本文選題：妊娠糖尿病 + 嬰幼兒��； 參考：《浙江大學(xué)》2016年博士論文

【摘要】：研究背景及目的妊娠糖尿病(Gestational diabetes mellitus,GDM)是指妊娠過程中發(fā)生或首次發(fā)現(xiàn)的不同程度的糖耐量受損,是一種常見的嚴(yán)重危害母嬰近遠(yuǎn)期健康的妊娠期合并癥。近年來,GDM的發(fā)生率快速上升,GDM患者宮內(nèi)高糖環(huán)境可能增加子代兒童青少年期及成年后肥胖的發(fā)生風(fēng)險(xiǎn)受到廣泛關(guān)注。然而,目前有關(guān)GDM與子代肥胖發(fā)生風(fēng)險(xiǎn)的研究結(jié)論并不完全一致,且研究主要集中在兒童青少年期肥胖,尚缺乏對(duì)GDM患者子代出生后嬰幼兒期生長(zhǎng)發(fā)育的研究；在中國人群中,也尚缺乏GDM與子代肥胖相關(guān)性的研究。此外,孕期不同時(shí)點(diǎn)血糖水平(孕早期血糖和孕中期血糖、孕中期口服葡萄糖耐量試驗(yàn)(OGTT)空腹血糖和糖負(fù)荷后(1 h或2 h)血糖)對(duì)子代肥胖的影響程度是否存在差別,目前尚無這方面的研究報(bào)道。GDM影響子代肥胖的生物學(xué)機(jī)制仍不明確,但宮內(nèi)高糖環(huán)境可能通過改變表觀遺傳學(xué)來參與子代肥胖的發(fā)生。過氧化物酶體增殖物激活受體γ(PPAR-γ)在調(diào)節(jié)代謝和脂肪形成中具有重要作用,瘦素、脂聯(lián)素、脂蛋白酯酶(LPL)和脂肪細(xì)胞型脂肪酸結(jié)合蛋白(AFABP)是PPAR-γ通路上的主要肥胖相關(guān)因子；而Trim28是最新發(fā)現(xiàn)的肥胖“開關(guān)”基因,它們可能都在“胎兒程序化”改變過程中起著十分重要的作用。然而,目前尚無關(guān)于GDM、胎兒PPAR-γ和Trim28基因甲基化以及子代肥胖間關(guān)系的研究,也無GDM、PPAR-γ通路肥胖相關(guān)因子水平以及出生后子代肥胖間關(guān)系的研究。因此,本研究選擇浙江省舟山市婦幼保健院為研究現(xiàn)場(chǎng),采用前瞻性隊(duì)列研究設(shè)計(jì)探討GDM與嬰幼兒(0、6、12、18和24個(gè)月)肥胖發(fā)生風(fēng)險(xiǎn)的關(guān)聯(lián)性,并在前瞻性隊(duì)列研究設(shè)計(jì)基礎(chǔ)上采用1：1匹配設(shè)計(jì),探討GDM、胎兒臍帶血PPAR-γ和Trim28基因甲基化以及PPAR-γ通路肥胖相關(guān)因子水平與嬰幼兒(0、6、12和18個(gè)月)肥胖發(fā)生風(fēng)險(xiǎn)間的關(guān)聯(lián),闡明GDM與子代肥胖發(fā)生風(fēng)險(xiǎn)的關(guān)聯(lián)性及其可能的分子機(jī)制。材料和方法本研究選擇浙江省舟山市婦幼保健院為研究現(xiàn)場(chǎng),采用前瞻性隊(duì)列(2011年8月至2015年5月)研究設(shè)計(jì),通過流行病學(xué)調(diào)查問卷收集研究對(duì)象一般社會(huì)人口學(xué)特征、生活行為方式等基本信息,從孕婦體檢醫(yī)療記錄中摘抄孕早期空腹血糖和糖化血紅蛋白以及OGTT數(shù)據(jù)(空腹血糖、糖負(fù)荷后1 h和2 h血糖)等信息,并利用醫(yī)院婦幼保健系統(tǒng)的孕婦妊娠合并癥、并發(fā)癥和產(chǎn)時(shí)并發(fā)癥、嬰幼兒身長(zhǎng)、體重等信息,選擇無其它妊娠合并癥、并發(fā)癥和產(chǎn)時(shí)并發(fā)癥的單胎足月新生兒及母親為研究對(duì)象,利用多元線性回歸和Logistic回歸模型探討GDM與嬰幼兒(0、6、12、18和24個(gè)月)肥胖相關(guān)指標(biāo)的關(guān)聯(lián)性。在已納入上述隊(duì)列研究分析的母子對(duì)中,排除孕期吸煙、飲酒、藥物濫用者后,按照1：1匹配設(shè)計(jì),以孕婦年齡、孕前BMI、分娩孕周、胎兒性別及采血季節(jié)為匹配條件,GDM組與對(duì)照組各納入50例。于分娩時(shí),采集每位研究對(duì)象的臍帶血。采用美國SEQUENOM MassArray(?) EpiTYPER技術(shù)平臺(tái)檢測(cè)臍帶血白細(xì)胞中PPAR-γ和Trim28基因甲基化水平,采用酶聯(lián)免疫吸附法檢測(cè)臍帶血血漿中瘦素、脂聯(lián)素、LPL和AFABP的蛋白表達(dá)水平,利用多元線性回歸和Logistic回歸模型探討GDM、PPAR-γ和Trim28基因甲基化以及PPAR-γ通路肥胖相關(guān)因子水平與嬰幼兒(0、6、12和18個(gè)月)肥胖發(fā)生風(fēng)險(xiǎn)間的關(guān)聯(lián)。結(jié)果前瞻性隊(duì)列研究共納入1232例孕婦,其中GDM有234例,占19.0%。調(diào)整混雜因素后,GDM、孕中期OGTT空腹血糖、糖負(fù)荷后1 h和2 h血糖均與出生體重、孕周別出生體重Z-Score呈明顯的正相關(guān),且均顯著增加巨大兒的發(fā)生風(fēng)險(xiǎn)(P0.05)；GDM和OGTT糖負(fù)荷后2 h血糖升高均顯著增加大于胎齡兒(LGA)的發(fā)生風(fēng)險(xiǎn)(OR=1.79,95%CI:1.11-2.89；OR=2.71,95%CI:1.33-5.53),未發(fā)現(xiàn)孕早期空腹血糖、糖化血紅蛋白與新生兒出生體重相關(guān)指標(biāo)存在關(guān)聯(lián)(P0.05)。此外,相對(duì)于OGTT空腹血糖異常,糖負(fù)荷后血糖異常對(duì)新生兒出生體重、孕周別出生體重Z-Score以及巨大兒發(fā)生風(fēng)險(xiǎn)影響程度更大,同時(shí)OGTT空腹血糖異常與糖負(fù)荷后血糖異常呈現(xiàn)明顯的聯(lián)合作用,兩者同時(shí)異常可顯著增加新生兒出生體重(β=161.4 g,P=0.0192)和孕周別出生體重Z-Score(p=0.42,P=0.0121)以及LGA(OR=3.24,95%CI:1.21-8.67)和巨大兒(OR=5.73,95%CI:2.20-14.90)的發(fā)生風(fēng)險(xiǎn)；相對(duì)于孕早期血糖異常,孕中期GDM對(duì)新生兒出生體重、孕周別出生體重Z-Score影響程度更大,同時(shí)孕早期血糖異常與GDM也呈現(xiàn)明顯的聯(lián)合作用,兩者同時(shí)異�？