于饲养第 2和第 6周末测定血清叶酸浓度和进行Morris水迷宫测试大鼠的学习记忆能力 ,记录平均逃避潜伏期和分析原平台象限游泳距离占游泳总距离的百分比 ,分离海马突触体 ,透射电镜作形态学证实 ,用荧光物质DPH标记突触体后测定荧光强度 ,后者反映突触体膜流动性。对血清叶酸浓度、平均逃避潜伏期及原平台象限游泳距离百分比、膜流动性作相关分析。结果 ,实验第2周除实验组血清叶酸浓度降低外 (P <0 0 1) ,其余各指标在三组间无明显差异 (P>0 0 5 )。实验组 (FD)从第 3周、对饲组 (PF)从第 4周开始摄食量减少 ,生长速度减慢 (P <0 0 5 )。第 6周实验组 (FD)的平均体重、血清叶酸浓度明显低于对照组 (AL)和对饲组 (PF) (P <0 0 1) ,平均逃避潜伏期明显延长 ,原平台象限游泳距离百分比及海马?     

母孕前和孕期高脂饮食对新生仔鼠骨骼生长的影响及机制探讨

目的 观察母鼠孕前和孕期高脂饮食对新生仔鼠骨骼生长的影响,并探讨影响骨骼生长的机制.方法 40 只雌性Sprague-Dawley 大鼠随机分为高脂组和对照组(n=20),分别喂养35% 高脂饲料和普通饲料.喂养8 周后,高脂组和对照组各取8 只雌鼠观察其肝脏组织病理;其余与普通饲料喂养的雄性大鼠交配,孕期分别继续给予高脂饲料或普通饲料喂养.待娩出新生仔鼠后24 h 内,测量两组仔鼠体长(鼻尾长度);酶联免疫吸附试验测定血清胰岛素样生长因子-I(IGF-I)水平;光镜下观察肝脏组织病理;免疫组织化学法检测长骨(胫骨、股骨)中胰岛素受体底物1(IRS-1)和磷酸化IRS-1(Phospho-IRS-1)的表达;蛋白质印迹技术检测长骨软骨细胞中促分裂原活化蛋白激酶(MAPK)和磷酸化MAPK(Phospho-MAPK)、磷酯酰肌醇3-激酶(PI3K)和磷酸化PI3K(Phospho-PI3K)、蛋白激酶B(AKT1)和磷酸化AKT1(Phospho-AKT1)的蛋白表达.结果 高脂组仔鼠的出生体长较对照组显著降低(P<0.05).高脂组仔鼠血清IGF-I 水平较对照组下降,但差异无统计学意义(P>0.05).高脂组母鼠及仔鼠肝组织可见脂肪样变,而对照组肝脏病理形态正常.两组仔鼠长骨软骨细胞中IRS-1 的表达差异无统计学意义(P>0.05).高脂组仔鼠长骨软骨细胞中MAPK 的表达水平高于对照组(P<0.05),而PI3K 及AKT1/Phospho-AKT1 的表达水平在两组间差异无统计学意义(P>0.05).结论 母鼠孕前和孕期高脂饮食会影响胎鼠在宫内的骨骼发育,可能与IGF-I 的下降有关,但未发现IGF-I 对骨骼影响的确切发病机制.     

