Research Topics
| Rebecca A SimmonsSummaryAffiliation: University of Pennsylvania Country: USA Publications
Research Grants
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Detail Information
Publications
Developmental origins of adult metabolic disease: concepts and controversiesRebecca Simmons
Department of Pediatrics Children s Hospital Philadelphia and University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
Trends Endocrinol Metab 16:390-4. 2005..Emerging data indicates that epigenetic regulation of gene expression might also play a crucial role in the pathogenesis of type 2 diabetes in individuals who are growth retarded at birth...- Role of metabolic programming in the pathogenesis of beta-cell failure in postnatal lifeRebecca A Simmons
Department of Pediatrics, Children s Hospital Philadelphia and University of Pennsylvania School of Medicine, BRB II III, Rm 1308, 421 Curie Blvd, Philadelphia, PA 19104, USA
Rev Endocr Metab Disord 8:95-104. 2007..Future research will be directed at elucidating the mechanisms underlying epigenetic modifications in offspring... 
Development of type 2 diabetes following intrauterine growth retardation in rats is associated with progressive epigenetic silencing of Pdx1Jun H Park
Department of Pediatrics, Children s Hospital of Philadelphia, Department of Medicine, and Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
J Clin Invest 118:2316-24. 2008..These results provide insight into the development of type 2 diabetes following IUGR and we believe they are the first to describe the ontogeny of chromatin remodeling in vivo from the fetus to the onset of disease in adulthood...- Developmental origins of diabetes: The role of oxidative stressRebecca A Simmons
Department of Pediatrics, Children s Hospital Philadelphia and University of Pennsylvania, Philadelphia, Philadelphia, PA 19104, USA
Best Pract Res Clin Endocrinol Metab 26:701-8. 2012..Emerging data suggests that oxidative stress and mitochondrial dysfunction may also play a critical role in the pathogenesis of type 2 diabetes in individuals who were growth retarded at birth... 
Epigenetics and maternal nutrition: nature v. nurtureRebecca Simmons
Department of Pediatrics, Children s Hospital Philadelphia and University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Proc Nutr Soc 70:73-81. 2011..The contributions of histone acetylation, histone methylation and DNA methylation to the process of adipogenesis in vivo remain to be evaluated...- Developmental origins of adult diseaseRebecca A Simmons
Department of Pediatrics, Children s Hospital, Philadelphia, PA, USA
Pediatr Clin North Am 56:449-66, Table of Contents. 2009..Future research will be directed at elucidating the mechanisms underlying epigenetic modifications in offspring... - Perinatal programming of obesityRebecca Simmons
Department of Pediatrics, Children s Hospital Philadelphia and University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
Semin Perinatol 32:371-4. 2008..Thus, both excess and reduced nutrient availability during fetal development can lead to the later development of obesity. This review summarizes both human and animal studies relating fetal exposures to later obesity... - Developmental origins of diabetes: the role of epigenetic mechanismsRebecca A Simmons
Department of Pediatrics, Children s Hospital Philadelphia and University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
Curr Opin Endocrinol Diabetes Obes 14:13-6. 2007..The purpose of this article is to review basic epigenetic mechanisms and familiarize the reader with the latest research linking epigenetics, fetal programming, and the development of type 2 diabetes... - Developmental origins of beta-cell failure in type 2 diabetes: the role of epigenetic mechanismsRebecca A Simmons
Department of Pediatrics Children s Hospital Philadelphia, University of Pennsylvania, PA 19104, USA
Pediatr Res 61:64R-67R. 2007..It is postulated that these epigenetic changes result in the observed increase in gene expression of GR and PPARgamma. Future research will be directed at elucidating the mechanisms underlying epigenetic modifications in offspring... - Developmental origins of diabetes: the role of oxidative stressRebecca A Simmons
