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Peixin Yang - One of the best experts on this subject based on the ideXlab platform.
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DNMT3a Conditional Deletion in Neuro-epithelium Restores Maternal Diabetes-suppressed Neural Tube Closure Essential Genes Expression and Blocks Maternal Diabetes-activated ER Stress
Free Radical Biology and Medicine, 2017Co-Authors: Penghua Yang, Cheng Xu, Peixin YangAbstract:Global DNA hypermethylation is induced in embryonic neuroepithelium by Maternal Diabetes, leading to neural tube defects (NTDs). However the underlying mechanism is not clear. Our previous study has demonstrated that the green tea polyphenal Epigallocatechin gallate (EGCG) inhibited DNA hypermethylation and ameliorated Maternal Diabetes-induced NTDs. To determine whether antioxidant enzymes can suppress DNA hypermethylation in diabetic embryos, SOD1 transgenic male mice are breed with diabetic wild type female mice. SOD1 overexpression reduces Maternal Diabetes-induced DNA hypermethylation leading to suppression of DNMT3a and DNMT3b, but not DNMT1. To further investigate whether Maternal Diabetes-increased DNA methyltransferase 3a (DNMT3a) is involved in the pathogenesis of diabetic embryopathy, the Dnmt3a gene was deleted using the Cre-Flox (f) approach by crossing DNMT3af/+ ;nestin-Cre male mice with DNMT3af/f female mice. Dnmt3a deletion specifically occurred in the developing neuroepithelium, and DNMT1 and DNMT3b expression were not affected. Conditional deletion of Dnmt3a significantly reduces the NTD rate from 27.2% in wild-type embryos to 4% in homozygous deletion embryos (DNMT3af/f ;nestin-Cre) under Maternal diabetic conditions and ameliorates Maternal Diabetes-induced DNA hyper-methylation. Moreover, Dnmt3a deficiency in the neuroepithelium abrogated Maternal Diabetes-induced hyper-methylation in the promoters region of neural tube closure essential genes including Pax3, Tulp3 and GRHL3, leading to activation of these genes. Furthermore Maternal Diabetes-induced ER stress in neuroepithelium is blocked by conditional deletion of Dnmt3a, which suppresses neuroepithelium apoptosis. Taken together, our findings demonstrate that Dnmt3a conditional deletion in neuroepithelium restores Maternal Diabetes-suppressed neural tube closure essential genes expression and blocks Maternal Diabetes-activated ER stress.
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The green tea polyphenol EGCG alleviates Maternal Diabetes–induced neural tube defects by inhibiting DNA hypermethylation
American Journal of Obstetrics and Gynecology, 2016Co-Authors: Jianxiang Zhong, Cheng Xu, E Albert Reece, Peixin YangAbstract:Background Maternal Diabetes increases the risk of neural tube defects in offspring. Our previous study demonstrated that the green tea polyphenol, Epigallocatechin gallate, inhibits high glucose-induced neural tube defects in cultured embryos. However, the therapeutic effect of Epigallocatechin gallate on Maternal Diabetes–induced neural tube defects is still unclear. Objective We aimed to examine whether Epigallocatechin gallate treatment can reduce Maternal Diabetes–induced DNA methylation and neural tube defects. Study Design Nondiabetic and diabetic pregnant mice at embryonic day 5.5 were given drinking water with or without 1 or 10 μM Epigallocatechin gallate. At embryonic day 8.75, embryos were dissected from the visceral yolk sac for the measurement of the levels and activity of DNA methyltransferases, the levels of global DNA methylation, and methylation in the CpG islands of neural tube closure essential gene promoters. embryonic day 10.5 embryos were examined for neural tube defect incidence. Results Epigallocatechin gallate treatment did not affect embryonic development because embryos from nondiabetic dams treated with Epigallocatechin gallate did not exhibit any neural tube defects. Treatment with 1 μM Epigallocatechin gallate did not reduce Maternal Diabetes–induced neural tube defects significantly. Embryos from diabetic dams treated with 10 μM Epigallocatechin gallate had a significantly lower neural tube defect incidence compared with that of embryos without Epigallocatechin gallate treatment. Epigallocatechin gallate reduced neural tube defect rates from 29.5% to 2%, an incidence that is comparable with that of embryos from nondiabetic dams. Ten micromoles of Epigallocatechin gallate treatment blocked Maternal Diabetes–increased DNA methyltransferases 3a and 3b expression and their activities, leading to the suppression of global DNA hypermethylation. Additionally, 10 μM Epigallocatechin gallate abrogated Maternal Diabetes–increased DNA methylation in the CpG islands of neural tube closure essential genes, including Grhl3 , Pax3 , and Tulp3 . Conclusion Epigallocatechin gallate reduces Maternal Diabetes–induced neural tube defects formation and blocks the enhanced expression and activity of DNA methyltransferases, leading to the suppression of DNA hypermethylation and the restoration of neural tube closure essential gene expression. These observations suggest that Epigallocatechin gallate supplements could mitigate the teratogenic effects of hyperglycemia on the developing embryo and prevent Diabetes–induced neural tube defects.