母鼠孕期补充α-亚麻酸或二十二碳六烯酸对其幼鼠脂质代谢的影响

目的了解母鼠孕期补充α-亚麻酸(LNA)或二十二碳六烯酸(DHA)对其新生幼鼠脂质代谢的影响。方法实验母鼠24只,随机分为三组,在母鼠孕期分别给予不同饲料喂养:对照组母鼠给予普通饲料;LNA组给予补充LNA(100mg/d);DHA组给予补充DHA(100mg/d)。三组母鼠分娩后,分别将其幼鼠杀死取血,测定各组幼鼠血浆中脂肪酸的含量,并与母鼠血中脂肪酸含量进行比较。结果母鼠孕期补充DHA组其幼鼠血浆中DHA的含量显著高于对照组和补充LNA组幼鼠;孕期补充LNA组其幼鼠血浆中LNA含量明显升高,血浆中DHA的含量也明显高于对照组;母鼠血中DHA和LNA的含量与其幼鼠血中DHA和LNA的含量显著相关(r=0.813、0.883,P均<0.01)。母鼠孕期补充DHA其幼鼠血浆中花生四烯酸(AA)的含量低于对照组和LNA组幼鼠。结论母鼠孕期补充DHA后可明显提高其新生幼鼠血中DHA的含量;母鼠孕期补充LNA后其新生幼鼠血中DHA含量也有升高,但升高程度没有补充DHA组显著;孕期补充DHA对婴儿脑和视网膜的发育有帮助,但补充DHA或LNA时应注意适当的剂量。     

左旋精氨酸对低出生体重仔鼠PI3K和PKB的影响

目的：生命早期应用左旋精氨酸（L-Arg）干预低出生体重仔鼠,检测其肝脏磷脂酰肌醇-3-激酶（PI3K）和蛋白激酶B(PKB)的表达,探讨L-Arg对改善胰岛素抵抗的影响。方法：以孕期低蛋白饮食法建立低出生体重仔鼠模型,18只孕鼠随机分为对照组、模型组和干预组,每组6只。对照组孕期给予21%正常蛋白饲料建立正常出生体重仔鼠模型,模型组及干预组孕期给予10%低蛋白饲料建立低出生体重仔鼠模型,3组孕鼠所生仔鼠分别纳入仔鼠对照组、模型组、干预组。生后21 d 仔鼠的哺乳期内,3组孕鼠均给予21%正常蛋白饲料喂养,对照组及模型组给予正常饮用水喂养,干预组给予富含L-Arg（200 mg/kg.d）的饮用水喂养。断乳后,3组仔鼠均给予21%正常蛋白饲料及正常饮用水喂养。于仔鼠生后1 周、3 周、8 周时,分别留取3组仔鼠的肝脏标本,用Western blot法检测肝脏PI3K和PKB的蛋白表达。结果：1 周时干预组仔鼠肝脏PI3K的蛋白表达高于模型组（P=0.045）,且与正常组相比差异无统计学意义（P=0.503）。8 周时干预组仔鼠肝脏PKB蛋白表达明显高于模型组（P=0.039）,且与正常组比较差异无统计学意义（P>0.05）。结论：生命早期补充L-Arg可促进蛋白质的合成,增加肝脏PI3K及PKB的蛋白表达,促进胰岛素信号传导,改善胰岛素抵抗。     

叶酸缺乏的离乳大鼠学习记忆能力与海马突触体膜流动性改变的相关性研究

初步探索叶酸缺乏的离乳大鼠学习记忆能力的改变与海马突触体膜流动性之间的关系,从膜功能的角度为叶酸缺乏影响学习记忆能力提供动物学方面的依据。对５４只刚离乳的健康雄性ＳＤ大鼠,随机分成实验组(ＦＤ)、对饲组(ＰＦ)和对照组(ＡＬ)三组。实验组饲以去叶酸的ＲＨＡＡ配方饲料,另二组饲以添加了８ｍｇ叶酸/ｋｇ膳食的ＲＨＡＡ饲料,对饲组按实验组的进食量加以控制,对照组不控制进食。每周记录体重和摄食量两次。分别于饲养第２和第６周末测定血清叶酸浓度和进行Ｍｏｒｒｉｓ水迷宫测试大鼠的学习记忆能力,记录平均逃避潜伏期和分析原平台象限游泳距离占游泳总距离的百分比;分离海马突触体,透射电镜作形态学证实,用荧光物质ＤＰＨ标记突触体后测定荧光强度,后者反映突触体膜流动性。对血清叶酸浓度、平均逃避潜伏期及原平台象限游泳距离百分比、膜流动性作相关分析。结果显示:实验第２周除实验组血清叶酸浓度降低外(Ｐ＜０．０１),其余各指标在三组间无明显差异(Ｐ＞０．０５);实验组(ＦＤ)从第３周、对饲组(ＰＦ)从第４周开始摄食量减少,生长速度减慢(Ｐ＜０．０５)。第６周实验组(ＦＤ)的平均体重、血清叶酸浓度明显低于对照组(ＡＬ)和对饲组(ＰＦ)(Ｐ＜０．０１),平均逃避潜伏期明显延长,原平台象     

