母鼠高脂饮食增加子代大鼠罹患代谢性疾病的危险性

目的观察母代高脂饮食和后天高脂饮食对子代大鼠代谢状态的不同影响,以探索母代高脂饮食与子代大鼠成年后代谢性疾病发生的关系。方法将成年SD大鼠分成对照组（C组）和高脂饮食组（H组）,至10周龄时交配怀孕生育子代大鼠,子代大鼠断乳后每组再分成高脂饮食组（HH组,CH组）和普通饮食组（HC组,CC组）,分别至子代大鼠3周龄和8周龄时观察其代谢相关性指标以及肝脏病理表现。结果H组母鼠孕前体质量、糖耐量曲线下面积、总胆固醇及三酰甘油均明显高于C组母鼠（P<0.05）;3周龄时H组母鼠所生育并喂养的子代大鼠其体质量明显高于C组母鼠生育的子代大鼠（P=0.002）,但两者的糖耐量曲线下面积差异无统计学意义（P＞0.05）;至8周龄时各组子代大鼠空腹血糖和胰岛素水平差异无统计学意义,而母鼠为H组的子代大鼠体质量和糖耐量曲线下面积大于母鼠为C组子代大鼠（母代饮食主效应P分别为0.024和0.013）,HH组和CH组子代大鼠糖耐量曲线下面积亦大于HC组和CC组的子代大鼠（子代饮食主效应P=0.041）;8周龄时HH组和CH组子代大鼠血清总胆固醇、三酰甘油和低密度脂蛋白水平均高于HC组和CC组（子代饮食主效应P分别为0.008,0.007和0.000）;8周龄时HH组、HC组和CH组子代大鼠表现出不同程度的脂肪肝;CC组子代大鼠肝脏镜下结构均显示正常。结论母代高脂饮食可以引起子代大鼠成年后体质量增加,糖耐量减退以及肝脏脂肪变,增加子代发生代谢性疾病的危险性。     

Lipin基因表达与宫内发育迟缓大鼠肝脏脂肪含量的相关性研究

目的 探讨宫内发育迟缓（intrauterine growth retardation,IUGR）大鼠肝脏Lipin2基因和内脏脂肪组织Lipin1基因的表达与肝脏脂肪含量的相关性。 方法 使用母孕期低蛋白（10%蛋白）饮食法喂养孕鼠制造IUGR仔鼠模型,对照组孕鼠在孕期使用正常蛋白饲料喂养（蛋白含量21%）。分别在两组仔鼠生后1 d、1周、3周、8周和12周时称体重并留取仔鼠的肝脏组织,在生后3周、8周和12周留取两组仔鼠的内脏脂肪组织。采用3.0T氢质子磁共振波谱法检测两组大鼠生后3周、8周、12周时肝脏脂肪含量;采用Real-time PCR法检测两组大鼠各时间点肝脏组织Lipin2、内脏脂肪组织Lipin1基因的mRNA表达水平;采用Western blot法检测两组大鼠肝脏组织Lipin2、内脏脂肪组织Lipin1蛋白表达水平。采用Pearson相关分析Lipin mRNA及其蛋白表达与肝脏脂肪含量的相关性。 结果 生后3周、8周、12周时,IUGR组仔鼠内脏脂肪组织Lipin1 mRNA及其蛋白表达水平均高于对照组（P<0.05）。生后1 d时IUGR组肝脏组织Lipin2 mRNA及其蛋白表达水平低于对照组（P<0.05）,而生后1周、3周、8周、12周时Lipin2 mRNA及其蛋白表达水平均高于对照组（P<0.05）。生后3周时IUGR仔鼠和对照组肝脏脂肪含量比较差异无统计意义（P>0.05）,生后8周、12周时IUGR组仔鼠肝脏脂肪含量显著高于对照组（P<0.05）。Lipin1蛋白和mRNA表达与肝脏脂肪含量呈正相关（分别r=0.628、0.521,P<0.05）,Lipin2蛋白和mRNA表达与脂肪含量呈正相关（分别r=0.601、0.524,P<0.05）。 结论 IUGR大鼠内脏脂肪组织Lipin1和肝脏组织Lipin2 mRNA及其蛋白表达上调可引起肝脏脂肪含量增加,可能与导致IUGR大鼠成年期肥胖有关。     