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The green tea polyphenol EGCG alleviates Maternal Diabetes-induced neural tube defects by inhibiting DNA hypermethylation.
American journal of obstetrics and gynecology, 2016Co-Authors: Jianxiang Zhong, Cheng Xu, E Albert Reece, Peixin YangAbstract:Maternal Diabetes increases the risk of neural tube defects in offspring. Our previous study demonstrated that the green tea polyphenol, Epigallocatechin gallate, inhibits high glucose-induced neural tube defects in cultured embryos. However, the therapeutic effect of Epigallocatechin gallate on Maternal Diabetes-induced neural tube defects is still unclear. We aimed to examine whether Epigallocatechin gallate treatment can reduce Maternal Diabetes-induced DNA methylation and neural tube defects. Nondiabetic and diabetic pregnant mice at embryonic day 5.5 were given drinking water with or without 1 or 10 μM Epigallocatechin gallate. At embryonic day 8.75, embryos were dissected from the visceral yolk sac for the measurement of the levels and activity of DNA methyltransferases, the levels of global DNA methylation, and methylation in the CpG islands of neural tube closure essential gene promoters. embryonic day 10.5 embryos were examined for neural tube defect incidence. Epigallocatechin gallate treatment did not affect embryonic development because embryos from nondiabetic dams treated with Epigallocatechin gallate did not exhibit any neural tube defects. Treatment with 1 μM Epigallocatechin gallate did not reduce Maternal Diabetes-induced neural tube defects significantly. Embryos from diabetic dams treated with 10 μM Epigallocatechin gallate had a significantly lower neural tube defect incidence compared with that of embryos without Epigallocatechin gallate treatment. Epigallocatechin gallate reduced neural tube defect rates from 29.5% to 2%, an incidence that is comparable with that of embryos from nondiabetic dams. Ten micromoles of Epigallocatechin gallate treatment blocked Maternal Diabetes-increased DNA methyltransferases 3a and 3b expression and their activities, leading to the suppression of global DNA hypermethylation. Additionally, 10 μM Epigallocatechin gallate abrogated Maternal Diabetes-increased DNA methylation in the CpG islands of neural tube closure essential genes, including Grhl3, Pax3, and Tulp3. Epigallocatechin gallate reduces Maternal Diabetes-induced neural tube defects formation and blocks the enhanced expression and activity of DNA methyltransferases, leading to the suppression of DNA hypermethylation and the restoration of neural tube closure essential gene expression. These observations suggest that Epigallocatechin gallate supplements could mitigate the teratogenic effects of hyperglycemia on the developing embryo and prevent Diabetes-induced neural tube defects. Copyright © 2016 Elsevier Inc. All rights reserved.
