妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠内嗅皮质神经颗粒素表达的影响

目的研究碘缺乏和甲状腺功能减退损伤内嗅皮质对神经颗粒素(neurogranin,Ng/RC3)表达的影响。方法将28只妊娠清洁级Wistar大鼠按体重随机分成对照组、碘缺乏组、甲状腺功能减退1、2组,每组7只。自妊娠第6天(GD6)起,碘缺乏组饲以缺碘地区粮食配制的饲料[碘含量为(14.11±1.96)ng/g],饮用自来水;甲状腺功能减退1、2组分别给予5和15mg/L丙基硫尿嘧啶(propylthiouracil,PTU)溶液作为饮用水,饲喂普通饲料[碘含量为(470.50±46.52)ng/g],直至仔鼠出生后第28天(PN28);对照组饮用自来水,饲喂普通饲料。分别于PN7、PN14、PN21、PN28和PN42时,每组随机取5只仔鼠,观察内嗅皮质Ng的表达。结果 PN7时,各组仔鼠内嗅皮质Ng表达水平间比较,差异无统计学意义。PN14时,甲状腺功能减退2组和碘缺乏组仔鼠内嗅皮质Ng表达水平低于对照组和甲状腺功能减退1组,差异均有统计学意义(P0.05)。PN21,PN28和PN42时,甲状腺功能减退2组和碘缺乏组仔鼠内嗅皮质Ng表达水平低于对照组,差异均有统计学意义(P0.05);PN42时,甲状腺功能减退1组仔鼠内嗅皮质Ng表达水平亦低于对照组,差异有统计学意义(P0.05)。与对照组比较,甲状腺功能减退1、2组和碘缺乏组内嗅皮质Ng染色强度明显降低。结论妊娠大鼠碘缺乏和甲状腺功能减退可降低仔鼠内嗅皮质Ng的表达。     

妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠海马神经颗粒素表达的影响

目的观察妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠海马神经颗粒素(neurogranin,Ng/RC3)表达的影响。方法将妊娠清洁级Wistar大鼠28只按体重随机分成对照组、碘缺乏组、甲状腺功能减退1、2组,每组7只。自妊娠第6天(GD6)起,碘缺乏组饲以缺碘地区粮食配制的饲料[碘含量为(14.11±1.96)ng/g],饮用自来水;甲状腺功能减退1、2组分别给予5和15mg/L丙基硫尿嘧啶(propylthiouracil,PTU)溶液作为饮用水,饲喂普通饲料[碘含量为(470.50±46.52)ng/g],直至仔鼠出生后第28天(PN28);对照组饮用自来水,饲喂普通饲料。分别于PN14、PN21、PN28和PN42时,每组随机取5只仔鼠,观察海马CA1、CA3和DG区Ng表达。结果在PN14时,碘缺乏组、甲状腺功能减退1、2组仔鼠海马CA1区Ng蛋白表达水平低于对照组,差异均有统计学意义(P0.05);在PN21时,碘缺乏组、甲状腺功能减退1、2组仔鼠海马CA1区以及碘缺乏组、甲状腺功能减退2组仔鼠海马CA3区Ng蛋白表达水平低于对照组,差异均有统计学意义(P0.05);在PN28时,碘缺乏组、甲状腺功能减退1、2组仔鼠海马CA3区以及碘缺乏组、甲状腺功能减退2组仔鼠海马CA1区Ng蛋白表达水平低于对照组,差异均有统计学意义(P0.05);在PN42时,碘缺乏组、甲状腺功能减退1、2组仔鼠海马CA3区和CA1区Ng蛋白表达水平低于对照组,差异均有统计学意义(P0.05)。结论妊娠大鼠碘缺乏和甲状腺功能减退可降低仔鼠海马CA1和CA3区Ng的表达。     

妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠海马脑源性神经营养因子表达的影响

目的观察妊娠大鼠碘缺乏和甲状腺功能减退对仔鼠海马脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)表达的影响。方法将妊娠清洁级Wistar大鼠28只按体重随机分成对照组、碘缺乏组、甲状腺功能减退1、2组,每组7只。自GD6起,碘缺乏组饲以缺碘地区粮食配制的饲料[碘含量为(14.11±1.96)ng/g],饮用自来水;甲状腺功能减退1、2组分别给予5和15mg/L丙基硫尿嘧啶(propylthiouracil,PTU)溶液作为饮用水,饲喂普通饲料[碘含量为(470.50±46.52)ng/g],直至仔鼠出生后第28天(PN28);对照组饮用自来水,饲喂普通饲料。分别于PN14、PN21、PN28和PN42时,每组随机取5只仔鼠,观察海马CA1、CA3和DG区BDNF表达。结果在PN14时,各组仔鼠海马CA1、CA3和DG区BDNF蛋白表达水平间比较,差异均无统计学意义。在PN21时,甲状腺功能减退2组和碘缺乏组仔鼠海马CA1、CA3和DG区BDNF蛋白表达水平低于对照组,差异均有统计学意义(P0.05);碘缺乏组仔鼠海马CA1区以及甲状腺功能减退2组和碘缺乏组仔鼠海马DG区BDNF蛋白水平低于甲状腺功能减退1组,差异均有统计学意义(P0.05)。在PN28时,甲状腺功能减退2组和碘缺乏组仔鼠海马CA1、CA3和DG区以及甲状腺功能减退1组仔鼠海马CA3区BDNF蛋白表达水平低于对照组,差异均有统计学意义(P0.05);甲状腺功能减退2组和碘缺乏组仔鼠海马CA1区BDNF蛋白表达水平低于甲状腺功能减退1组,差异均有统计学意义(P0.05)。在PN42时,甲状腺功能减退1、2组和碘缺乏组仔鼠海马CA1、CA3和DG区BDNF蛋白表达水平低于对照组,差异均有统计学意义(P0.05);甲状腺功能减退2组和碘缺乏组仔鼠海马CA1和DG区BDNF蛋白表达水平低于甲状腺功能减退1组,差异均有统计学意义(P0.05)。结论妊娠大鼠碘缺乏和甲状腺功能减退可降低仔鼠海马BDNF的表达。     

碘缺乏和甲状腺功能减退对大鼠仔鼠小脑cAMP反应元件结合蛋白表达的影响

目的 研究碘缺乏和甲状腺功能减退对大鼠仔鼠小脑cAMP反应元件结合蛋白(CREB)表达的影响.方法 分别选用低碘饲料及丙基硫尿啼啶(propylthiouracil,PTU)饮水诱导建立低碘及甲状腺功能减退Wistar大鼠动物模型,按体重随机分成对照组、甲状腺功能减退组(5 mg/L PTU组、15 mg/L PTU组)和碘缺乏组,出生后第14天(PN14)、PN21、PN28、PN42时,测定仔鼠小脑重量,PN7、PN14、PN21、PN28、PN42时取小脑组织进行免疫组织化学链霉菌抗生物素蛋白-过氧化物酶(SP)染色,用图像分析方法分析大鼠仔鼠小脑皮质CREB表达情况.结果 PN14、PN21、PN28、PN42时,碘缺乏组小脑重量显著低于对照组和甲状腺功能减退组(P＜0.05).PN7时,各组之间小脑组织CREB平均积分光密度值差别不明显,而PN14,PN21,PN28和PN42时,5、15 mg/L PTU组和碘缺乏组平均积分光密度值均低于对照组(P＜0.05).结论 碘缺乏和甲状腺功能减退可降低大鼠仔鼠小脑组织CREB表达,影响神经系统的发育.

Abstract：

Objective To study the effects of iodine deftcieney and hypothyrosis on protein expression of CREB in the cerebellum of rats.Methods Iodine deficient rats were administered with iodine-deficient diet and hypothyroid rats were administered with PTU in drinking water.Female Wistar pregnant rats (n=28)were randomly divided into four groups:control group,iodine deficient group,5 mg/L PTU group and 15 mg/L PTU group.On PN14,PN21,PN28,pups cerebellum in each group were weighed.On PN7.PN14,PN21,PN28,cerebellum tissue were determined for CREB protein detection by immunohistochemistry.Results Cerebellum weights of pup from iodine-deftcient were significantly lighter than control,5 mg/L and 15 mg/L groups on PN14,PN21,PN28 and PN42.In the result of immunohistochemistry:on PN7,there was no significant difference in all the groups.On PN14,PN21,PN28 and PN42,CREB expression in 5,15 mg/L and iodine-deficient groups was significantly lower than that of the control group(P＜0.05).Conclusion Iodine deficiency and hypothyrosis during critical periods brain development may down regulate the protein expression of CREB,which may result in damage of serebellum development.     