大鼠不同时期高脂饮食对子代糖脂代谢的影响及机制研究

目的 探讨Sprague-Dawley母鼠不同时期高脂饮食对子代糖脂代谢的影响及相关机制。 方法 根据孕前及孕期哺乳期饮食的不同,将母鼠随机分为4组（n=9）：CC组（孕前、孕期哺乳期均正常饮食）、HC组（孕前高脂饮食、孕期哺乳期正常饮食）、CH组（孕前正常饮食、孕期哺乳期高脂饮食）、HH组（孕前、孕期哺乳期均高脂饮食）;子代生后3周断奶后,全部给予正常饮食。记录母鼠孕前、孕期体重及仔鼠体重。取各组幼年期（3周）、成年期（12周）雄性仔鼠,检测空腹血糖（glucose,GLU）、胰岛素（insulin,INS）及肝脏三酰甘油（triglyceride,TG）、总胆固醇（total cholesterol,TC）水平,计算胰岛素抵抗指数（homeostasis model assessment of insulin resistance,HOMA-IR）、糖耐量试验（glucose tolerance test,GTT）及胰岛素耐量试验（insulin tolerance test,ITT）的曲线下面积（area under the curve,AUC）;取肝脏组织行苏木精-伊红染色和油红O染色,观察肝脏脂质沉积;检测肝脏糖脂代谢关键基因IR、IRS、AKT和FASN、SREBP1c、PPARα的mRNA及其蛋白表达水平。 结果 孕前高脂饮食组（HC组、HH组）母鼠体重较正常饮食组（CC组、CH组）显著增加（P<0.001）;HC组、CH组、HH组母鼠孕期增重较CC组显著增加（P<0.001）。生后3周时,HC组、CH组、HH组的仔鼠体重、肝脏TG及TC含量,以及FASN、SREBP1c、PPARα的mRNA及其蛋白表达水平均较CC组显著增加（P<0.05）,肝脏脂质沉积增加,其中HH组增加最显著;HH组的空腹GLU及INS水平、HOMA-IR、GTT-AUC、ITT-AUC及肝脏p-IRS蛋白表达水平均较CC组显著增加,肝脏IR、IRS的mRNA及其蛋白表达水平均较CC组显著降低（P<0.05）。生后12周时,HC组、CH组、HH组的仔鼠体重、空腹GLU及INS水平、HOMA-IR、GTT-AUC、ITT-AUC、肝脏TG及TC含量、p-IRS蛋白表达水平,以及FASN、SREBP1c、PPARα的mRNA及其蛋白表达水平均较CC组显著增加（P<0.05）,肝脏脂质沉积增加,其中HH组增加最显著;HC组、CH组、HH组IR、IRS、AKT的mRNA水平均较CC组显著降低,IR、IRS、p-AKT蛋白表达水平均较CC组显著降低（P<0.05）。HC组与CH组在不同时期的糖脂代谢水平未见显著性差异（P>0.05）。 结论 大鼠怀孕前后不同时期的高脂饮食对子代的糖脂代谢具有不同的影响,孕前、孕期、哺乳期全程高脂饮食对子代糖脂代谢影响最大;大鼠高脂饮食对其子代糖脂代谢的影响考虑与糖脂代谢基因的表达改变有关。 引用格式:     