娠@著增加新生兒出生體重(β=125.8 g,P=0.0010)和孕周別出生體重Z-Score(β=0.30,P=0.0013)以及LGA(OR=2.34,95%CI:1.28-4.30)和巨大兒(OR=2.53,95%CI:1.37-4.67)的發(fā)生風(fēng)險(xiǎn)。GDM與6個(gè)月嬰兒的BMI(β=0.31 kg/m2,P=0.0113)和年齡別BMI Z-Score(β=-0.19,P=0.0116)呈負(fù)相關(guān),且可降低6個(gè)月嬰兒超重或肥胖的發(fā)生風(fēng)險(xiǎn)(OR=0.59,95%CI:0.33-1.04；P=0.0686)；然而,未發(fā)現(xiàn)孕早期血糖水平或孕中期血糖水平(包括GDM)與12、18和24個(gè)月嬰幼兒體重、增重、BMI.BMI變化、年齡別體重Z-Score.年齡別BMI Z-Score以及超重或肥胖存在關(guān)聯(lián)(P0.05)。1：1匹配的前瞻性隊(duì)列研究中主要發(fā)現(xiàn)GDM以及孕中期OGTT空腹血糖與Trim28基因CpG10-11位點(diǎn)的甲基化水平呈明顯的正相關(guān),且該位點(diǎn)甲基化水平又與18個(gè)月幼兒的BMI、年齡別BMI Z-Score存在明顯的正相關(guān)(P0.05)。GDM以及OGTT空腹血糖也與Trim28基因各CpG位點(diǎn)的平均甲基化(CpGM)水平呈正相關(guān)趨勢(shì)；Trim28基因CpGM水平的升高又可增加巨大兒的發(fā)生風(fēng)險(xiǎn)(OR=1.37,95%CI：1.03-1.81),且與12、18個(gè)月嬰幼兒的體重、年齡別體重Z-Score、BMI和年齡別BMI Z-Score呈正相關(guān)(P0.05)。同時(shí),GDM與18個(gè)月幼兒的BMI(β=0.67 kg/m2,P=0.0177)和年齡別BMI Z-Score(p=0.58,P=0.0221)也呈正相關(guān)。但本研究未發(fā)現(xiàn)孕期血糖水平、Trim28其它CpG位點(diǎn)基因甲基化水平以及嬰幼兒肥胖間存在關(guān)聯(lián),也未發(fā)現(xiàn)孕期血糖水平、PPAR-γ基因甲基化水平、PPAR-γ通路肥胖相關(guān)因子(瘦素、脂聯(lián)素、LPL和AFABP)水平以及嬰幼兒肥胖間存在關(guān)聯(lián)(P0.05)。結(jié)論1.本研究發(fā)現(xiàn)GDM可增加新生兒出生體重、巨大兒和LGA的發(fā)生風(fēng)險(xiǎn)以及可能降低6個(gè)月嬰兒的BMI、超重或肥胖的發(fā)生風(fēng)險(xiǎn)；OGTT空腹血糖異常與糖負(fù)荷后血糖異常、孕早期血糖異常與GDM均呈現(xiàn)明顯的聯(lián)合作用,均可顯著增加新生兒出生體重、巨大兒和LGA的發(fā)生風(fēng)險(xiǎn)；未發(fā)現(xiàn)孕早期血糖水平或孕中期血糖水平(包括GDM)與12、18和24個(gè)月嬰幼兒肥胖相關(guān)指標(biāo)的關(guān)聯(lián)性。提示孕婦在孕前及孕期應(yīng)合理膳食,加強(qiáng)孕早期及孕中期血糖水平的監(jiān)測(cè),積極治療GDM,以降低不良妊娠結(jié)局及子代肥胖的發(fā)生風(fēng)險(xiǎn)。2.我們的研究結(jié)果還提示,GDM可能通過增加Trim28基因CpG10-11位點(diǎn)的甲基化以及CpGM水平來引起18個(gè)月幼兒BMI的增加,但未發(fā)現(xiàn)孕期血糖水平、PPAR-γ基因甲基化水平、PPAR-γ通路肥胖相關(guān)因子(瘦素、脂聯(lián)素、LPL和AFABP)水平以及嬰幼兒肥胖間存在關(guān)聯(lián)。然而,機(jī)制部分的研究結(jié)果還需大樣本的流行病研究予以驗(yàn)證。
[Abstract]:Background and objective Gestational diabetes mellitus (GDM) refers to the varying degrees of impaired glucose tolerance occurring during pregnancy or for the first time. It is a common serious harm to maternal and infant healthy pregnancy complications. In recent years, the incidence of GDM has risen rapidly, and the high glucose environment in GDM patients may increase. The risk of childhood obesity in children and adolescents is widely concerned. However, the current research conclusions about the risk of GDM and offspring obesity are not entirely consistent, and the study is mainly focused on childhood obesity, and there is still a lack of research on the growth and development of postnatal infants in GDM patients; among Chinese people, There is also a lack of study on the correlation between GDM and offspring obesity. In addition, whether there is a difference in the influence of the blood glucose level in the early pregnancy (early pregnancy glucose and midtrimester glucose, OGTT) fasting glucose tolerance test (OGTT) and glucose load (1 h or 2 h) on the offspring obesity, there is no research report on this aspect at present,.GDM The