碘缺乏和甲状腺功能减退仔鼠海马CaMKⅡ表达的改变

目的观察多功能钙/钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)在碘缺乏和甲状腺功能减退的大鼠仔鼠海马中蛋白表达的影响。方法健康2月龄雌性Wistar大鼠,交配妊娠后,取孕鼠28只,按体重随机分成对照组、甲状腺功能减退组和碘缺乏组,甲状腺功能减退组根据饮水中含丙基硫尿嘧啶(PTU)剂量分为5和15mg/L组,每组7只孕鼠。分别于出生后(PN)7、14、和21天时,每组随机取5只仔鼠,灌流固定大脑,进行组织病理切片和免疫组化染色,观察分析海马CaMKⅡ表达。结果对照组仔鼠海马CA1、CA3和DG区均呈强阳性染色,在神经元细胞胞浆内充满CaMKⅡ。5、15mg/L和碘缺乏组仔鼠海马免疫反应产物的分布与对照组一致,但与对照组相比染色强度逐渐降低。PN21和PN14时,仔鼠海马CA1、CA3和DG区平均积分光密度在碘缺乏组[PN21:(26.05±4.98)、(30.79±3.22)、(26.40±2.63);PN14:(25.48±4.87)、(44.17±5.91)、(26.41±3.01)]和15mg/L组[PN21:(17.02±2.68)、(24.57±6.62)、(20.18±4.05);PN14:(20.66±3.51)、(34.94±5.09)、(27.32±4.97)]明显低于对照组[PN21:(57.75±13.22)、(65.03±6.20)、(49.39±8.41),P0.05;PN14:(54.08±12.00)、(71.04±5.07)、(78.52±12.42),P0.05]。PN7时,碘缺乏组和15mg/L组仔鼠海马CA1区平均积分光密度在碘缺乏组(25.74±3.33)和15mg/L组(26.89±5.25)明显低于对照组(40.53±3.65),P0.05。结论碘缺乏和甲状腺功能减退可下调海马组织CaMKⅡ蛋白表达。     

甲状腺功能减退妊娠大鼠的仔鼠海马络丝蛋白和脑源性神经营养因子的表达及意义

目的探讨妊娠大鼠甲状腺功能减退对仔鼠海马络丝蛋白(RELN)和脑源性神经营养因子(BDNF)表达的影响。方法采用放射免疫法测定妊娠第15天对照组、甲状腺功能减退组、甲状腺功能减退孕期治疗组和甲状腺功能减退产后治疗组4组,每组7只孕鼠的血清中甲状腺激素水平。采用免疫组织化学方法分析对照组、甲状腺功能减退组、甲状腺功能减退孕期治疗组和甲状腺功能减退产后治疗组,每组6只仔鼠海马CA1区RELN和BDNF蛋白的表达。结果 1妊娠第15天甲状腺功能减退组、甲状腺功能减退孕期治疗组和甲状腺功能减退产后治疗组3组母鼠血清中总甲状腺素(TT4)水平明显低于对照组(P0.05),促甲状腺激素(TSH)水平明显高于对照组(P0.05);2甲状腺功能减退组、甲状腺功能减退产后治疗组仔鼠海马RELN和BDNF蛋白表达明显低于对照组,差异均有统计学意义(P0.05)。3甲状腺功能减退组、甲状腺功能减退产后治疗组仔鼠海马RELN和BDNF蛋白表达明显低于甲状腺功能减退孕期治疗组,差异均有统计学意义(P0.05)。结论甲状腺功能减退的孕期治疗RELN和BDNF蛋白表达改变不明显,但产后治疗RELN和BDNF蛋白表达降低,影响子代脑发育。孕期补充甲状腺激素治疗甲状腺功能减退组对减轻子代脑发育异常有益,在临床上为预防及治疗甲状腺功能减退组所致的胎儿脑发育异常提供新的理论依据。     