运动康复训练对支气管哮喘儿童运动能力和生活质量干预效果的系统评价

目的 系统评价运动康复训练对支气管哮喘儿童运动能力和生活质量的干预效果。 方法 检索PubMed、Cochrane Library、Web of Science、EBSCO、中国知网、维普数据库、万方数据库等数据库从建库至2021年2月关于运动康复训练对支气管哮喘儿童影响的随机对照试验。采用RevMan 5.3软件进行Meta分析。 结果 共纳入14项研究,共计990例受试者。Meta分析结果显示：（1）运动康复组运动能力优于常规治疗组：6 min步行试验的步行距离（MD=108.13,P<0.01）、自我疲劳感觉值（MD=-2.16,P<0.001）、峰值功率（MD=0.94,P=0.001）均显著优于常规治疗组;（2）在儿科哮喘生活质量问卷中,运动康复组生活质量总评分（SMD=1.28,P=0.0002）显著高于常规治疗组,活动受限评分（SMD=1.38,P=0.0002）、症状评分（SMD=1.02,P<0.001）、情感功能评分（SMD=0.86,P<0.001）均显著高于常规治疗组。 结论 运动康复训练对支气管哮喘儿童运动能力和生活质量具有一定的改善作用,但受纳入研究数量和质量的限制,作为指导临床应用还需进一步研究和验证。     

MTHFR基因多态性与儿童支气管哮喘易感性及糖皮质激素疗效的相关性

目的 探讨亚甲基四氢叶酸还原酶（methylenetetrahydrofolate reductase,MTHFR）基因多态性与儿童支气管哮喘易感性及糖皮质激素（glucocorticoid,GC）疗效的相关性。 方法 选取2018年6月至2020年12月住院治疗的儿童支气管哮喘患儿173例为观察组,均接受GC雾化吸入治疗,连续3个月。选取同期体检的健康儿童178例为对照组。采用PCR检测两组受试儿MTHFR基因C677T位点的基因型,分析两组基因型分布差异性;比较观察组不同基因型患儿治疗前后血清免疫球蛋白E、白细胞介素-8（interleukin-8,IL-8）、白三烯B4（leukotriene B4,LTB4）水平,肺功能指标差异及临床疗效差异。 结果 与对照组相比,观察组TT基因型及T等位基因频率均显著升高（P<0.001）;TT/CT基因型及T等位基因是支气管哮喘易感性的独立危险因素（OR分别为6.615、7.055,P<0.001）。GC治疗后3种基因型患儿免疫球蛋白E、IL-8和LTB4水平较治疗前显著降低,第1秒用力呼气容积（forced expiratory volume in 1 second,FEV1）、用力肺活量（forced vital capacity,FVC）、FEV1/FVC%较治疗前显著升高（P<0.001）;TT基因型患儿IL-8和LTB4水平显著低于CC基因型患儿,LTB4水平明显低于CT基因型患儿,TT基因型患儿FVC明显高于CT基因型患儿,FEV1/FVC%显著高于CC基因型患儿（P<0.05）;治疗后3种基因型患儿临床GC治疗疗效比较差异有统计学意义,其中TT基因型患儿GC疗效良好比例显著高于CC基因型患儿（P<0.05）,且TT基因型是GC疗效良好的独立影响因素（OR=2.111,P=0.018）。 结论 MTHFR基因多态性与儿童哮喘易感性及GC疗效相关,携带TT/CT基因型儿童支气管哮喘发病风险更高,TT基因型对GC治疗具有更高的敏感性。     

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.     

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.     

