中华围产医学杂志
中華圍產醫學雜誌
중화위산의학잡지
CHINESE JOURNAL OF PERINATAL MEDICINE
2013年
6期
362-368
,共7页
妊娠并发症%营养不良%葡萄糖代谢障碍%脂代谢障碍%巨大胎儿%婴儿,出生时低体重%疾病模型,动物
妊娠併髮癥%營養不良%葡萄糖代謝障礙%脂代謝障礙%巨大胎兒%嬰兒,齣生時低體重%疾病模型,動物
임신병발증%영양불량%포도당대사장애%지대사장애%거대태인%영인,출생시저체중%질병모형,동물
Pregnancy complications%Malnutrition%Glucose metabolism disorders%Lipid metabolism disorders%Fetal macrosomia%Infant,low birth weight%Disease models,animal
目的 研究妊娠期营养不良(营养过剩及营养不足)对大鼠糖、脂代谢及子代出生体重的影响.方法 Wistar大鼠从确定妊娠第1天起按摄入食物的不同,分别分为高脂高热量组、正常饮食组及低热量饮食组,每组10只.比较孕鼠妊娠期体重变化以及妊娠晚期血清甘油三酯、高密度脂蛋白、低密度脂蛋白、空腹血糖、胰岛素的水平、口服葡萄糖耐量试验和胰岛素释放试验结果的差异,观察各组子代出生体重及仔鼠巨大儿和低体重的发生率.采用单因素方差分析、LSD或DunnettT3检验、卡方检验进行统计学分析.结果 高脂高热量饮食组大鼠妊娠期体重明显增加,妊娠晚期血清甘油三酯及低密度脂蛋白分别为(1.68±0.13) mmol/L及(0.57±0.04) mmol/L,均高于正常饮食组[(0.78±0.08) mmol/L及(0.35±0.07) mmol/L),P均＜0.01],而高密度脂蛋白低于正常饮食组[(0.56±0.06) mmol/L与(1.09±0.08) mmol/L,P＜0.05]；低热量饮食组甘油三酯、低密度脂蛋白及高密度脂蛋白分别为[(0.47±0.06) mmol/L、(0.21±0.06) mmol/L及(0.42±0.05) mmol/L],均低于正常饮食组(P均＜0.05).营养不良组(高脂高热量饮食组和低热量饮食组)孕鼠均出现了糖耐量受损,口服葡萄糖耐量试验和胰岛素释放试验异常；高脂高热量饮食组鼠妊娠晚期空腹血糖高于正常饮食组[(6.63±0.53) mmol/L与(4.90±0.26) mmol/L,P＜0.05],低热量饮食组空腹血糖为(4.18±0.26) mmol/L,与正常饮食组比较,差异无统计学意义(P＞0.05).3组孕鼠妊娠晚期空腹血清胰岛素水平比较,差异均无统计学意义.高脂高热量饮食组子代平均出生体重高于正常饮食组[(6.14±0.31)g与(5.73±0.26)g,P＜0.05],仔鼠巨大儿发生率高于正常饮食组[19.20％(19/99)与7.84％(8/102),P＜0.05]；低热量饮食组子代平均出生体重为(4.54±0.23)g,低于正常饮食组(P＜0.05),仔鼠巨大儿发生率为13.40％(11/76),高于正常饮食组(P＜0.05)；低体重儿发生率高于正常饮食组[15.90％(13/76)与3.92％(4/102),P＜0.05]；仔鼠总数量少于正常饮食组(76只与102只)(P＜0.05),高脂高热量饮食组仔鼠总数量为99只,少于正常饮食组,但差异无统计学意义(P＞0.05).结论 妊娠期营养不良可引起大鼠妊娠期脂质代谢异常、糖耐量受损和胰岛素抵抗,同时也对子代出生体重,包括仔鼠巨大儿及低体重儿的发生率产生不良影响.