妊娠期和哺乳期碘缺乏对子代大鼠小脑stathmin表达的影响

目的研究妊娠期和哺乳期碘缺乏对大鼠子代小脑stathmin表达的影响。方法将21只健康清洁级雌性Wistar大鼠按体重随机分成3组,分别为对照(7.0μg/d)组、轻度碘缺乏(3.0μg/d)组和重度碘缺乏(1.5μg/d)组,每组7只。各组大鼠均喂养碘缺乏饲料(碘含量约为60 ng/g),饮用不同剂量KI溶液。继续饲养3个月后,将雌鼠与正常雄鼠按2∶1交配。在仔鼠出生后(PN),母鼠继续染毒,仔鼠采用母乳染毒。分别于PN7、PN14和PN21时,测定仔鼠小脑浦肯野细胞树突长度及stathmin蛋白的表达情况。结果 PN7、PN14和PN21时,仔鼠小脑浦肯野细胞树突总长度依次为对照组轻度碘缺乏组重度碘缺乏组,stathmin蛋白的表达水平依次为对照组轻度碘缺乏组重度碘缺乏组,差异均有统计学意义(P0.05)。结论妊娠期和哺乳期碘缺乏可促进子代大鼠小脑中stathmin蛋白的表达,影响小脑发育。     

碘缺乏、甲状腺功能减退对仔鼠海马RKC活性及表达的影响

目的 :研究碘缺乏、甲状腺功能减退对仔鼠海马蛋白激酶C活性的影响 ,并测定碘缺乏、甲状腺功能减退大鼠仔鼠海马组织c -fos、c-jun的表达 ,以探讨碘缺乏、甲状腺功能减退调节脑发育的机制。方法 :分别选用低碘饲料及他巴唑诱导建立低碘及甲减大鼠动物模型 ,收集生后 30d时仔鼠海马组织 ,测定海马细胞浆、细胞膜PKC活性。免疫组织化学S -P法染色 ,观察生后 30d时低碘组、甲状腺功能减退组 (甲减组 )及对照组大鼠仔鼠海马c-fos、c -jun表达情况并进行图像分析。结果 :生后 30d低碘组和甲减组仔鼠海马胞液PKC活性略低于对照组 ,而胞膜PKC活性稍高于对照组 ,低碘组、甲减组仔鼠海马胞膜PKC活性与胞浆PKC活性比值 (1. 4 1± 0 .12 ,1. 19± 0 . 14 )较对照组 (0 . 6 5± 0. 0 9)升高 ,差异有统计学意义 (P <0 .0 1)。生后 30天低碘组和甲减组仔鼠海马组织c -fos、c-jun灰度值均显著高于对照组P <0 .0 1) ,提示其表达水平明显降低。结论 :碘缺乏、甲状腺功能减退可引起仔鼠海马胞浆PKC向胞膜的转运 ,并可降低仔鼠海马组织原癌基因c -fos、c-jun表达 ,进而影响神经系统及智力发育 ,可能是低碘、甲减引起海马损害导致学习记忆功能减退的机制之一。     

碘缺乏、甲减对仔鼠海马相关酶及蛋白影响

目的 研究碘缺乏、甲状腺功能减退(甲减)对仔鼠海马蛋白激酶C活性的影响,并测定碘缺乏、甲减大鼠仔鼠海马组织c-fos、c-jun的表达,以探讨碘缺乏、甲减调节脑发育的机制.方法 分别选用低碘饲料及他巴唑诱导建立低碘及甲减大鼠动物模型,收集生后30 d时仔鼠海马组织,测定海马细胞浆、细胞膜PKC活性.免疫组织化学S-P法染色,观察生后30d时低碘组、甲减组及对照组大鼠仔鼠海马即早基因c-fos、c-jun表达情况并进行图像分析.结果 生后30 d低碘组和甲减组仔鼠海马胞液PKC活性略低于对照组,而胞膜PKC活性稍高于对照组,低碘组、甲减组仔鼠海马胞膜PKC活性与胞浆PKC活性比值(1.1871±0.4325,1.4143±0.3940)较对照组(0.6493±0.2943)升高,差异有统计学意义(P＜0.01).生后30d低碘组和甲减组仔鼠海马组织c-fos、c-jun灰度值均显著高于对照组(P＜0.0l),提示其表达水平明显降低.结论 碘缺乏、甲状腺功能减退可影响神经系统及智力发育,可能是低碘、甲减引起海马损害导致学习记忆功能减退的机制之一.     

