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1、瘦素基因甲基化對(duì)孕鼠糖代謝變化的影響[基金項(xiàng)目]國(guó)家自然科學(xué)基金面上項(xiàng)目(30973203)辛靜,女,碩士研究生,研究方向:圍產(chǎn)醫(yī)學(xué),E-mail:dsjydxj@126.com通訊作者:李真,E-mail:drlizhen@yahoo.com.cn辛靜黃金通訊作者:李真第三軍醫(yī)大學(xué)附屬新橋醫(yī)院婦產(chǎn)科(重慶400037)摘要目的:探討不同孕期小鼠體內(nèi)孕激素、胰島素、瘦素的動(dòng)態(tài)水平及瘦素基因啟動(dòng)子區(qū)甲基化變化特點(diǎn),分析其相互關(guān)系及對(duì)孕期糖代謝的影響。方法:采用隨機(jī)的方式取孕前、孕早期、孕中期、孕晚
2、期及產(chǎn)后7天的雌鼠各五只,進(jìn)行葡萄糖耐量的測(cè)定從而了解孕期糖代謝的變化,并測(cè)定不同孕期血清中孕酮、胰島素和瘦素水平,以了解三者間的動(dòng)態(tài)關(guān)系,通過(guò)檢測(cè)瘦素基因啟動(dòng)子的甲基化水平進(jìn)一步了解影響瘦素水平變化的機(jī)制。結(jié)果:孕鼠血清中胰島素、孕酮、瘦素水平明顯高于非妊娠期,并隨孕期逐漸升高(P<0.01),孕期空腹血糖偏低,糖耐量較非孕期有降低的趨勢(shì),胎盤中瘦素基因啟動(dòng)子區(qū)的甲基化水平隨妊娠進(jìn)展降低。結(jié)論:孕期孕激素、胰島素和瘦素的高水平共同參與妊娠期生理性胰島素抵抗的發(fā)生,使空腹血糖降低,糖耐量下調(diào)。正
3、常妊娠期瘦素水平的變化與胎盤組織瘦素基因的甲基化水平有關(guān)。關(guān)鍵詞妊娠;瘦素;胰島素抵抗;糖代謝;甲基化TheeffectoftheleptingenemethylationonglucosemetabolisminpregnantmiceXinJingHuangJin(DepartmentofObstericsandGynecology,XinQiaoHospital,ThirdMilitaryMedicalUniversity,ChongQing400037,China)Correspongd
4、ingauthor:LIZhenAbstract:[Purpose]Toinvestigatethechangesofprogesterone,insulinandleptininpregnantmiceandthecorrelativemechanismamongthem,aswellastheeffectsonthechangeofglucosemetabolism.[Methods]Femalemiceweredividedrandomlytofivedifferentgroups,non
5、-pregnancy,early-gestation,mid-gestation,late-gestationandpostpartummicerespectively,inordertoidentifythechangeofglucosemetabolismduringthewholedurationofpregnancy.Thelevelsofprogesterone,insulinandleptinindifferentperiodsofpregnancyweremeasuredtocla
6、rifytherelationshipamongthem.Alsothelevelofmethylationoftheleptinpromotergenewasdetectedtofindoutthemechanismofthechangeonthelevelofleptin.[Results]Theserumlevelsofprogesterone,insulinandleptinofpregnantmicearedramaticallyhigherthanthatofthenon-pregn
7、antmice,andrisinginaccordwiththedevelopmentofpregnancy(P<0.01).Fastingserumglucoseindurationofpregnancyislowerandglucosetolerancestayinadecreasingtendencyuntiltheendofgestation.Withthehigherexpressionofleptin,methylationoftheleptinpromoterisreduceddu
8、ringgestationalperiod.[Conclusion]Highlevelofprogesterone,insulinandleptintakespartinthephysiologicalinsulinresistanceduringgestation.Thechangeofleptinexpressionmaybeattributabletoreducedmethylationoftheleptinpromotergeneinplacentaltissue.Keywords:pr