Department of Pediatrics, Children s Hospital Philadelphia and University of Pennsylvania, Philadelphia, PA 19104, USA
Free Radic Biol Med 40:917-22. 2006..Emerging data suggest that oxidative stress and mitochondrial dysfunction may also play critical roles in the pathogenesis of type 2 diabetes in individuals who were growth retarded at birth... - Developmental origins of adult metabolic diseaseRebecca Simmons
Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA, USA
Endocrinol Metab Clin North Am 35:193-204, viii. 2006 - Perinatal programming of obesityRebecca Simmons
Department of Pediatrics Children's Hospital Philadelphia and University of Pennsylvania School of Medicine, BRB II/III, Rm 1308, 421 Curie Blvd, Pennsylvania, Philadelphia, PA 19104, USA
Exp Gerontol 40:863-6. 2005 - Intrauterine growth retardation leads to the development of type 2 diabetes in the ratR A Simmons
Division of Neonatology, Department of Pediatrics, University of Pennsylvania and Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA
Diabetes 50:2279-86. 2001..05). The data presented here support the hypothesis that an abnormal intrauterine milieu can induce permanent changes in glucose homeostasis after birth and lead to type 2 diabetes in adulthood... - Progressive accumulation of mitochondrial DNA mutations and decline in mitochondrial function lead to beta-cell failureRebecca A Simmons
Department of Pediatrics Children s Hospital Philadelphia and University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
J Biol Chem 280:28785-91. 2005..A self-reinforcing cycle of progressive deterioration in mitochondrial function leads to a corresponding decline in beta-cell function. Finally, a threshold in mitochondrial dysfunction and ROS production is reached, and diabetes ensues... - Neonatal exendin-4 treatment reduces oxidative stress and prevents hepatic insulin resistance in intrauterine growth-retarded ratsElisabeth L Raab
Department of Pediatrics, Children s Hospital Los Angeles, Los Angeles, California, USA
Am J Physiol Regul Integr Comp Physiol 297:R1785-94. 2009..These results indicate that exposure to exendin-4 in the newborn period reverses the adverse consequences of fetal programming and prevents the development of hepatic insulin resistance... - Epigenetic mechanisms in the development of type 2 diabetesSara E Pinney
Department of Pediatrics, The Children s Hospital Philadelphia, Philadelphia, PA 19104, USA
Trends Endocrinol Metab 21:223-9. 2010.... - Exendin-4 normalizes islet vascularity in intrauterine growth restricted rats: potential role of VEGFJ Nina Ham
Department of Medicine and The Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA
Pediatr Res 66:42-6. 2009.... - Impaired oxidative phosphorylation in hepatic mitochondria in growth-retarded ratsIyalla E Peterside
Department of Pediatrics, Children's Hospital and University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
Am J Physiol Endocrinol Metab 285:E1258-66. 2003.... - Neonatal exendin-4 prevents the development of diabetes in the intrauterine growth retarded ratDoris A Stoffers
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Clinical Research Building 611B, University of Pennsylvania School of Medicine, 415 Curie Boulevard, Philadelphia, PA 19104, USA
Diabetes 52:734-40. 2003..These results indicate that exposure to Ex-4 in the newborn period reverses the adverse consequences of fetal programming and prevents the development of diabetes in adulthood... - Gestational diabetes leads to the development of diabetes in adulthood in the ratJudd Boloker
Division of Neonatology, Department of Pediatrics, University of Pennsylvania and Children's Hospital of Philadelphia, Philadelphia, Pennsylvani, USA
Diabetes 51:1499-506. 2002..These data demonstrate that the altered metabolic milieu of the diabetic pregnancy causes permanent defects in glucose homeostasis in the offspring that lead to the development of diabetes later in life... - Neonatal exendin-4 leads to protection from reperfusion injury and reduced rates of oxidative phosphorylation in the adult rat heartSuzanne B Brown
Hospital of the University of Pennsylvania, Philadelphia, PA, USA