高超二倍体核型儿童急性淋巴细胞白血病的临床特征及预后——福建省多中心回顾性研究

目的 检测儿童急性淋巴细胞白血病（acute lymphoblastic leukemia,ALL）患儿骨髓单个核细胞中E-钙黏蛋白（E-cadherin）mRNA及蛋白水平表达和基因甲基化状态,探讨E-cadherin在儿童ALL的意义及甲基化状态与预后的关系。 方法 采集42例初次确诊的ALL患儿确诊时（治疗前组）及诱导化疗第33天（治疗后组）的骨髓血5 mL,应用RT-qPCR、Westerm blot及甲基化特异性PCR法检测骨髓单个核细胞中E-cadherin mRNA及蛋白表达和E-cadherin基因甲基化水平,并比较治疗前后各指标的变化。 结果 治疗后组E-cadherin mRNA及蛋白的表达水平均高于治疗前组（P<0.05）;治疗后组E-cadherin基因甲基化阳性率较治疗前组下降（P<0.05）;至试验终点时,甲基化阴性者总生存率和无事件生存率均高于甲基化阳性者（P<0.05）。 结论 E-cadherin表达与儿童ALL发展相关,表达降低及甲基化水平增高可能提示预后不良。     

青少年抑郁情绪及自杀意念与父母教养方式之间的关联研究

目的 研究青少年抑郁情绪及自杀意念与父母教养方式之间的关系。 方法 采用整群抽样法,于2014~2018年抽取河南省新乡市6 195名初高中生进行调查研究。调查工具包括一般社会资料问卷、父母教养方式问卷及Kutcher青少年抑郁量表（11项）。采用多因素logistic回归分析评估青少年抑郁情绪及自杀意念与父母教养方式之间的关联。 结果 有效问卷为6 194份,其中男性2 586名（41.75%）,女性3 608（58.25%）;年龄（16.4±1.9）岁（范围：11~20岁）。在6 194名青少年中,1 333名（21.52%）青少年有抑郁情绪,508名（8.20%）青少年有自杀意念。青少年的抑郁情绪与母亲的控制（OR=1.059,P<0.001）和父亲的控制呈明显正关联（OR=1.061,P<0.001）,而与母亲的关爱（OR=0.937,P<0.001）和父亲的关爱（OR=0.917,P<0.001）呈明显负关联。青少年的自杀意念与母亲的控制（OR=1.110,P<0.001）和父亲的控制（OR=1.076,P<0.001）呈明显正关联,而与母亲的关爱（OR=0.895,P<0.001）和父亲的关爱（OR=0.914,P<0.001）呈明显负关联。 结论 父母的关爱可降低青少年抑郁情绪的发生风险,而父母控制性可增加青少年抑郁情绪及自杀意念的发生风险。 引用格式:     

儿童急性淋巴细胞白血病中E-钙黏蛋白甲基化对预后的影响

目的 通过Meta分析探讨在儿童及青少年成熟B细胞非霍奇金淋巴瘤治疗中应用利妥昔单抗联合化疗的疗效与安全性,为更加合理地应用利妥昔单抗提供理论依据。 方法 检索PubMed、Embase、Cochrane Library、ClinicalTrials.gov、Web of Science、中国知网、万方、维普数据库的文献,共筛选出从建库至2022年6月公开发表的利妥昔单抗治疗儿童及青少年成熟B细胞非霍奇金淋巴瘤的10篇文献,共计886例患儿。以3年无事件生存率、3年总生存率、完全缓解率、病死率和不良反应发生率作为结局指标,采用RevMan 5.4软件进行Meta分析、亚组分析、敏感性分析和发表偏倚分析。 结果 与单纯化疗组相比,利妥昔单抗联合化疗组3年无事件生存率显著提高（HR=0.38,95%CI：0.25~0.59,P<0.001）,3年总生存率显著提高（HR=0.29,95%CI：0.14~0.61,P=0.001）,完全缓解率显著提高（OR=3.72,95%CI：1.89~7.33,P<0.001）,病死率显著降低（OR=0.31,95%CI：0.17~0.57,P<0.001）。而两组的不良反应发生率差异无统计学意义（OR=1.28,95%CI：0.85~1.92,P=0.24）。 结论 在儿童及青少年成熟B细胞非霍奇金淋巴瘤治疗方案中添加利妥昔单抗可带来明显的生存益处,且不会增加不良反应的发生。     