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Maternal Diabetes triggers dna damage and dna damage response in neurulation stage embryos through oxidative stress
Biochemical and Biophysical Research Communications, 2015Co-Authors: Daoyin Dong, Jingwen Yu, Yanqing Wu, Noah Fu, Natalia Arias Villela, Peixin YangAbstract:DNA damage and DNA damage response (DDR) in neurulation stage embryos under Maternal Diabetes conditions are not well understood. The purpose of this study was to investigate whether Maternal Diabetes and high glucose in vitro induce DNA damage and DDR in the developing embryo through oxidative stress. In vivo experiments were conducted by mating superoxide dismutase 1 (SOD1) transgenic male mice with wild-type (WT) female mice with or without Diabetes. Embryonic day 8.75 (E8.75) embryos were tested for the DNA damage markers, phosphorylated histone H2A.X (p-H2A.X) and DDR signaling intermediates, including phosphorylated checkpoint 1 (p-Chk1), phosphorylated checkpoint 2 (p-Chk2), and p53. Levels of the same DNA damage markers and DDR signaling intermediates were also determined in the mouse C17.2 neural stem cell line. Maternal Diabetes and high glucose in vitro significantly increased the levels of p-H2A.X. Levels of p-Chk1, p-Chk2, and p53, were elevated under both Maternal diabetic and high glucose conditions. SOD1 overexpression blocked Maternal Diabetes-induced DNA damage and DDR in vivo. Tempol, a SOD1 mimetic, diminished high glucose-induced DNA damage and DDR in vitro. In conclusion, Maternal Diabetes and high glucose in vitro induce DNA damage and activates DDR through oxidative stress, which may contribute to the pathogenesis of Diabetes-associated embryopathy.
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Trehalose prevents neural tube defects by correcting Maternal Diabetes-suppressed autophagy and neurogenesis
American Journal of Physiology-endocrinology and Metabolism, 2013Co-Authors: Cheng Xu, Xuezheng Li, Fang Wang, Hongbo Weng, Peixin YangAbstract:Preexisting Maternal Diabetes increases the risk of neural tube defects (NTDs). The mechanism underlying Maternal Diabetes-induced NTDs is not totally defined, and its prevention remains a challenge. Autophagy, an intracellular process to degrade dysfunction protein and damaged cellular organelles, regulates cell proliferation, differentiation, and apoptosis. Because autophagy impairment causes NTDs reminiscent of those observed in diabetic pregnancies, we hypothesize that Maternal Diabetes-induced autophagy impairment causes NTD formation by disrupting cellular homeostasis, leading to endoplasmic reticulum (ER) stress and apoptosis, and that restoration of autophagy by trehalose, a natural disaccharide, prevents Diabetes-induced NTDs. Embryos from nondiabetic and type 1 diabetic mice fed with or without 2 or 5% trehalose water were used to assess markers of autophagy, ER stress, and neurogenesis, numbers of autophagosomes, gene expression that regulates autophagy, NTD rates, indices of mitochondrial dysfunction, and neuroepithelial cell apoptosis. Maternal Diabetes suppressed autophagy by significantly reducing LC3-II expression, autophagosome numbers, and GFP-LC3 punctate foci in neuroepithelial cells and by altering autophagy-related gene expression. Maternal Diabetes delayed neurogenesis by blocking Sox1 neural progenitor differentiation. Trehalose treatment reversed autophagy impairment and prevented NTDs in diabetic pregnancies. Trehalose resolved homeostatic imbalance by correcting mitochondrial defects, dysfunctional proteins, ER stress, apoptosis, and delayed neurogenesis in the neural tubes exposed to hyperglycemia. Our study demonstrates for the first time that Maternal Diabetes suppresses autophagy in neuroepithelial cells of the developing neural tube, leading to NTD formation, and provides evidence for the potential efficacy of trehalose as an intervention against hyperglycemia-induced NTDs.
Shao-ling Zhang - One of the best experts on this subject based on the ideXlab platform.
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post weaning high fat diet accelerates kidney injury but not hypertension programmed by Maternal Diabetes
Pediatric Research, 2016Co-Authors: Yessoufou Aliou, Isabelle Chenier, Julie R. Ingelfinger, Xin-ping Zhao, Min-chun Liao, Shiao-ying Chang, Shao-ling ZhangAbstract:Post-weaning high-fat diet accelerates kidney injury, but not hypertension programmed by Maternal Diabetes
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Maternal Diabetes modulates kidney formation in murine progeny: the role of hedgehog interacting protein (HHIP).
Diabetologia, 2014Co-Authors: Xin-ping Zhao, Isabelle Chenier, Julie R. Ingelfinger, Min-chun Liao, Shiao-ying Chang, Shaaban Abdo, Yessoufou Aliou, Shao-ling ZhangAbstract:Aims/hypothesis We hypothesised that Maternal Diabetes impairs kidney formation in offspring via augmented expression of hedgehog interacting protein (HHIP). Our gene-array results were performed in neonatal kidneys from our murine model of Maternal Diabetes and indicated that Hhip expression was significantly modulated by Maternal Diabetes.