目的 研究妊娠期營養不良(營養過剩及營養不足)對大鼠糖、脂代謝及子代齣生體重的影響.方法 Wistar大鼠從確定妊娠第1天起按攝入食物的不同,分彆分為高脂高熱量組、正常飲食組及低熱量飲食組,每組10隻.比較孕鼠妊娠期體重變化以及妊娠晚期血清甘油三酯、高密度脂蛋白、低密度脂蛋白、空腹血糖、胰島素的水平、口服葡萄糖耐量試驗和胰島素釋放試驗結果的差異,觀察各組子代齣生體重及仔鼠巨大兒和低體重的髮生率.採用單因素方差分析、LSD或DunnettT3檢驗、卡方檢驗進行統計學分析.結果 高脂高熱量飲食組大鼠妊娠期體重明顯增加,妊娠晚期血清甘油三酯及低密度脂蛋白分彆為(1.68±0.13) mmol/L及(0.57±0.04) mmol/L,均高于正常飲食組[(0.78±0.08) mmol/L及(0.35±0.07) mmol/L),P均＜0.01],而高密度脂蛋白低于正常飲食組[(0.56±0.06) mmol/L與(1.09±0.08) mmol/L,P＜0.05]；低熱量飲食組甘油三酯、低密度脂蛋白及高密度脂蛋白分彆為[(0.47±0.06) mmol/L、(0.21±0.06) mmol/L及(0.42±0.05) mmol/L],均低于正常飲食組(P均＜0.05).營養不良組(高脂高熱量飲食組和低熱量飲食組)孕鼠均齣現瞭糖耐量受損,口服葡萄糖耐量試驗和胰島素釋放試驗異常；高脂高熱量飲食組鼠妊娠晚期空腹血糖高于正常飲食組[(6.63±0.53) mmol/L與(4.90±0.26) mmol/L,P＜0.05],低熱量飲食組空腹血糖為(4.18±0.26) mmol/L,與正常飲食組比較,差異無統計學意義(P＞0.05).3組孕鼠妊娠晚期空腹血清胰島素水平比較,差異均無統計學意義.高脂高熱量飲食組子代平均齣生體重高于正常飲食組[(6.14±0.31)g與(5.73±0.26)g,P＜0.05],仔鼠巨大兒髮生率高于正常飲食組[19.20％(19/99)與7.84％(8/102),P＜0.05]；低熱量飲食組子代平均齣生體重為(4.54±0.23)g,低于正常飲食組(P＜0.05),仔鼠巨大兒髮生率為13.40％(11/76),高于正常飲食組(P＜0.05)；低體重兒髮生率高于正常飲食組[15.90％(13/76)與3.92％(4/102),P＜0.05]；仔鼠總數量少于正常飲食組(76隻與102隻)(P＜0.05),高脂高熱量飲食組仔鼠總數量為99隻,少于正常飲食組,但差異無統計學意義(P＞0.05).結論 妊娠期營養不良可引起大鼠妊娠期脂質代謝異常、糖耐量受損和胰島素牴抗,同時也對子代齣生體重,包括仔鼠巨大兒及低體重兒的髮生率產生不良影響.
목적 연구임신기영양불량(영양과잉급영양불족)대대서당、지대사급자대출생체중적영향.방법 Wistar대서종학정임신제1천기안섭입식물적불동,분별분위고지고열량조、정상음식조급저열량음식조,매조10지.비교잉서임신기체중변화이급임신만기혈청감유삼지、고밀도지단백、저밀도지단백、공복혈당、이도소적수평、구복포도당내량시험화이도소석방시험결과적차이,관찰각조자대출생체중급자서거대인화저체중적발생솔.채용단인소방차분석、LSD혹DunnettT3검험、잡방검험진행통계학분석.결과 고지고열량음식조대서임신기체중명현증가,임신만기혈청감유삼지급저밀도지단백분별위(1.68±0.13) mmol/L급(0.57±0.04) mmol/L,균고우정상음식조[(0.78±0.08) mmol/L급(0.35±0.07) mmol/L),P균＜0.01],이고밀도지단백저우정상음식조[(0.56±0.06) mmol/L여(1.09±0.08) mmol/L,P＜0.05]；저열량음식조감유삼지、저밀도지단백급고밀도지단백분별위[(0.47±0.06) mmol/L、(0.21±0.06) mmol/L급(0.42±0.05) mmol/L],균저우정상음식조(P균＜0.05).영양불량조(고지고열량음식조화저열량음식조)잉서균출현료당내량수손,구복포도당내량시험화이도소석방시험이상；고지고열량음식조서임신만기공복혈당고우정상음식조[(6.63±0.53) mmol/L여(4.90±0.26) mmol/L,P＜0.05],저열량음식조공복혈당위(4.18±0.26) mmol/L,여정상음식조비교,차이무통계학의의(P＞0.05).3조잉서임신만기공복혈청이도소수평비교,차이균무통계학의의.고지고열량음식조자대평균출생체중고우정상음식조[(6.14±0.31)g여(5.73±0.26)g,P＜0.05],자서거대인발생솔고우정상음식조[19.20％(19/99)여7.84％(8/102),P＜0.05]；저열량음식조자대평균출생체중위(4.54±0.23)g,저우정상음식조(P＜0.05),자서거대인발생솔위13.40％(11/76),고우정상음식조(P＜0.05)；저체중인발생솔고우정상음식조[15.90％(13/76)여3.92％(4/102),P＜0.05]；자서총수량소우정상음식조(76지여102지)(P＜0.05),고지고열량음식조자서총수량위99지,소우정상음식조,단차이무통계학의의(P＞0.05).결론 임신기영양불량가인기대서임신기지질대사이상、당내량수손화이도소저항,동시야대자대출생체중,포괄자서거대인급저체중인적발생솔산생불량영향.