Regional Brazilian diet-induced low birth weight is correlated with changes in renal hemodynamics and glomerular morphometry in adult age

Number of nephrons, renal hemodynamics, and glomerular morphometry were assessed in rats submitted to a multideficient diet which was developed from a basic regional diet consumed in a Brazilian region of sugarcane cultivation. We evaluated three groups of male Wistar rat offspring: (1) from dams fed a standard diet throughout mating, pregnancy and lactation (control group) and (2) from dams fed the multideficient diet during mating and pregnancy (MalN1 group) or (3) throughout mating, pregnancy, and lactation (MalN2 group). At adult age, the animals were anesthetized to measure mean arterial blood pressure and renal hemodynamics. The MalN1 group, as compared with the control group, showed unaltered body and kidney weights, nephron deficiency, a high mean arterial blood pressure, glomerular hypertrophy, and renal vasoconstriction. The MalN2 group showed the same nephron deficiency and mean arterial blood pressure levels as the MalN1 group. These animals exhibited lower body and kidney weights and no glomerular hypertrophy. In conclusion, the alterations induced by intrauterine malnutrition are compatible with the development of chronic renal failure.     

Moderate zinc deficiency influences arterial blood pressure and vascular nitric oxide pathway in growing rats

There is an increasing interest in the involvement of trace elements such as zinc in the pathogenesis of cardiovascular diseases. This study was designed to examine whether moderate zinc deficiency during growth influences blood pressure (BP) and vascular nitric oxide (NO) pathway. Three-week-old weaned male Wistar rats were randomly divided into two dietary groups and fed either a moderately zinc-deficient diet (zinc content 9 mg/kg; n = 12) or a control diet (zinc content 30 mg/kg; n = 12) for 60 d. The following were measured: systolic BP, nitrates and nitrites urinary excretion, urinary chemiluminescence intensity, NADPH-diaphorase activity in the thoracic aorta and intestinal arterioles, and NO synthase (NOS) catalytic activity using L-[U14C]-arginine as substrate in the thoracic aorta. Zinc deficiency during growth induced an increase in BP from day 30 of the experimental period, leading to hypertension on day 60. Animals that were fed the zinc-deficient diet had lower urinary excretion levels of nitrates and nitrites and higher intensity of spontaneous luminescence on day 60. At the end of the experiment, zinc-deficient rats showed decreased NADPH diaphorase activity in endothelium and smooth muscle of the thoracic aorta and intestinal arterioles and decreased activity of NOS in thoracic aortic tissue. An imbalance in zinc bioavailability during postnatal and growing periods may be may be a risk factor in development of cardiovascular alterations in adult life. The mechanisms involved may include an impaired vascular NO system as a result of decreased NOS activity and higher systemic oxidative stress.     

Perinatal salt restriction: a new pathway to programming insulin resistance and dyslipidemia in adult wistar rats

Several studies support the hypothesis that chronic diseases in adulthood might be triggered by events that occur during fetal development. This study examined the consequences of perinatal salt intake on blood pressure (BP) and carbohydrate and lipid metabolism in adult offspring of dams on high-salt [HSD; 8% (HSD2) or 4% (HSD1)], normal-salt (NSD; 1.3%), or low-salt (LSD; 0.15% NaCl) diet during pregnancy and lactation. At 12 wk of age, female Wistar rats were matched with adult male rats that were fed NSD. Weekly tail-cuff BP measurements were performed before, during, and after pregnancy. After weaning, the offspring received only NSD and were housed in metabolic cages for 24-h urine collection for sodium and potassium and nitrate and nitrite excretion measurements. At 12 wk of age, intra-arterial mean BP was measured, a euglycemic-hyperinsulinemic clamp was performed, and plasma lipids and nitrate and nitrite concentrations were determined. Tail-cuff BP was higher during pregnancy in HSD2 and HSD1 than in NSD and LSD dams. Mean BP (mm Hg) was also higher in the offspring of HSD2 (110 +/- 5) and HSD1 (107 +/- 5) compared with NSD (100 +/- 2) and LSD (92 +/- 2). Lower glucose uptake and higher plasma cholesterol and triacylglycerols were observed in male offspring from LSD dams (glucose uptake: HSD2 17 +/- 4, HSD1 15 +/- 3, NSD 11 +/- 3, LSD 4 +/- 1 mg . kg(-1) . min(-1); cholesterol: HSD2 62 +/- 6, HSD1 82 +/- 11, NSD 68 +/- 10, LSD 98 +/- 17 mg/dL; triacylglycerols: HSD2 47 +/- 15, HSD1 49 +/- 12, NSD 56 +/- 19, LSD 83 +/- 11 mg/dL). In conclusion, maternal salt intake during pregnancy and lactation has long-term influences on arterial pressure, insulin sensitivity, and plasma lipids of the adult offspring.     