biological mechanism that affects offspring obesity is still unclear, but the intrauterine high glucose environment may be involved in the generation of offspring obesity by changing epigenetics. Peroxisome proliferator activated receptor gamma (PPAR- gamma) plays an important role in regulating metabolism and fat formation, leptin, adiponectin, lipoprotein esterase (LPL) and fat cell fat Acid binding protein (AFABP) is a major obesity related factor in the PPAR- gamma pathway; and Trim28 is the most recently discovered obesity "switch" gene, which may play a very important role in "fetal programmed" changes. However, there is no relationship between GDM, fetal PPAR- gamma and Trim28 gene methylation and offspring obesity. There is no GDM, PPAR- gamma pathway obesity related factor and postnatal obesity relationship. Therefore, this study selected the Zhoushan maternal and child health care hospital in Zhejiang Province as the research site, using prospective cohort study to explore the association between the risk of obesity in GDM and infants (0,6,12,18 and 24 months), and in the prospective team On the basis of the study design, the 1:1 matching design was used to explore the correlation between GDM, fetal umbilical cord blood PPAR- gamma and Trim28 methylation, the association of obesity related factors in PPAR- gamma pathway and the risk of obesity in infants (0,6,12 and 18 months), and to elucidate the relationship between GDM and the risk of offspring obesity and its possible molecular mechanism. The study selected Zhoushan maternal and child health care hospital of Zhejiang Province as the research site, and used a prospective cohort (August 2011 to May 2015) to study and design, collect the basic information of the general social demography, life behavior and so on through the epidemiological survey questionnaire, and extract the fasting blood glucose in the early pregnancy from the medical records of the pregnant women. Glycosylated hemoglobin and OGTT data (fasting blood glucose, 1 h and 2 h blood sugar after sugar load), and using the maternal and child health system of pregnant women with pregnancy complications, complications and complications, infant length, weight and other information, select no other pregnancy complications, complications and complications of single full-term newborns and mothers Study subjects, using multiple linear regression and Logistic regression model to explore the correlation between GDM and infant (0,6,12,18 and 24 months) obesity related indicators. In the mother and child, who had been included in the above cohort study, excluded from pregnancy smoking, drinking, and drug abusers, according to the 1:1 matching design, the age of pregnant women, BMI before pregnancy, pregnancy week, fetus. The sex and the blood sampling season were matched, the GDM group and the control group were included in 50 cases. The umbilical