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Maternal Diabetes programs hypertension and kidney injury in offspring.
Pediatric Nephrology, 2010Co-Authors: Yun Wen Chen, Stella Tran, Isabelle Chenier, Shiao-ying Chang, Michael Scotcher, Shao-ling ZhangAbstract:We investigated whether Maternal Diabetes programs the offspring to develop hypertension and kidney injury in adulthood and examined potential underlying mechanisms. In a murine model we studied the offspring of three groups of dams (non-diabetic, diabetic, and diabetic treated with insulin). Mean systolic blood pressure in the offspring was monitored from 8 to 20 weeks. Body and kidney weights in the offspring of diabetic mothers were significantly lower than in offspring of non-diabetic mothers. Offspring of diabetic mothers developed hypertension, microalbuminuria, and glucose intolerance. Increased accumulation of extracellular matrix proteins in the glomeruli and marked upregulation of angiotensinogen, angiotensin II type 1 receptor, angiotensin-converting enzyme, transforming growth factor beta-1 (TGF-β1), and plasminogen activator inhibitor-1 (PAI-1) gene expression were evident in the renal cortex of hypertensive offspring of diabetic mothers. By contrast, angiotensin-converting enzyme-2 (ACE2) gene expression was lower in the hypertensive offspring of diabetic mothers than in that of non-diabetic mothers. These changes were prevented in the offspring of insulin-treated diabetic mothers. These data indicate that Maternal Diabetes induces perinatal programming of hypertension, renal injury, and glucose intolerance in the offspring and suggest a central role for the activation of the intrarenal renin–angiotensin system and TGF-β1 gene expression in this process.
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Maternal Diabetes Modulates Renal Morphogenesis in Offspring
Journal of The American Society of Nephrology, 2008Co-Authors: Stella Tran, Yun Wen Chen, Isabelle Chenier, John S.d. Chan, Susan E. Quaggin, Marie-josée Hébert, Julie R. Ingelfinger, Shao-ling ZhangAbstract:Maternal Diabetes leads to an adverse in utero environment, but whether Maternal Diabetes impairs nephrogenesis is unknown. Diabetes was induced with streptozotocin in pregnant Hoxb7–green fluorescence protein mice at embryonic day 13, and the offspring were examined at several time points after birth. Compared with offspring of nondiabetic controls, offspring of diabetic mice had lower body weight, body size, kidney weight, and nephron number. The observed renal dysmorphogenesis may be the result of increased apoptosis, because immunohistochemical analysis revealed significantly more apoptotic podocytes as well as increased active caspase-3 immunostaining in the renal tubules compared with control mice. Regarding potential mediators of these differences, offspring of diabetic mice had increased expression of intrarenal angiotensinogen and renin mRNA, upregulation of NF-κB isoforms p50 and p65, and activation of the NF-κB pathway. In conclusion, Maternal Diabetes impairs nephrogenesis, possibly via enhanced intrarenal activation of the renin-angiotensin system and NF-κB signaling.
Kabirou Moutairou - One of the best experts on this subject based on the ideXlab platform.
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Maternal Diabetes in pregnancy early and long term outcomes on the offspring and the concept of metabolic memory
Experimental Diabetes Research, 2011Co-Authors: Akadiri Yessoufou, Kabirou MoutairouAbstract:The adverse outcomes on the offspring from Maternal Diabetes in pregnancy are substantially documented. In this paper, we report main knowledge on impacts of Maternal Diabetes on early and long-term health of the offspring, with specific comments on Maternal obesity. The main adverse outcome on progenies from pregnancy complicated with Maternal Diabetes appears to be macrosomia, as it is commonly known that intrauterine exposure to hyperglycemia increases the risk and programs the offspring to develop Diabetes and/or obesity at adulthood. This “fetal programming”, due to intrauterine diabetic milieu, is termed as “metabolic memory”. In gestational Diabetes as well as in macrosomia, the complications include metabolic abnormalities, degraded antioxidant status, disrupted immune system and potential metabolic syndrome in adult offspring. Furthermore, there is evidence that Maternal obesity may also increase the risk of obesity and Diabetes in offspring. However, women with GDM possibly exhibit greater macrosomia than obese women. Obesity and Diabetes in pregnancy have independent and additive effects on obstetric complications, and both require proper management. Management of gestational Diabetes mellitus and Maternal obesity is essential for Maternal and offspring's good health. Increasing physical activity, preventing gestational weight gain, and having some qualitative nutritional habits may be beneficial during both the pregnancy and offspring's future life.