Dietary zinc supplementation ameliorates LPS-induced teratogenicity in mice

Maternal infection during the first trimester of pregnancy has been associated with preterm birth, spontaneous abortion, growth retardation, and congenital anomalies. Previously, our group has shown that subcutaneous injection of zinc prevents endotoxin [lipopolysaccharide (LPS)]-induced teratogenicity. The purpose of this study was to investigate whether increasing or decreasing dietary zinc alters the teratogenic effects of LPS. Female C57BL6 mice were mated and fed diets containing 5, 35, or 100 mg/kg zinc. On gestational day (GD) 8, pregnant dams were injected with either LPS (0.5 mg/kg s.c.) or saline and killed on GD18. LPS-treated fetuses from dams fed 5 and 35 mg/kg zinc diet had a significantly higher number of abnormalities per litter (2- and 1- fold saline controls, respectively) compared with those from LPS + zinc supplemented dams, which were not significantly different from the saline control groups. The beneficial effect and importance of zinc was also reflected in the larger size of fetuses (weight and crown-rump length) from the LPS + zinc-supplemented treatment group. We have demonstrated that low dietary zinc during exposure to infection (i.e. LPS) in pregnancy augments the negative impact of LPS alone, and that dietary zinc supplementation throughout pregnancy ameliorates LPS-induced teratogenicity.     

Chronic caffeine intake by rat dams during gestation and lactation affects various parts of the neonatal brain

Timed-pregnant rats were randomly divided into 2 groups on day 13 of gestation. Group 1 received a 20% protein diet. Group 2 was pair-fed to group 1 with a 20% protein diet containing caffeine (1 mg/100 g body weight). At parturition, the dams of each group were continued on their respective diets until day 22 postpartum. At the time of weaning (day 22), only male rats were continued in the study. At this time, rats from both groups were fed the control diet containing 20% protein. On day 57 and 58, rats were killed, the brains divided into six areas, and DNA, RNA and protein contents were measured. In certain areas of the brain, weight, cholesterol, DNA, RNA and protein contents were different even long after returning to the caffeine-free control diet. The present study demonstrates that even if a relatively small amount of caffeine is taken during gestation and lactation, a time during which the growth rate is greater than in any other period of life, certain areas of the brain may be affected. These findings suggest that future central nervous system impairment may be expressed later in life in these offspring.     

Influence of marginal maternal zinc deficiency on pregnancy outcome and infant zinc status in rhesus monkeys