cord blood of each study was collected during childbirth. The SEQUENOM MassArray (?) EpiTYPER technology platform was used to detect the methylation level of PPAR- gamma and Trim28 gene in the umbilical cord blood white blood cells and the ELISA was used to detect the leptin in the umbilical cord blood plasma. The protein expression levels of adiponectin, LPL and AFABP, using multiple linear regression and Logistic regression models to explore the correlation between the methylation of GDM, PPAR- gamma and Trim28 genes and the levels of obesity related factors in PPAR- gamma pathway and the risk of obesity in infants (0,6,12 and 18 months). Results a prospective cohort study was included in 1232 pregnant women, of which GDM was found. 234 cases, after 19.0%. adjustment of confounding factors, GDM, OGTT fasting glucose in the middle of pregnancy, 1 h and 2 h blood glucose after sugar load were all positively correlated with birth weight and gestational birth weight Z-Score, and significantly increased the risk of macrosomia (P0.05), and the increase of 2 h blood glucose after GDM and OGTT sugar load were significantly higher than that of gestational age infants (LGA). The risk (OR=1.79,95%CI:1.11-2.89; OR=2.71,95%CI:1.33-5.53) was not found in early pregnancy with fasting blood glucose, glycated hemoglobin and newborn birth weight related indicators (P0.05). In addition, compared with OGTT abnormal fasting blood glucose, abnormal blood glucose after sugar load on newborn birth weight, gestational birth weight Z-Score and huge hair hair. There was a greater degree of impact on the risk of birth, at the same time, there was a significant combination of abnormal OGTT fasting blood glucose and abnormal glucose load. Both of them also significantly increased the birth weight of the newborn (beta =161.4 g, P=0.0192) and the birth weight Z-Score (p=0.42, P=0.0121), and LGA (OR=3.24,95%CI:1.21-8.67) and giant infants (OR=5.73,95%CI:2.20). The risk of -14.90); relative to the abnormal blood glucose in the early pregnancy, the mid trimester GDM has a greater impact on the birth weight of the newborn and the birth weight Z-Score in the gestational week, and the abnormal blood glucose in the early pregnancy also has a significant combined effect on the GDM, and both of the two can significantly increase the birth weight of newborn infants (beta =125.8 g, P=0.0010) and the birth of the gestational weeks. The risk.GDM of weight Z-Score (beta =0.30, P=0.0013) and LGA (OR=2.34,95%CI:1.28-4.30) and macrosomia (OR=2.53,95%CI:1.37-4.67) was negatively correlated with the BMI (beta =0.31 kg/m2, P=0.0113) of 6 months infants and the age BMI (beta), and reduced the risk of overweight or obesity in 6 months. 