Gestational oxidative stress protects against adult obesity and insulin resistance
Pregnancy complications such as preeclampsia cause increased fetal oxidative stress and fetal growth restriction, and associate with a higher incidence of adult metabolic syndrome. However, the pathophysiological contribution of oxidative stress per se is experimentally difficult to discern and has...
Main Authors: | , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Elsevier
2020-01-01
|
Series: | Redox Biology |
Online Access: | http://www.sciencedirect.com/science/article/pii/S2213231719305087 |
id |
doaj-65cde675473e4dd789ae3c14a75611a1 |
---|---|
record_format |
Article |
spelling |
doaj-65cde675473e4dd789ae3c14a75611a12020-11-25T01:35:51ZengElsevierRedox Biology2213-23172020-01-0128Gestational oxidative stress protects against adult obesity and insulin resistanceLidiya G. Dimova0Simone Battista1Torsten Plösch2Rosalie A. Kampen3Fan Liu4Rikst Nynke Verkaik-Schakel5Domenico Pratico6Henkjan J. Verkade7Uwe J.F. Tietge8Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, the NetherlandsDepartment of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, the NetherlandsDepartment of Obstetrics and Gynecology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, the NetherlandsDepartment of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, the NetherlandsDepartment of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, the Netherlands; Division of Clinical Chemistry, Department of Laboratory Medicine, Karolinska Institutet, Alfred Nobels Alle 8, Stockholm, SwedenDepartment of Obstetrics and Gynecology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, the NetherlandsAlzheimer's Center at Temple, Lewis Katz School of Medicine, Temple University, 3500 N Broad St, Philadelphia, PA, USADepartment of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, the NetherlandsDepartment of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, the Netherlands; Division of Clinical Chemistry, Department of Laboratory Medicine, Karolinska Institutet, Alfred Nobels Alle 8, Stockholm, Sweden; Clinical Chemistry, Karolinska University Laboratory, Karolinska University Hospital, Stockholm, Sweden; Corresponding author. Division of Clinical Chemistry, Department of Laboratory Medicine (LABMED), H5, Alfred Nobels Alle 8, Karolinska Institutet, S‐141 83, Stockholm, Sweden.Pregnancy complications such as preeclampsia cause increased fetal oxidative stress and fetal growth restriction, and associate with a higher incidence of adult metabolic syndrome. However, the pathophysiological contribution of oxidative stress per se is experimentally difficult to discern and has not been investigated. This study determined, if increased intrauterine oxidative stress (IUOx) affects adiposity, glucose and cholesterol metabolism in adult Ldlr−/−xSod2+/+ offspring from crossing male Ldlr−/−xSod2+/+ mice with Ldlr−/−xSod2 +/- dams (IUOx) or Ldlr−/−xSod2 +/- males with Ldlr−/−xSod2+/+ dams (control). At 12 weeks of age mice received Western diet for an additional 12 weeks. Adult male IUOx offspring displayed lower body weight and reduced adiposity associated with improved glucose tolerance compared to controls. Reduced weight gain in IUOx was conceivably due to increased energy dissipation in white adipose tissue conveyed by higher expression of Ucp1 and an accompanying decrease in DNA methylation in the Ucp1 enhancer region. Female offspring did not show comparable phenotypes. These results demonstrate that fetal oxidative stress protects against the obesogenic effects of Western diet in adulthood by programming energy dissipation in white adipose tissue at the level of Ucp1. Keywords: Fetal oxidative stress, Mitohormesis, Metabolic programming, Adiposity, Epigenetics, Methylationhttp://www.sciencedirect.com/science/article/pii/S2213231719305087 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Lidiya G. Dimova Simone Battista Torsten Plösch Rosalie A. Kampen Fan Liu Rikst Nynke Verkaik-Schakel Domenico Pratico Henkjan J. Verkade Uwe J.F. Tietge |
spellingShingle |
Lidiya G. Dimova Simone Battista Torsten Plösch Rosalie A. Kampen Fan Liu Rikst Nynke Verkaik-Schakel Domenico Pratico Henkjan J. Verkade Uwe J.F. Tietge Gestational oxidative stress protects against adult obesity and insulin resistance Redox Biology |
author_facet |
Lidiya G. Dimova Simone Battista Torsten Plösch Rosalie A. Kampen Fan Liu Rikst Nynke Verkaik-Schakel Domenico Pratico Henkjan J. Verkade Uwe J.F. Tietge |
author_sort |
Lidiya G. Dimova |
title |
Gestational oxidative stress protects against adult obesity and insulin resistance |
title_short |
Gestational oxidative stress protects against adult obesity and insulin resistance |
title_full |
Gestational oxidative stress protects against adult obesity and insulin resistance |
title_fullStr |
Gestational oxidative stress protects against adult obesity and insulin resistance |
title_full_unstemmed |
Gestational oxidative stress protects against adult obesity and insulin resistance |
title_sort |
gestational oxidative stress protects against adult obesity and insulin resistance |
publisher |
Elsevier |
series |
Redox Biology |
issn |
2213-2317 |
publishDate |
2020-01-01 |
description |
Pregnancy complications such as preeclampsia cause increased fetal oxidative stress and fetal growth restriction, and associate with a higher incidence of adult metabolic syndrome. However, the pathophysiological contribution of oxidative stress per se is experimentally difficult to discern and has not been investigated. This study determined, if increased intrauterine oxidative stress (IUOx) affects adiposity, glucose and cholesterol metabolism in adult Ldlr−/−xSod2+/+ offspring from crossing male Ldlr−/−xSod2+/+ mice with Ldlr−/−xSod2 +/- dams (IUOx) or Ldlr−/−xSod2 +/- males with Ldlr−/−xSod2+/+ dams (control). At 12 weeks of age mice received Western diet for an additional 12 weeks. Adult male IUOx offspring displayed lower body weight and reduced adiposity associated with improved glucose tolerance compared to controls. Reduced weight gain in IUOx was conceivably due to increased energy dissipation in white adipose tissue conveyed by higher expression of Ucp1 and an accompanying decrease in DNA methylation in the Ucp1 enhancer region. Female offspring did not show comparable phenotypes. These results demonstrate that fetal oxidative stress protects against the obesogenic effects of Western diet in adulthood by programming energy dissipation in white adipose tissue at the level of Ucp1. Keywords: Fetal oxidative stress, Mitohormesis, Metabolic programming, Adiposity, Epigenetics, Methylation |
url |
http://www.sciencedirect.com/science/article/pii/S2213231719305087 |
work_keys_str_mv |
AT lidiyagdimova gestationaloxidativestressprotectsagainstadultobesityandinsulinresistance AT simonebattista gestationaloxidativestressprotectsagainstadultobesityandinsulinresistance AT torstenplosch gestationaloxidativestressprotectsagainstadultobesityandinsulinresistance AT rosalieakampen gestationaloxidativestressprotectsagainstadultobesityandinsulinresistance AT fanliu gestationaloxidativestressprotectsagainstadultobesityandinsulinresistance AT rikstnynkeverkaikschakel gestationaloxidativestressprotectsagainstadultobesityandinsulinresistance AT domenicopratico gestationaloxidativestressprotectsagainstadultobesityandinsulinresistance AT henkjanjverkade gestationaloxidativestressprotectsagainstadultobesityandinsulinresistance AT uwejftietge gestationaloxidativestressprotectsagainstadultobesityandinsulinresistance |
_version_ |
1725065813344387072 |