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Maternal Diabetes in Pregnancy: Early and Long-Term Outcomes on the Offspring and the Concept of “Metabolic Memory”
Experimental Diabetes Research, 2011Co-Authors: Akadiri Yessoufou, Kabirou MoutairouAbstract:The adverse outcomes on the offspring from Maternal Diabetes in pregnancy are substantially documented. In this paper, we report main knowledge on impacts of Maternal Diabetes on early and long-term health of the offspring, with specific comments on Maternal obesity. The main adverse outcome on progenies from pregnancy complicated with Maternal Diabetes appears to be macrosomia, as it is commonly known that intrauterine exposure to hyperglycemia increases the risk and programs the offspring to develop Diabetes and/or obesity at adulthood. This “fetal programming”, due to intrauterine diabetic milieu, is termed as “metabolic memory”. In gestational Diabetes as well as in macrosomia, the complications include metabolic abnormalities, degraded antioxidant status, disrupted immune system and potential metabolic syndrome in adult offspring. Furthermore, there is evidence that Maternal obesity may also increase the risk of obesity and Diabetes in offspring. However, women with GDM possibly exhibit greater macrosomia than obese women. Obesity and Diabetes in pregnancy have independent and additive effects on obstetric complications, and both require proper management. Management of gestational Diabetes mellitus and Maternal obesity is essential for Maternal and offspring's good health. Increasing physical activity, preventing gestational weight gain, and having some qualitative nutritional habits may be beneficial during both the pregnancy and offspring's future life.
Kelle H. Moley - One of the best experts on this subject based on the ideXlab platform.
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Maternal Diabetes and oocyte quality
Mitochondrion, 2010Co-Authors: Qiang Wang, Kelle H. MoleyAbstract:Maternal Diabetes has been demonstrated to adversely affect preimplantation embryo development and pregnancy outcomes. Emerging evidence has implicated that these effects are associated with compromised oocyte competence. Several developmental defects during oocyte maturation in diabetic mice have been reported over past decades. Most recently, we further identified the structural, spatial and metabolic dysfunction of mitochondria in oocytes from diabetic mice, suggesting the impaired oocyte quality. These defects in the oocyte may be Maternally transmitted to the embryo and then manifested later as developmental abnormalities in preimplantation embryo, congenital malformations, and even metabolic disease in the offspring. In this paper, we briefly review the effects of Maternal Diabetes on oocyte quality, with a particular emphasis on the mitochondrial dysfunction. The possible connection between dysfunctional oocyte mitochondria and reproductive failure of diabetic females, and the mechanism(s) by which Maternal Diabetes exerts its effects on the oocyte are also discussed.
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Maternal Diabetes causes mitochondrial dysfunction and meiotic defects in murine oocytes
Molecular Endocrinology, 2009Co-Authors: Qiang Wang, Ann M Ratchford, Erica L Schoeller, Antonina Frolova, Tim Schedl, Kelle H. MoleyAbstract:The adverse effects of Maternal Diabetes on embryo development and pregnancy outcomes have recently been shown to occur as early as the one-cell zygote stage. The hypothesis of this study was that Maternally inherited mitochondria in oocytes from diabetic mice are abnormal and thus responsible in part for this latency of developmental compromise. In ovulated oocytes from diabetic mice, transmission electron microscopy revealed an alteration in mitochondrial ultrastructure, and the quantitative analysis of mitochondrial DNA copy number demonstrated an increase. The levels of ATP and tricarboxylic acid cycle metabolites in diabetic oocytes were markedly reduced compared with controls, suggesting a mitochondrial metabolic dysfunction. Abnormal distribution of mitochondria within maturing oocytes also was seen in diabetic mice. Furthermore, oocytes from diabetic mice displayed a higher frequency of spindle defects and chromosome misalignment in meiosis, resulting in increased aneuploidy rates in ovulated oocytes. Collectively, our results suggest that Maternal Diabetes results in oocyte defects that are transmitted to the fetus by two routes: first, meiotic spindle and chromatin defects result in nondisjunction leading to embryonic aneuploidy; second, structural and functional abnormalities of oocyte mitochondria, through Maternal transmission, provide the embryo with a dysfunctional complement of mitochondria that may be propagated during embryogenesis.