血清miR-922及miR-506对儿童急性淋巴细胞白血病诊断及预后判断的价值

目的 探讨血清miR-922及miR-506表达水平对儿童急性淋巴细胞白血病（acute lymphoblastic leukemia,ALL）诊断及预后判断的价值。 方法 前瞻性选取132例ALL患儿（ALL组）和80例健康儿童（健康对照组）纳入本研究,采用实时荧光定量PCR技术检测ALL组和健康对照组血清miR-922及miR-506表达水平。绘制受试者工作特征曲线分析miR-922及miR-506对儿童ALL的诊断价值。应用Kaplan-Meier法绘制生存曲线,采用多因素COX回归模型分析影响ALL患儿预后不良的因素。 结果 ALL组血清miR-922及miR-506表达水平均明显高于健康对照组（P<0.001）。受试者工作特征曲线分析结果显示,miR-922及miR-506诊断儿童ALL的最佳截断值分别为1.46、2.17。miR-922高表达组（≥1.46）及miR-506高表达组（≥2.17）的淋巴结肿大、白细胞计数≥50×10⁹/L、中高危险度分层、MLL基因重排、染色体核型异常的发生率均明显高于miR-922及miR-506低表达组（P<0.05）。Kaplan-Meier分析结果显示,miR-922及miR-506高表达与ALL患儿生存期短有关（P<0.05）。多因素COX回归分析结果显示,白细胞计数≥50×10⁹/L、危险度分层为中高危、MLL基因重排、miR-922≥1.46及miR-506≥2.17可提示ALL患儿预后不良（P<0.05）。 结论 miR-922及miR-506表达水平对儿童ALL诊断及预后判断均有较好的价值。     

宫内生长迟缓和高脂饮食对大鼠血脂及肝脏相关基因转录水平的影响

目的 探讨宫内生长迟缓(IUGR)和高脂饮食对大鼠生长、脂代谢及肝脏相关基因的作用。方法 采用母鼠孕期全程限食法建立IUGR 大鼠模型。断奶后,将32 只正常子鼠和24 只IUGR 子鼠随机分配到标准饮食组和高脂饮食组。10 周龄时,测量空腹血糖、血脂,观察肝脏组织病理切片,并测定肝脏相关基因转录水平。结果 IUGR 大鼠与正常大鼠比较,10 周龄时,标准饮食下两者体重差异有统计学意义,而高脂饮食下两者体重差异无统计学意义。和正常大鼠相比,两种饮食下的IUGR 大鼠均出现能量摄入增加、空腹血糖、总胆固醇和甘油三酯水平升高。无论在正常大鼠还是IUGR 大鼠,高脂饮食均降低了血清甘油三酯浓度。IUGR和高脂饮食均加重了肝脏的脂肪堆积。双因素方差分析显示,10 周龄时,与正常大鼠比较, IUGR 大鼠肝脏脂代谢相关基因PGC-1α、CPT-1、SREBF-2、HMGR、LDLR 和SREBF-1 的表达差异有统计学意义;与标准饮食比较,高脂饮食增加了正常大鼠和IUGR 大鼠PPARα、SREBF-1、SREBF-2、ABCG5 和CYP7A1 的表达;IUGR 和高脂饮食对LDLR 水平存在交互作用。结论 IUGR 大鼠呈现出高血脂和肝脏脂肪堆积,可能与IUGR 大鼠的食欲增强和转录水平上脂肪酸氧化相关基因调节紊乱有关。高脂饮食可加重大鼠的肝脏脂肪堆积,可能与转录水平上调节脂肪酸合成的相关基因表达增加和甘油三酯分泌减少相关。     

孕期和哺乳期轻度缺锌对仔鼠学习记忆能力的影响

目的探讨孕期和哺乳期母鼠缺锌对仔鼠幼年期学习记忆能力的影响。方法怀孕1 d的孕鼠随机分为轻度缺锌组和对照组,每组3只。缺锌饲料、正常饲料含锌量分别为5 mg/kg、25 mg/kg。产后每窝随机保留4只。至21 d断乳去母鼠,每组12只仔鼠,继续饲以缺锌和正常饲料,分别于28 d及58 d以Morris水迷宫测试仔鼠的短期及长期学习记忆能力。结果学习获得实验(短期记忆)及记忆保持实验(长期记忆):对照组定位能力较好,游泳轨迹以目标象限为主;而缺锌组定位能力较差,游泳轨迹比较分散;缺锌组仔鼠找到平台的潜伏期、总游程大于对照组(P<0.01);两组游速的差异无统计学意义(P>0.05)。随着训练天数的增加,对照组上述各项记录都随着训练天数增加而变化,其中潜伏期和总游程随着训练天数增加而逐步减少,游泳速度、目标象限游程占总游程的百分比随着训练天数的增加而增加,缺锌组的变化趋势不如对照组明显。结论孕期及哺乳期母鼠轻度缺锌影响仔代生长期幼鼠短期与长期学习记忆能力。     