04; P=0.0686); however, it was not found that early pregnancy blood glucose level or midtrimester glucose level (including GDM) and 12,18 and 24 months infant weight, weight gain, BMI.BMI change, Z-Score. age BMI Z-Score, and overweight or obesity associated (P0.05).1: 1 matching in prospective cohort study of GDM and mid pregnancy OG There was a positive correlation between TT fasting blood glucose and the level of methylation of the Trim28 gene CpG10-11 locus, and the level of methylation of the site was also positively correlated with the BMI of 18 months young children, the P0.05.GDM and the OGTT fasting blood glucose also had a positive correlation with the average methylation (CpGM) level of the CpG loci of the Trim28 gene. The increase in the CpGM level of the 28 gene could also increase the risk of the occurrence of macrosomia (OR=1.37,95%CI:1.03-1.81), as well as the weight of the infants in 12,18 months, the age other body weight Z-Score, the BMI and the age BMI Z-Score (P0.05). Meanwhile, GDM and the BMI of the 18 month children were also present. Positive correlation. However, there was no pregnancy glucose level in this study. There was a association between Trim28 other CpG locus methylation levels and infant obesity, and no pregnancy glucose levels, PPAR- gamma methylation levels, PPAR- gamma pathway obesity related factors (leptin, adiponectin, LPL and AFABP) levels and association between infant obesity (P0.05) Conclusion the 1. study found that GDM could increase the birth weight of the newborn, the risk of the occurrence of giant infants and LGA, and the risk of reducing the BMI, overweight or obesity in the 6 month infant; the abnormal OGTT fasting blood glucose and the abnormal glucose load, the abnormal blood glucose in the early pregnancy and the GDM have a clear combined effect, which can significantly increase the birth rate of the newborn. The risk of birth weight, macrosomia and LGA, and the association between the blood glucose level in the early pregnancy or the mid trimester blood glucose level (including GDM) and the obesity related indexes of 12,18 and 24 months infants. It is suggested that pregnant women should have a reasonable diet before and during pregnancy, strengthen the monitoring of blood glucose level in the early pregnancy and midtrimester, and actively treat GDM in order to reduce the bad pregnancy. The outcome and the risk of offspring obesity.2. our results also suggest that GDM may increase the BMI increase in 18 month children by increasing the methylation of the Trim28 gene CpG10-11 site and the CpGM level, but no pregnancy glucose level, the PPAR- gamma methylation level, and PPAR- gamma pathway obesity related factors (leptin, adiponectin, LPL and AFA) are not found. There is a correlation between BP level and infant obesity. However, the results of part of the mechanism need to be verified by large sample epidemiological studies.
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2016
【分類號(hào)】：R714.256;R723.14

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