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Modeling intrauterine growth retardation in rodents: Impact on pancreas development and glucose homeostasis

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Published in Molecular and cellular endocrinology. 2009, vol. 304, no. 1-2, p. 78-83
Abstract Fetal adverse environment, such as insufficient maternal nutrition, placental insufficiency and stress, alters organ development and leads to poor fetal growth, also called intrauterine growth retardation (IUGR). IUGR is associated with an increased risk of perinatal mortality and morbidity as well as late-onset metabolic diseases, such as obesity, diabetes and hypertension in adulthood. In the rodent model, IUGR can be induced by fetal caloric restriction, fetal protein restriction, by exposure to high levels of glucocorticoids or by restricted placental blood supply. Such experimental IUGR models show a decreased beta cell mass and lower pancreatic insulin content. Recent research has provided an insight into the mechanisms responsible for the loss of beta cells. Here we review models that give further details about the molecular determinants of fetal and postnatal pancreatic islet development that are required to understand the consequences of fetal insults.
Keywords AnimalsAnimals, NewbornBlood Glucose/metabolismCaloric RestrictionDisease Models, AnimalFemaleFetal Growth Retardation/blood/physiopathologyGlucocorticoids/pharmacologyHomeostasisHumansInsulin/metabolismPancreas/drug effects/embryology/growth & development/metabolismPregnancy
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PMID: 19433251
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Article (Author postprint) (482 Kb) - document accessible for UNIGE members only Limited access to UNIGE
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Research group Diabète et métabolisme (178)
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SCHWITZGEBEL LUSCHER, Valérie, SOMM, Emmanuel, KLEE, Philippe. Modeling intrauterine growth retardation in rodents: Impact on pancreas development and glucose homeostasis. In: Molecular and cellular endocrinology, 2009, vol. 304, n° 1-2, p. 78-83. https://archive-ouverte.unige.ch/unige:3837

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Deposited on : 2009-10-20

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