Maternal protein restriction increases hepatic glycogen storage in young rats

This study aimed to determine whether maternal protein restriction alters hepatic glycogen metabolism. Mated female rats were fed diets containing 20% protein throughout pregnancy and lactation (CONT), 8% protein throughout pregnancy and lactation (LP), or 8% protein during the last week of pregnancy only and lactation (LLP). Weights and lengths were reduced in the LLP and LP offspring compared with the CONT offspring. The LLP and LP offspring demonstrated reduced insulin concentrations at both 10 and 26 d and also failed to show the increase in insulin seen with time in the CONT offspring. Serum glucose and leptin levels increased with time but were not different among the groups; however, in relation to adiposity leptin levels were greater in the LLP and LP offspring at 26 d. The LLP and LP offspring had increased hepatic glycogen at day 10 (CONT, 75.1 +/- 9.8; LLP, 103.4 +/- 11.0; LP, 116.0 +/- 18.4 glucose residues/g tissue) and d 26 (CONT, 183.1 +/- 38.9; LLP, 395.3 +/- 16.8; LP, 396.6 +/- 15.1 glucose residues/g tissue). Glycogen synthase expression was increased in the LLP and LP offspring at 10 d but not 26 d; glucose transporter 2 and glycogen phosphorylase expressions were not different at either time. At 26 d glycogen synthase activity was not different; however, glycogen phosphorylase a activity was reduced. The enhanced capacity to store glycogen despite reductions in insulin secretion suggests increased insulin sensitivity possibly acting with an alternative non-insulin-dependent glycogen storage mechanism.     

Menhaden fish oil, n-3 polyunsaturated fatty acids, and protection of newborn rats from oxygen toxicity

We have previously reported that newborn rats born to mothers fed a high n-6 polyunsaturated fatty acid (PUFA) (safflower oil) diet demonstrated increased n-6 PUFA in lung lipids and superior tolerance to high oxygen exposure. In the present study, we explored whether high n-3 PUFA might also protect against hyperoxic damage and by what mechanism. Adult female rats were fed either regular rat chow, a high n-3 (menhaden fish oil-based) diet, or a high n-6 (safflower oil-based) diet for 6 wk before and then throughout pregnancy and lactation. Newborn offspring of the high n-3 (fish oil) dams demonstrated increased n-3 PUFA (i.e. eicosapentaenoic and docosahexaenoic acid) and decreased n-6 PUFA (i.e. linoleic and arachidonic acid) in their lung lipids compared to the other two diet groups. The high n-6 (safflower oil) offspring had the opposite PUFA lung lipid pattern (with increases in total n-6 fatty acids and decreases in total n-3 fatty acids). The high n-3 offspring demonstrated markedly decreased lung levels of prostaglandin E2, F2 alpha and thromboxane B2, whereas the high n-6 offspring had higher eicosanoid levels than the regular diet offspring. Offspring of both high n-6 and high n-3 diet dams demonstrated essentially the same superior hyperoxic tolerance compared to regular diet offspring [7-d (greater than 95% O2) survival rates of 110/115 and 99/109, respectively, versus 70/91, p less than 0.01].(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of dietary fat on fat absorption and concomitant plasma and tissue fat composition in a rat model of short bowel syndrome

