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Maternal resistance to diet-induced obesity partially protects newborn and post-weaning male mice offspring from metabolic disturbances

Published online by Cambridge University Press:  07 October 2020

Laís Angélica de Paula Simino Open the ORCID record for Laís Angélica de Paula Simino [Opens in a new window] ,
Carolina Panzarin Open the ORCID record for Carolina Panzarin [Opens in a new window] ,
Marcio Alberto Torsoni Open the ORCID record for Marcio Alberto Torsoni [Opens in a new window] ,
Letícia Martins Ignácio-Souza Open the ORCID record for Letícia Martins Ignácio-Souza [Opens in a new window] ,
Marciane Milanski Open the ORCID record for Marciane Milanski [Opens in a new window]  and
Adriana Souza Torsoni Open the ORCID record for Adriana Souza Torsoni [Opens in a new window]
Laís Angélica de Paula Simino
Affiliation:
Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas – UNICAMP, Limeira, São Paulo, Brazil
Carolina Panzarin
Affiliation:
Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas – UNICAMP, Limeira, São Paulo, Brazil
Marcio Alberto Torsoni
Affiliation:
Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas – UNICAMP, Limeira, São Paulo, Brazil
Letícia Martins Ignácio-Souza
Affiliation:
Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas – UNICAMP, Limeira, São Paulo, Brazil
Marciane Milanski
Affiliation:
Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas – UNICAMP, Limeira, São Paulo, Brazil
Adriana Souza Torsoni*
Affiliation:
Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas – UNICAMP, Limeira, São Paulo, Brazil
*
Address for correspondence: Adriana Souza Torsoni, Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas – UNICAMP, Limeira, São Paulo, Brazil. Email: [email protected]
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Abstract

The rising rate of childhood overweight follows the increase in maternal obesity, since perinatal events impact offspring in a diversity of metabolic disorders. Despite many studies that have linked dietary consumption, overnutrition, or maternal obesity as the mediators of fetal metabolic programming, there are gaps regarding the knowledge about the contribution of different maternal phenotypes to the development of metabolic disturbances in offspring. This study aimed to investigate whether maternal high-fat diet (HFD) consumption without the development of the obese phenotype would protect offspring from metabolic disturbances. Female mice were fed standard chow diet or a HFD for 4 weeks before mating. HFD females were classified into obesity-resistant (OR) or obesity-prone (OP), according to weight gain. OP females presented with higher adiposity, fasting serum glucose and insulin, cholesterol and non-esterified fatty acid (NEFA). Newborn offspring from OP dams showed higher serum glucose and insulin and alteration in hepatic gene expression that may have contributed to the rise in hepatic fat content and decline of glycogen levels in the liver. Despite offspring from OR and OP females having showed similar growth after the day of delivery, offspring from OP females had higher caloric intake, fasting glucose, serum triglycerides and altered hepatic gene expression, as well as glucose and pyruvate intolerance and lower insulin sensitivity at d28 compared with offspring from OR females. Maternal pre-pregnancy serum glucose, insulin, and NEFA positively correlated with serum glucose and fat liver content and negatively correlated with hepatic glycogen in offspring. In conclusion, our results show that maternal resistance to diet-induced obesity partially protects offspring from early metabolic disturbances.

Keywords

Maternal programminghigh-fat dietobesity-resistantobesity-prone
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 12 , Issue 4 , August 2021 , pp. 660 - 670
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Copyright
© The Author(s), 2020. Published by Cambridge University Press in association with International Society for Developmental Origins of Health and Disease

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