Isabelle Chenier - One of the best experts on this subject based on the ideXlab platform.
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post weaning high fat diet accelerates kidney injury but not hypertension programmed by Maternal Diabetes
Pediatric Research, 2016Co-Authors: Yessoufou Aliou, Isabelle Chenier, Julie R. Ingelfinger, Xin-ping Zhao, Min-chun Liao, Shiao-ying Chang, Shao-ling ZhangAbstract:Post-weaning high-fat diet accelerates kidney injury, but not hypertension programmed by Maternal Diabetes
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Maternal Diabetes modulates kidney formation in murine progeny: the role of hedgehog interacting protein (HHIP).
Diabetologia, 2014Co-Authors: Xin-ping Zhao, Isabelle Chenier, Julie R. Ingelfinger, Min-chun Liao, Shiao-ying Chang, Shaaban Abdo, Yessoufou Aliou, Shao-ling ZhangAbstract:Aims/hypothesis We hypothesised that Maternal Diabetes impairs kidney formation in offspring via augmented expression of hedgehog interacting protein (HHIP). Our gene-array results were performed in neonatal kidneys from our murine model of Maternal Diabetes and indicated that Hhip expression was significantly modulated by Maternal Diabetes.
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Maternal Diabetes programs hypertension and kidney injury in offspring.
Pediatric Nephrology, 2010Co-Authors: Yun Wen Chen, Stella Tran, Isabelle Chenier, Shiao-ying Chang, Michael Scotcher, Shao-ling ZhangAbstract:We investigated whether Maternal Diabetes programs the offspring to develop hypertension and kidney injury in adulthood and examined potential underlying mechanisms. In a murine model we studied the offspring of three groups of dams (non-diabetic, diabetic, and diabetic treated with insulin). Mean systolic blood pressure in the offspring was monitored from 8 to 20 weeks. Body and kidney weights in the offspring of diabetic mothers were significantly lower than in offspring of non-diabetic mothers. Offspring of diabetic mothers developed hypertension, microalbuminuria, and glucose intolerance. Increased accumulation of extracellular matrix proteins in the glomeruli and marked upregulation of angiotensinogen, angiotensin II type 1 receptor, angiotensin-converting enzyme, transforming growth factor beta-1 (TGF-β1), and plasminogen activator inhibitor-1 (PAI-1) gene expression were evident in the renal cortex of hypertensive offspring of diabetic mothers. By contrast, angiotensin-converting enzyme-2 (ACE2) gene expression was lower in the hypertensive offspring of diabetic mothers than in that of non-diabetic mothers. These changes were prevented in the offspring of insulin-treated diabetic mothers. These data indicate that Maternal Diabetes induces perinatal programming of hypertension, renal injury, and glucose intolerance in the offspring and suggest a central role for the activation of the intrarenal renin–angiotensin system and TGF-β1 gene expression in this process.
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Maternal Diabetes Modulates Renal Morphogenesis in Offspring
Journal of The American Society of Nephrology, 2008Co-Authors: Stella Tran, Yun Wen Chen, Isabelle Chenier, John S.d. Chan, Susan E. Quaggin, Marie-josée Hébert, Julie R. Ingelfinger, Shao-ling ZhangAbstract:Maternal Diabetes leads to an adverse in utero environment, but whether Maternal Diabetes impairs nephrogenesis is unknown. Diabetes was induced with streptozotocin in pregnant Hoxb7–green fluorescence protein mice at embryonic day 13, and the offspring were examined at several time points after birth. Compared with offspring of nondiabetic controls, offspring of diabetic mice had lower body weight, body size, kidney weight, and nephron number. The observed renal dysmorphogenesis may be the result of increased apoptosis, because immunohistochemical analysis revealed significantly more apoptotic podocytes as well as increased active caspase-3 immunostaining in the renal tubules compared with control mice. Regarding potential mediators of these differences, offspring of diabetic mice had increased expression of intrarenal angiotensinogen and renin mRNA, upregulation of NF-κB isoforms p50 and p65, and activation of the NF-κB pathway. In conclusion, Maternal Diabetes impairs nephrogenesis, possibly via enhanced intrarenal activation of the renin-angiotensin system and NF-κB signaling.