The aim of this study was to investigate the effect of dietary fat on the time course of changes in fat absorption and tissue and plasma lipid composition in a rat model of short bowel syndrome (SBS). Male Sprague-Dawley rats underwent either a bowel transection with re-anastomosis (Sham rats) or 75% small bowel resection (SBS rats). Animals were randomly assigned to one of three groups: Sham rats fed normal chow (Sham-NC), SBS rats fed normal chow (SBS-NC), or SBS rats fed a high-fat diet (SBS-HFD). Rats were sacrificed on day 3 or 14. Body weight, food intake, food clearance (dry fecal mass), and fat clearance (total fecal fat) were measured twice a week. Fat and energy intakes were calculated according to the amount of ingested food. Food and fat absorbability were calculated as intake minus clearance and were expressed as percent of intake. Serum cholesterol, triglyceride, and albumin were measured. Total lipid composition of the liver, epididymal adipose tissue, and the small intestine was determined. Statistical analysis was performed by a Students test, with p values <0.05 considered significant. Both food and fat absorbability diminished after bowel resection in rats fed NC. This was accompanied by a decrease in body weight gain, plasma triglyceride and protein levels, and total lipid content of the liver at day 3 and of a decrease in adipose tissue at day 14 following operation. SBS-HFD rats experienced a significant increase ( p <0.05) in food absorbability after 7 days and fat absorbability after 3 days compared with Sham-NC and SBS-NC rats ( p <0.05), as well as increases in serum cholesterol, triglycerides, and glucose compared with SBS-NC rats. On day 14, plasma lipid levels in SBS-HFD rats were not different from SBS-NC or control rats; however, albumin levels were higher. A high-fat diet increased total fat content of the liver early after operation. In conclusion, in a rat model of SBS, an early high-fat diet increased the absorptive capacity of the intestinal remnant as seen by increased food and fat absorbability. These findings suggest a benefit of a high-fat diet on intestinal adaptation in general and on lipid absorption in particular.     

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.     

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.     

Effects of a maternal low protein isocaloric diet on milk leptin and progeny serum leptin concentration and appetitive behavior in the first 21 days of neonatal life in the rat

Suboptimal developmental environments program offspring to lifelong metabolic problems. We evaluated effects of maternal isocaloric low protein diet during pregnancy and/or lactation on milk quantity and leptin concentration at postnatal day 7, 14, and 21. Control mothers ate 20% casein (C) and restricted mothers (R) 10% casein to provide four groups: CC, RR, CR, and RC (first letter pregnancy and second lactation diet) to enable evaluation of effects influenced by maternal diet during pregnancy and lactation. Milk leptin was not a determinant of pup serum leptin. Pup serum leptin did not inhibit milk appetite at any postnatal age. Pup serum leptin did not correlate with pup adipose tissue. Finally, the normal postnatal leptin rise in pup serum was delayed by prenatal undernutrition. These data suggest that fetal nutrition modifies timing of neonatal leptin surge and may contribute to the development of altered appetite and metabolic disorders in later life.     

生长追赶宫内发育迟缓大鼠肝细胞细胞因子信号转导抑制因子3表达与胰岛素抵抗的发生机制

目的研究生长追赶宫内发育迟缓(CG-IUGR)大鼠肝细胞中细胞因子信号转导抑制因子3(SOCS3)以及胰岛素信号转导途径中关键分子胰岛素受体底物1(IRS1)和胰岛素受体底物2(IRS2)的表达变化,探讨CG-IUGR大鼠发生胰岛素抵抗的机制。方法采用孕期全程限食及缩减每产子鼠数量的方法建立CG-IUGR大鼠模型。正常摄食孕鼠所产子鼠设为正常对照组(AGA组)。运用改良原位两步非循环灌流法分离并培养原代大鼠肝细胞;用实时定量PCR和Western blot法检测胰岛素抵抗CG-IUGR大鼠肝细胞于基础状态和胰岛素刺激状态下SOCS3、IRS1和IRS2分子mRNA和蛋白水平表达变化。结果 CG-IUGR大鼠肝细胞在基础状态和胰岛素刺激状态下,SOCS3 mRNA和蛋白水平表达量均较AGA组高(Pa<0.05),IRS1 mRNA和蛋白水平表达量均较AGA组低(Pa<0.05),而IRS2 mRNA和蛋白水平表达量与AGA组比较均无统计学差异(Pa>0.05)。结论 CG-IUGR大鼠肝细胞中SOCS3表达量增加,并通过负性调节下调IRS1表达,这可能是CG-IUGR大鼠发生以胰岛素抵抗为核心的疾病分子机制之一。