Pregnancy environment, and not preconception, leads to fetal growth restriction and congenital abnormalities associated with diabetes
Maternal diabetes can lead to pregnancy complications and impaired fetal development. The goal of this study was to use a mouse model of reciprocal embryo transfer to distinguish between the preconception and gestational effects of diabetes. To induce diabetes female mice were injected with a single...
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| Veröffentlicht in: | Scientific reports 2020-07, Vol.10 (1), p.12254, Article 12254 |
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| description | Maternal diabetes can lead to pregnancy complications and impaired fetal development. The goal of this study was to use a mouse model of reciprocal embryo transfer to distinguish between the preconception and gestational effects of diabetes. To induce diabetes female mice were injected with a single high dose of streptozotocin and 3 weeks thereafter used as oocyte donors for in vitro fertilization (IVF) and as recipients for embryo transfer. Following IVF embryos were cultured to the blastocyst stage in vitro or transferred to diabetic and non-diabetic recipients. Diabetic and non-diabetic females did not differ in regard to the number of oocytes obtained after ovarian stimulation, oocytes ability to become fertilized, and embryo development in vitro. However, diabetic females displayed impaired responsiveness to superovulation. Reciprocal embryo transfer resulted in similar incidence of live fetuses and abortions, and no changes in placental size. However, fetuses carried by diabetic recipients were smaller compared to those carried by non-diabetic recipients, regardless hyperglycemia status of oocyte donors. Congenital abnormalities were observed only among the fetuses carried by diabetic recipients. The findings support that the diabetic status during pregnancy, and not the preconception effect of diabetes on oogenesis, leads to fetal growth restriction and congenital deformities. |
| doi_str_mv | 10.1038/s41598-020-69247-w |
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The goal of this study was to use a mouse model of reciprocal embryo transfer to distinguish between the preconception and gestational effects of diabetes. To induce diabetes female mice were injected with a single high dose of streptozotocin and 3 weeks thereafter used as oocyte donors for in vitro fertilization (IVF) and as recipients for embryo transfer. Following IVF embryos were cultured to the blastocyst stage in vitro or transferred to diabetic and non-diabetic recipients. Diabetic and non-diabetic females did not differ in regard to the number of oocytes obtained after ovarian stimulation, oocytes ability to become fertilized, and embryo development in vitro. However, diabetic females displayed impaired responsiveness to superovulation. Reciprocal embryo transfer resulted in similar incidence of live fetuses and abortions, and no changes in placental size. However, fetuses carried by diabetic recipients were smaller compared to those carried by non-diabetic recipients, regardless hyperglycemia status of oocyte donors. Congenital abnormalities were observed only among the fetuses carried by diabetic recipients. The findings support that the diabetic status during pregnancy, and not the preconception effect of diabetes on oogenesis, leads to fetal growth restriction and congenital deformities.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-020-69247-w</identifier><identifier>PMID: 32703993</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/136 ; 692/308 ; Animals ; Congenital Abnormalities - diagnosis ; Congenital Abnormalities - etiology ; Diabetes ; Diabetes Complications ; Diabetes Mellitus ; Disease Models, Animal ; Disease Susceptibility ; Embryo Transfer ; Embryonic Development ; Embryos ; Female ; Females ; Fetal Growth Retardation - diagnosis ; Fetal Growth Retardation - etiology ; Fetuses ; Humanities and Social Sciences ; Humans ; Hyperglycemia ; In vitro fertilization ; Incidence ; Male ; Maternal Exposure ; Mice ; multidisciplinary ; Oocytes ; Oogenesis ; Ovulation ; Phenotype ; Placenta ; Pregnancy ; Pregnancy complications ; Prenatal Exposure Delayed Effects ; Science ; Science (multidisciplinary) ; Streptozocin</subject><ispartof>Scientific reports, 2020-07, Vol.10 (1), p.12254, Article 12254</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. 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The goal of this study was to use a mouse model of reciprocal embryo transfer to distinguish between the preconception and gestational effects of diabetes. To induce diabetes female mice were injected with a single high dose of streptozotocin and 3 weeks thereafter used as oocyte donors for in vitro fertilization (IVF) and as recipients for embryo transfer. Following IVF embryos were cultured to the blastocyst stage in vitro or transferred to diabetic and non-diabetic recipients. Diabetic and non-diabetic females did not differ in regard to the number of oocytes obtained after ovarian stimulation, oocytes ability to become fertilized, and embryo development in vitro. However, diabetic females displayed impaired responsiveness to superovulation. Reciprocal embryo transfer resulted in similar incidence of live fetuses and abortions, and no changes in placental size. However, fetuses carried by diabetic recipients were smaller compared to those carried by non-diabetic recipients, regardless hyperglycemia status of oocyte donors. Congenital abnormalities were observed only among the fetuses carried by diabetic recipients. The findings support that the diabetic status during pregnancy, and not the preconception effect of diabetes on oogenesis, leads to fetal growth restriction and congenital deformities.