Diet-Induced Maternal Obesity Alters Insulin Signalling in Male Mice Offspring Rechallenged with a High-Fat Diet in Adulthood

Modern lifestyle has resulted in an increase in the prevalence of obesity and its comorbidities in pregnant women and the young population. It has been well established that the consumption of a high-fat diet (HFD) has many direct effects on glucose metabolism. However, it is important to assess whe...

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Published inPloS one Vol. 11; no. 8; p. e0160184
Main Authors Fante, Thaís de, Simino, Laís Angélica, Reginato, Andressa, Payolla, Tanyara Baliani, Vitoréli, Débora Cristina Gustavo, Souza, Monique de, Torsoni, Márcio Alberto, Milanski, Marciane, Torsoni, Adriana Souza
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 01.08.2016
Public Library of Science (PLoS)
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Abstract Modern lifestyle has resulted in an increase in the prevalence of obesity and its comorbidities in pregnant women and the young population. It has been well established that the consumption of a high-fat diet (HFD) has many direct effects on glucose metabolism. However, it is important to assess whether maternal consumption of a HFD during critical periods of development can lead to metabolic changes in the offspring metabolism. This study evaluated the potential effects of metabolic programming on the impairment of insulin signalling in recently weaned offspring from obese dams. Additionally, we investigated if early exposure to an obesogenic environment could exacerbate the impairment of glucose metabolism in adult life in response to a HFD. Swiss female mice were fed with Standard Chow (SC) or a HFD during gestation and lactation and tissues from male offspring were analysed at d28 and d82. Offspring from obese dams had greater weight gain and higher adiposity and food intake than offspring from control dams. Furthermore, they showed impairment in insulin signalling in central and peripheral tissues, which was associated with the activation of inflammatory pathways. Adipose tissue was ultimately the most affected in adult offspring after HFD rechallenge; this may have contributed to the metabolic deregulation observed. Overall, our results suggest that diet-induced maternal obesity leads to increased susceptibility to obesity and impairment of insulin signalling in offspring in early and late life that cannot be reversed by SC consumption, but can be aggravated by HFD re-exposure.
AbstractList Modern lifestyle has resulted in an increase in the prevalence of obesity and its comorbidities in pregnant women and the young population. It has been well established that the consumption of a high-fat diet (HFD) has many direct effects on glucose metabolism. However, it is important to assess whether maternal consumption of a HFD during critical periods of development can lead to metabolic changes in the offspring metabolism. This study evaluated the potential effects of metabolic programming on the impairment of insulin signalling in recently weaned offspring from obese dams. Additionally, we investigated if early exposure to an obesogenic environment could exacerbate the impairment of glucose metabolism in adult life in response to a HFD. Swiss female mice were fed with Standard Chow (SC) or a HFD during gestation and lactation and tissues from male offspring were analysed at d28 and d82. Offspring from obese dams had greater weight gain and higher adiposity and food intake than offspring from control dams. Furthermore, they showed impairment in insulin signalling in central and peripheral tissues, which was associated with the activation of inflammatory pathways. Adipose tissue was ultimately the most affected in adult offspring after HFD rechallenge; this may have contributed to the metabolic deregulation observed. Overall, our results suggest that diet-induced maternal obesity leads to increased susceptibility to obesity and impairment of insulin signalling in offspring in early and late life that cannot be reversed by SC consumption, but can be aggravated by HFD re-exposure.
Audience Academic
Author Vitoréli, Débora Cristina Gustavo
Torsoni, Márcio Alberto
Reginato, Andressa
Souza, Monique de
Torsoni, Adriana Souza
Payolla, Tanyara Baliani
Fante, Thaís de
Simino, Laís Angélica
Milanski, Marciane
AuthorAffiliation Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas–UNICAMP, Limeira, São Paulo, Brazil
Universidade do Estado do Rio de Janeiro, BRAZIL
AuthorAffiliation_xml – name: Universidade do Estado do Rio de Janeiro, BRAZIL
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  surname: Simino
  fullname: Simino, Laís Angélica
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  surname: Payolla
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  givenname: Marciane
  surname: Milanski
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  givenname: Adriana Souza
  surname: Torsoni
  fullname: Torsoni, Adriana Souza
  organization: Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas-UNICAMP, Limeira, São Paulo, Brazil
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2016 Fante et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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– notice: 2016 Fante et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Conceptualization: TF AST. Formal analysis: TF AST. Funding acquisition: TF AST. Investigation: TF LAS AR TBP DCGV MS. Methodology: TF LAS AR TBP AST. Project administration: AST. Resources: TF AST. Supervision: AST MM MAT. Validation: TF LAS AR TBP DCGV MS AST. Visualization: TF AST MM MAT. Writing - original draft: TF AST MAT. Writing - review & editing: TF AST MM MAT.
Competing Interests: The authors have declared that no competing interests exist.
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SSID ssj0053866
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Snippet Modern lifestyle has resulted in an increase in the prevalence of obesity and its comorbidities in pregnant women and the young population. It has been well...
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doaj
pubmedcentral
proquest
gale
crossref
pubmed
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
StartPage e0160184
SubjectTerms Adipose tissue
Adiposity
Adults
Analysis
Animal tissues
Animals
Biology and Life Sciences
Blood Glucose - analysis
Body Weight
Body weight gain
Consumption
Cytokines
Dams
Deregulation
Diet
Diet, High-Fat
Endoplasmic reticulum
Exposure
Fatty acids
Female
Food intake
Gene expression
Gestation
Glucose
Glucose metabolism
Glucose Tolerance Test
Glycogen - metabolism
Health aspects
High fat diet
Homeostasis
Hypothalamus - metabolism
Impairment
Inflammation
Insulin
Insulin - blood
Insulin - metabolism
Insulin resistance
Kinases
Laboratory animals
Lactation
Leptin - blood
Lipids
Liver
Liver - metabolism
Male
Medicine and Health Sciences
Metabolic disorders
Metabolic syndrome
Metabolism
Mice
Muscle, Skeletal - metabolism
Nervous system
Neural networks
Obesity
Obesity - etiology
Obesity - metabolism
Offspring
Phosphatase
Pregnancy
Pregnant women
Prenatal Exposure Delayed Effects
Proteins
Risk factors
Rodents
Signal Transduction
Signaling
Weaning
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Title Diet-Induced Maternal Obesity Alters Insulin Signalling in Male Mice Offspring Rechallenged with a High-Fat Diet in Adulthood
URI https://www.ncbi.nlm.nih.gov/pubmed/27479001
https://www.proquest.com/docview/1808041792
https://search.proquest.com/docview/1808601722
https://search.proquest.com/docview/1811891196
https://pubmed.ncbi.nlm.nih.gov/PMC4968809
https://doaj.org/article/4cd8baec72c94f0e93b48251037eec1a
http://dx.doi.org/10.1371/journal.pone.0160184
Volume 11
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