碘缺乏和甲状腺功能减退对大鼠仔鼠海马ERK1/2表达的影响

目的观察碘缺乏和甲状腺功能减退对大鼠仔鼠海马细胞外信号调节蛋白激酶1及2(ERK1/2)表达的影响。方法健康2月龄孕Wistar大鼠28只,按体重随机分成对照组、甲状腺功能减退组[按饮水中含丙基硫尿嘧啶(PTU)剂量分为5mg/L组和15mg/L组]和碘缺乏组,每组7只。分别于出生后第7、14、21、28和42天每组随机取5只仔鼠,灌流固定大脑,用组织病理切片和免疫组化染色观察分析海马的ERK1/2表达。结果在出生后14、21、28和42天时,海马CA1和CA3区的ERK1/2表达在PTU5mg/L组、PTU15mg/L组和碘缺乏组显著低于对照组(P0.05)。DG区的ERK1/2表达与对照组相比差异无显著性。出生后7天时,各组间ERK1/2表达差异无显著性。结论碘缺乏和甲状腺功能减退可降低海马CA1和CA3区的ERK1/2表达。     

Protein nutrition of the neonate

The period of growth and development between birth and weaning is crucial for the long-term well-being of the organism. Protein deposition is very rapid, is achieved with a high nutritional efficiency, and is accompanied by marked differences in the growth rates of individual tissues and a series of maturational processes. These important aspects of development occur while the neonate is consuming a single and highly-specific food source, milk. Surprisingly, although there is a clear relationship between the nutrient density of milk and the growth rate of its recipient, this relationship does not apply to the overall amino acid composition of mixed milk proteins. Some amino acids, notably glycine and arginine, are supplied in milk in quantities that are much less than the needs of the neonate. The milk-fed neonate is therefore capable of carrying out a tightly-regulated transfer of N from amino acids in excess to those that are deficient. The rapid growth of the neonate is supported by a high rate of tissue protein synthesis. This process appears to be activated by the consumption of the first meals of colostrum. Recent research has identified that skeletal muscle and the brain are specifically responsive to an unidentified factor in colostrum. Following the initial anabolic response the rate of protein synthesis in some tissues, notably muscle, falls from birth to weaning. This decrease reflects a progressively smaller anabolic response to nutrient intake, which not only involves an overall fall in the capacity for protein synthesis, but also in responses to insulin and amino acids. The study of growth and protein metabolism, and their regulation in the neonate is not only important for pediatrics, but may provide important pointers to more general aspects of regulation that could be applied to the nutrition of the mature animal.     

Protein Requirements in the Elderly

No abstract available for this article.     

Protein requirements in the elderly

Adequate protein intake and the maintenance of nitrogen equilibrium are of particular importance in the elderly because this age group is at increased risk of illness and malnutrition. The current recommendation for protein intake of healthy elderly subjects is 0.8 g/kg body weight/day, the same as for younger adults. Nitrogen balance studies in the elderly, however, revealed conflicting results; some studies suggest that not all elderly can achieve a nitrogen balance with a protein intake of 0.8 g/kg body weight/day, particularly if energy supply is not adequate. Beyond the amount of protein needed for nitrogen balance, the optimal protein intake for preservation of lean body mass, body functions, and health is of paramount interest. At present, there is insufficient longer-term research with defined health outcomes to derive recommendations in this regard. Very little is also known about the protein needs of frail and unhealthy elderly. Until more evidence is available, it seems reasonable to ensure a protein intake of at least 0.8 g/kg body weight/day in all elderly persons, particularly in those at risk of malnutrition (e.g., frail and multimorbid elderly). In addition to ascertaining adequate protein and energy intake, physical activity should be encouraged in order to increase energy expenditure and food intake and to facilitate muscle protein anabolism.     

Protein metabolism and the gut

This paper reviews the recent literature concerning the importance of the gut in extraintestinal protein metabolism. A growing body of evidence suggests that the gut modulates amino acid flux and inter-organ relationships in various metabolic states. This may be particularly true during the absorptive period, when the gut: (1) controls amino acid absorption; (2) may modulate catabolism and uptake for synthesis of absorbed amino acid; and (3) consequently influences the availability of liver and extrasplanchnic amino acids, as well as their pattern and kinetics through portal flow delivery.