Objective To explore the glucose and liplid metabolism changes of pregnant rats and the birth weight of their offsprings due to pregnancy malnutrition,including overnutrition and undernutrition.Methods Thirty pregnant Wistar rats were randomly divided into three groups on the day of conception,the high-fat-diet group,normal control group and 50％ food-restricted diet group.Increase of body weight and serum level of triglycerides,high-density lipoprotein,low-density lipoprotein,oral glucose tolerance test (OGTT) and insulin release test(IRT) levels during pregnancy were measured.The birth weight of offsprings was recorded within 12 h after birth.One-way ANOVA,LSD or Dunnett T3,and Chi-square test were applied for statistical analysis.Results The body weight at late pregnancy and the level of triglycerides and low-density lipoprotein were significantly increased in the high-fat-diet rats compared to normal control ones [(1.68±0.13) mmol/L vs (0.78±0.08) mmol/L,(0.57±0.04) mmol/L vs (0.35±0.07) mmol/L; both P＜0.01].While the level of high-density lipoprotein of high-fat-diet rats was lower than that of the normal control rats [(0.56±0.06) mmol/L vs (1.09±0.08) mmol/L,P＜0.05].The level of triglycerides,low density lipoprotein and high density lipoprotein in 50％ food restricted group [(0.47±0.06) mmol/L,(0.21±0.06) mmol/L and (0.42±0.05) mmol/L] were lower than the control group (all P＜0.05).Impaired glucose tolerance,abnormal OGTT and IRT results were found in both high-fat-diet and 50％ foodrestricted diet rats.The fasting plasma glucose level in high-fat-diet group was significantly increased in late pregnancy compared to the control [(6.63±0.53) mmol/L vs (4.90±0.26) mmol/L,P＜0.05],while there was no significant difference between rats in 50％ food-restricted diet [(4.18±0.26) mmol/L]and control group (P＞0.05).There was no statistical difference in fasting serum insulin level among the three groups.The average birth weight was significantly increased in high-fat-diet rats than in the control group [(6.14±0.31) g vs (5.73±0.26) g,P＜0.05],and the incidence of macrosomic newborn rats in the high-fat-diet group was also higher than that of the control group [19.2 ％ (19/99)vs 7.84％(8/102),P＜0.05].The birth weight of offspring in 50％ food-restricted diet group was decreased with their average birth weight of (4.54±0.23) g,which was lower than that of the control group (P＜0.05).The incidence of macrosomic [13.40％ (11/76)] and low birth weight newborn rats [15.90％ (13/76) vs 3.92％(4/102)] in food-restricted diet group were both higher than in the control group (P＜0.05); and smaller number of offsprings was obtained than the control group (76 vs 102,P＜0.05),the number of offsprings in high-fat-diet group was 99,which was less than the control group without statistical difference (P＞0.05).Conclusions Pregnancy malnutrition,including overnutrition and undernutrition,may affect the lipid metabolism and glucose tolerance of pregnant rats,leading to insulin resistance,and may also contribute to the abnormal birth weight of the offspring,including macrosomia and low birth weight.