Cardiovasc Drugs Ther 24:197-205. 2010..We sought to evaluate whether neonatal Ex-4 can exert the same effect in the normal rat heart, as well as whether Ex-4 could affect susceptibility to cardiac reperfusion injury... - Impaired oxidative phosphorylation in skeletal muscle of intrauterine growth-retarded ratsMary A Selak
Department of Pediatrics, Children's Hospital of Philadelphia and University of Pennsylvania, 19104, USA
Am J Physiol Endocrinol Metab 285:E130-7. 2003..Impaired ATP synthesis in muscle compromises energy-dependent GLUT4 recruitment to the cell surface, glucose transport, and glycogen synthesis, which contribute to insulin resistance and hyperglycemia of type 2 diabetes... - Oxidative stress disrupts oligodendrocyte maturationHeather Morein French
Department of Pediatrics, Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA
J Neurosci Res 87:3076-87. 2009..Both of these mechanisms result in the arrest of oligodendrocyte differentiation without an increase in cell death... - Metabolic programming, epigenetics, and gestational diabetes mellitusSara E Pinney
Division of Endocrinology and Diabetes, Department of Pediatrics, The Children s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA
Curr Diab Rep 12:67-74. 2012.... - Maternal antioxidant supplementation prevents adiposity in the offspring of Western diet-fed ratsSarbattama Sen
Department of Pediatrics, The Children s Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
Diabetes 59:3058-65. 2010.... - Delayed myelination in an intrauterine growth retardation model is mediated by oxidative stress upregulating bone morphogenetic protein 4Mary V Reid
Department of Neurology, Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA
J Neuropathol Exp Neurol 71:640-53. 2012..Together, these findings suggest that IUGR results in delayed myelination through the generation of oxidative stress that leads to BMP4 upregulation... - Mice deficient for testis-brain RNA-binding protein exhibit a coordinate loss of TRAX, reduced fertility, altered gene expression in the brain, and behavioral changesVargheese Chennathukuzhi
Center for Research on Reproduction and Women s Health, School of Medicine, Department of Biology, University of Pennsylvania, 1310 Biomedical Research Building II III, 421 Curie Boulevard, Philadelphia, PA 19104 6142, USA
Mol Cell Biol 23:6419-34. 2003..Behavioral abnormalities were also seen. Compared to littermates, the TB-RBP-null mice appeared docile and exhibited reduced Rota-Rod performance... - Clinical features and insulin regulation in infants with a syndrome of prolonged neonatal hyperinsulinismFrancis M Hoe
Divisions of Endocrinology and Neonatology, Department of Pediatrics, Children's Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Philadelphia, PA 19104, USA
J Pediatr 148:207-12. 2006..AIR tests suggest that both the K(ATP) channel and GDH have normal function... - Placental expression of insulin-like growth factor receptor-1 and insulin receptor in the growth-restricted fetal ratGregory J Reid
Department of Obstetrics and Gynecology, Northwestern University Medical School, Children s Memorial Hospital, Chicago, Illinois, USA
J Soc Gynecol Investig 9:210-4. 2002..The regulation of fetal growth by IGFs and insulin might reflect their actions on the placenta. This study compared the placental expression of IGF-R1 and INS-R in growth-restricted and normal pregnancies...
Research Grants
- MECHANISMS BY WHICH IUGR LEADS TO DIABETESRebecca Simmons; Fiscal Year: 2007....
- Mechanisms by which GDM Leads to Diabetes in OffspringRebecca Simmons; Fiscal Year: 2005..non-F2 animals. ..
- MECHANISMS BY WHICH IUGR LEADS TO DIABETESRebecca Simmons; Fiscal Year: 2003..insufficiency to the beta-cell phenotype observed in type II diabetes, the investigators will induce beta-cell failure in vitro by transferring damaged mitochondria from IUGR animals into beta-cells from unaffected, non-IUGR animals ..
- Mechanisms by which Obesity in Pregnancy Leads to Obesity in OffspringRebecca A Simmons; Fiscal Year: 2010..Since the incidence of obesity is rapidly increasing in the United States, these studies will have great impact on health. ..