To investigate the effects of marginal zinc deficiency on early development, rhesus monkeys were fed a diet marginally deficient in zinc (M; 4 micrograms/g) throughout pregnancy and during the first month of lactation. Despite the low concentration of zinc in the diet. M dams did not develop overt signs of zinc deficiency. However, compared to control dams fed diets adequate in zinc (C; 100 micrograms Zn/g), M dams showed a low response to the mitogens concanavalin A and phytohemagglutinin. Pregnancy outcome was similar in the two groups and all of the neonates were judged to be healthy at delivery. From birth until d 30 of age, the infants were closely monitored for signs of zinc deficiency, and at d 30, they were killed and tissues were removed and analyzed for a number of parameters reported to be affected by zinc status. At birth, M infants had low plasma zinc concentrations compared to controls; however, this difference was not observed at d 30. D 30 M infants showed a normal response to the mitogens concanavalin A and phytohemagglutinin, but showed a low response to pokeweed mitogen. Tissue (liver, brain, spleen, kidney, and heart) trace element concentrations were similar in the two groups of infants, as were liver metallothionein concentrations and 65Zn uptake/retention by isolated hepatocytes. Infant wt gain was inversely correlated with plasma zinc, liver zinc, and liver metallothionein concentrations in both the M and C groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Polyunsaturated fatty acids and protection of newborn rats from oxygen toxicity

To test whether polyunsaturated fatty acids (PUFA) might be associated with protection against oxygen toxicity in newborn experimental animals, we performed two series of experiments. In the first series, adult female rats were fed one of three diets--regular Rat Chow, a high-PUFA (safflower oil-based) diet, or a low-PUFA (palm oil-based) diet--for several weeks before and throughout pregnancy and lactation. Newborn offspring of the three diet groups had similar antioxidant enzyme activities and surfactant development. Offspring of dams fed the high-PUFA diet had total lung lipid fatty acids characterized by increased linoleic acid (18:2 omega 6) and arachidonic acid (20:4 omega 6) and a significantly increased PUFA/saturated fatty acid ratio, compared with offspring of dams fed the regular diet or low-PUFA diet; associated with this increased PUFA pattern was markedly superior survival (80 of 84 (95%) vs 56 of 84 (67%) for regular-diet offspring, P less than 0.01) after 7 days in greater than 95% oxygen. Conversely, offspring born to dams fed the low-PUFA diet had decreased lung PUFA content and inferior tolerance to prolonged high O2 exposure (survival 38 of 84 (45%)). In the second experimental series, the postnatal provision of high PUFA rat milk to offspring born to dams fed the low-PUFA diet (via "cross-nurturing" by high-PUFA diet dams) rapidly increased their lung lipid PUFA and improved their hyperoxic survival (44 of 50 vs 25 of 50 for low-PUFA diet newborn animals kept with their low-PUFA mother rats, P less than 0.01). These studies suggest that increasing lung lipid PUFA can confer a protective effect against the toxic effects of hyperoxia on the newborn animal lung.     

Congenital malformations in offspring of diabetic rats: experimental study on the influence of the diet composition and magnesium intake

In spite of improvements in the treatment of diabetes, the risk of congenital malformations in diabetic pregnancy is three to four times higher than in normal pregnancy. This might be due to the metabolic abnormalities of diabetic pregnancy that also affect mineral metabolism. Since diabetes can lower both maternal and fetal blood Mg levels, and Mg deficiency has been shown to be teratogenic in laboratory animals, we decided to investigate which effects Mg deficiency would have in inducing embryopathy in diabetic animals. Female CD rats were divided into six groups. Groups 1 and 2 were fed a standard diet (Mg content 4,200 ppm), groups 3-6 a purified diet (Mg contents 4,200, 500, 250, or 125 ppm). Groups 2-6 had been made diabetic by an intravenous injection of 50 mg/kg streptozocin 1 week before mating. The rats were killed on day 21 of pregnancy, and the live fetuses were examined for external, skeletal, and visceral malformations. The maternal and fetal blood glucose levels were the same in all diabetic groups. The maternal Mg levels in groups 2 and 3 were the same as in controls, but definitely lower in groups 4-6. Embryotoxicity (embryonic deaths, delayed development, congenital malformations) was higher in the groups fed the purified diet than in group 2, but without a clear relation to the dietary Mg levels. We cannot draw any conclusions about the effects of Mg deficiency in diabetic pregnancy from our results, but they show that the quality of the diet is of major importance in the manifestation of embryotoxicity in diabetes.