Literature DB >> 27037899

Maternal glucose intolerance reduces offspring nephron endowment and increases glomerular volume in adult offspring.

Stacey Hokke1, Nicole Arias1, James A Armitage1,2, Victor G Puelles1, Karen Fong1, Stefania Geraci3, Norbert Gretz3, John F Bertram1, Luise A Cullen-McEwen4.   

Abstract

BACKGROUND: Animal studies report a nephron deficit in offspring exposed to maternal diabetes, yet are limited to models of severe hyperglycaemia which do not reflect the typical clinical condition and which are associated with foetal growth restriction that may confound nephron endowment. We aimed to assess renal morphology and function in offspring of leptin receptor deficient mice (Leprdb /+) and hypothesized that exposure to impaired maternal glucose tolerance (IGT) would be detrimental to the developing kidney.
METHODS: Nephron endowment was assessed in offspring of C57BKS/J Leprdb /+ and +/+ mice at embryonic day (E)18 and postnatal day (PN)21 using design-based stereology. Transcutaneous measurement of renal function and total glomerular volume were assessed in 6-month-old offspring. Only +/+ offspring of Leprdb /+ dams were analysed.
RESULTS: Compared with +/+ dams, Leprdb /+ dams had a 20% and 35% decrease in glucose tolerance prior to pregnancy and at E17.5 respectively. Offspring of IGT Leprdb /+ dams had approximately 15% fewer nephrons at E18.5 and PN21 than offspring of +/+ dams. There was no difference in offspring bodyweight. Despite normal renal function, total glomerular volume was 13% greater in 6-month-old offspring of IGT Leprdb /+ dams than in +/+ offspring.
CONCLUSIONS: IGT throughout gestation resulted in a nephron deficit that was established early in renal development. Maternal IGT was associated with glomerular hypertrophy in adult offspring, likely a compensatory response to maintain normal renal function. Given the increasing prevalence of IGT, monitoring glucose from early in gestation may be important to prevent altered kidney morphology.
Copyright © 2016 John Wiley & Sons, Ltd. Copyright © 2016 John Wiley & Sons, Ltd.

Entities:  

Keywords:  developmental programming; impaired glucose tolerance; kidney development; maternal diabetes; nephron number; renal function

Mesh:

Substances:

Year:  2016        PMID: 27037899     DOI: 10.1002/dmrr.2805

Source DB:  PubMed          Journal:  Diabetes Metab Res Rev        ISSN: 1520-7552            Impact factor:   4.876


  7 in total

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Authors:  Débora M Cerqueira; Shelby L Hemker; Andrew J Bodnar; Daniella M Ortiz; Favour O Oladipupo; Elina Mukherjee; Zhenwei Gong; Corynn Appolonia; Radhika Muzumdar; Sunder Sims-Lucas; Jacqueline Ho
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3.  The Impact of Kidney Development on the Life Course: A Consensus Document for Action.

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5.  Prematurity disrupts glomeruli development, whereas prematurity and hyperglycemia lead to altered nephron maturation and increased oxidative stress in newborn baboons.

Authors:  Danielle A Callaway; Lisa L McGill-Vargas; Amy Quinn; Jasmine L Jordan; Lauryn A Winter; Diana Anzueto; Edward J Dick; Cynthia L Blanco
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6.  Normal foetal kidney volume in offspring of women treated for gestational diabetes.

Authors:  Stacey Hokke; Natasha de Zoysa; Bethany L Carr; Veronica Abruzzo; Peter R Coombs; Carolyn A Allan; Christine East; Julie R Ingelfinger; Victor G Puelles; Mary J Black; Danica Ryan; James A Armitage; Euan M Wallace; John F Bertram; Luise A Cullen-McEwen
Journal:  Endocrinol Diabetes Metab       Date:  2019-08-30

7.  Dysglycemia in Pregnancy and Maternal/Fetal Outcomes.

Authors:  Corinne M Silva; Matthew E Arnegard; Christine Maric-Bilkan
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  7 in total

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