</description><subject>631/136</subject><subject>692/308</subject><subject>Animals</subject><subject>Congenital Abnormalities - diagnosis</subject><subject>Congenital Abnormalities - etiology</subject><subject>Diabetes</subject><subject>Diabetes Complications</subject><subject>Diabetes Mellitus</subject><subject>Disease Models, Animal</subject><subject>Disease Susceptibility</subject><subject>Embryo Transfer</subject><subject>Embryonic Development</subject><subject>Embryos</subject><subject>Female</subject><subject>Females</subject><subject>Fetal Growth Retardation - diagnosis</subject><subject>Fetal Growth Retardation - etiology</subject><subject>Fetuses</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>In vitro fertilization</subject><subject>Incidence</subject><subject>Male</subject><subject>Maternal Exposure</subject><subject>Mice</subject><subject>multidisciplinary</subject><subject>Oocytes</subject><subject>Oogenesis</subject><subject>Ovulation</subject><subject>Phenotype</subject><subject>Placenta</subject><subject>Pregnancy</subject><subject>Pregnancy complications</subject><subject>Prenatal Exposure Delayed Effects</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Streptozocin</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kU1OHDEQha0oUUCEC2QRWcqWBrd_utsbpAglgISULJK1VW1XD0Y99mB7GM0Bcu94GAJkE29sqb73qsqPkI8tO22ZGM6ybJUeGsZZ02ku-2bzhhxyJlXDBedvX70PyHHOd6wexbVs9XtyIHjPhNbikPz-kXARINgtxfDgUwxLDOWEQnA0xEJXCW0MFlfFx3BCZwSXaYl0wgIzXaS4Kbc0YS7J2x3yKKyKBQa_I2AMMS1h9sVjppBztB4KOrrxVeg8jFgwfyDvJpgzHj_dR-TXt68_L66am--X1xdfbhore1ma3tlpgBF0i3xQSgndDd3ELZ-gdQjgOhCWWen0KLQaJjVxxTQwaxlKpzpxRM73vqv1uERn66oJZrNKfglpayJ4828l-FuziA-mF_0wCF0NPj8ZpHi_rmubu7hOoc5suOSdUKoVqlJ8T9kUc044PXdomdmlZ_bpmZqeeUzPbKro0-vZniV_s6qA2AO5luoHp5fe_7H9A16oqw4</recordid><startdate>20200723</startdate><enddate>20200723</enddate><creator>Tsai, Pai-Jong Stacy</creator><creator>Yamauchi, Yasuhiro</creator><creator>Riel, Jonathan M.</creator><creator>Ward, Monika A.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20200723</creationdate><title>Pregnancy environment, and not preconception, leads to fetal growth restriction and congenital abnormalities associated with diabetes</title><author>Tsai, Pai-Jong Stacy ; 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The goal of this study was to use a mouse model of reciprocal embryo transfer to distinguish between the preconception and gestational effects of diabetes. To induce diabetes female mice were injected with a single high dose of streptozotocin and 3 weeks thereafter used as oocyte donors for in vitro fertilization (IVF) and as recipients for embryo transfer. Following IVF embryos were cultured to the blastocyst stage in vitro or transferred to diabetic and non-diabetic recipients. Diabetic and non-diabetic females did not differ in regard to the number of oocytes obtained after ovarian stimulation, oocytes ability to become fertilized, and embryo development in vitro. However, diabetic females displayed impaired responsiveness to superovulation. Reciprocal embryo transfer resulted in similar incidence of live fetuses and abortions, and no changes in placental size. However, fetuses carried by diabetic recipients were smaller compared to those carried by non-diabetic recipients, regardless hyperglycemia status of oocyte donors. Congenital abnormalities were observed only among the fetuses carried by diabetic recipients. The findings support that the diabetic status during pregnancy, and not the preconception effect of diabetes on oogenesis, leads to fetal growth restriction and congenital deformities.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32703993</pmid><doi>10.1038/s41598-020-69247-w</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 631/136 692/308 Animals Congenital Abnormalities - diagnosis Congenital Abnormalities - etiology Diabetes Diabetes Complications Diabetes Mellitus Disease Models, Animal Disease Susceptibility Embryo Transfer Embryonic Development Embryos Female Females Fetal Growth Retardation - diagnosis Fetal Growth Retardation - etiology Fetuses Humanities and Social Sciences Humans Hyperglycemia In vitro fertilization Incidence Male Maternal Exposure Mice multidisciplinary Oocytes Oogenesis Ovulation Phenotype Placenta Pregnancy Pregnancy complications Prenatal Exposure Delayed Effects Science Science (multidisciplinary) Streptozocin |
| title | Pregnancy environment, and not preconception, leads to fetal growth restriction and congenital abnormalities associated with diabetes |
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