The maternal reduced uteroplacental perfusion model of preeclampsia induces sexually dimorphic metabolic responses in rat offspring

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Abstract

Background

Offspring born to preeclamptic mothers are prone to obesity, diabetes and hypertension in later life, but still, studies investigating the underlying mechanism are limited. Here, we aimed to investigate the impact of the reduced uteroplacental perfusion (RUPP) rat preeclampsia model on offspring metabolic outcomes.

Methods

Timed pregnant Wistar rats underwent RUPP or sham surgeries on day 14 of gestation. Glucometabolic parameters were evaluated on postnatal days (PND), 14 (childhood), and 60 (young adult). In addition, intraperitoneal glucose tolerance test (IPGTT), homeostatic model assessment of insulin resistance (HOMA-IR), immunohistochemical staining for insulin in pancreatic islets, arterial blood pressure and 24-h urine protein (24hUP) excretion were performed at PND60.

Results

Male, but not female, young adult rats (PND60) of RUPP dams exhibited an impaired IPGTT, decreased circulatory insulin and weakened pancreatic insulin immunoreactivity. Compared to the male offspring of the sham group, the body mass of male RUPP offspring significantly caught up after PND42, but it was not sex-specific. RUPP pups also exhibited upregulations in glucagon (only males) and ghrelin (both sexes with a more significant increase in males) during PND14–PND60. However, in sham offspring (both sexes), glucagon levels were downregulated and ghrelin levels unchanged during PND14–PND60. The blood pressure, HOMA-IR and 24hUP values did not alter in RUPP pups.

Conclusions

The overall results suggest that maternal RUPP has negative and sex-specific impacts on insulin, glucagon and ghrelin regulations in offspring and that, as young adults, male RUPP rats may be more prone to develop obesity and diabetes.

Highlights

Pancreatic insulin production was reduced in adult male offspring born to reduced uteroplacental perfusion (RUPP) rats.
Offspring born to RUPP dams exhibited sex-specific alterations in insulin, ghrelin and glucagon changes.

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Most cited references 52

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The hypertensive disorders of pregnancy: ISSHP classification, diagnosis & management recommendations for international practice

Fergus McCarthy, Mark Brown, Laura Magee … (2018)

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Influence of maternal obesity on the long-term health of offspring.

Keith M. Godfrey, Rebecca M Reynolds, Susan Prescott … (2017)

In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life. Observational studies provide evidence for effects of maternal obesity on her offspring's risks of obesity, coronary heart disease, stroke, type 2 diabetes, and asthma. Maternal obesity could also lead to poorer cognitive performance and increased risk of neurodevelopmental disorders, including cerebral palsy. Preliminary evidence suggests potential implications for immune and infectious-disease-related outcomes. Insights from experimental studies support causal effects of maternal obesity on offspring outcomes, which are mediated at least partly through changes in epigenetic processes, such as alterations in DNA methylation, and perhaps through alterations in the gut microbiome. Although the offspring of obese women who lose weight before pregnancy have a reduced risk of obesity, few controlled intervention studies have been done in which maternal obesity is reversed and the consequences for offspring have been examined. Because the long-term effects of maternal obesity could have profound public health implications, there is an urgent need for studies on causality, underlying mechanisms, and effective interventions to reverse the epidemic of obesity in women of childbearing age and to mitigate consequences for offspring.

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Is Open Access

Intrauterine programming of obesity and type 2 diabetes

Denise S Fernandez-Twinn, Line Hjort, Boris Novakovic … (2019)

The type 2 diabetes epidemic and one of its predisposing factors, obesity, are major influences on global health and economic burden. It is accepted that genetics and the current environment contribute to this epidemic; however, in the last two decades, both human and animal studies have consolidated considerable evidence supporting the ‘developmental programming’ of these conditions, specifically by the intrauterine environment. Here, we review the various in utero exposures that are linked to offspring obesity and diabetes in later life, including epidemiological insights gained from natural historical events, such as the Dutch Hunger Winter, the Chinese famine and the more recent Quebec Ice Storm. We also describe the effects of gestational exposure to endocrine disruptors, maternal infection and smoking to the fetus in relation to metabolic programming. Causal evidence from animal studies, motivated by human observations, is also discussed, as well as some of the proposed underlying molecular mechanisms for developmental programming of obesity and type 2 diabetes, including epigenetics (e.g. DNA methylation and histone modifications) and microRNA interactions. Finally, we examine the effects of non-pharmacological interventions, such as improving maternal dietary habits and/or increasing physical activity, on the offspring epigenome and metabolic outcomes. Electronic supplementary material The online version of this article (10.1007/s00125-019-4951-9) contains a slideset of the figures for download, which is available to authorised users.

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Author and article information

Contributors

Mehran Hosseini:

ORCID: http://orcid.org/0000-0002-6793-2035

mehranhosseiny@yahoo.co.in , mehranhosseiny@bums.ac.ir

Journal

Journal ID (nlm-ta): Biol Sex Differ

Journal ID (iso-abbrev): Biol Sex Differ

Title: Biology of Sex Differences

Publisher: BioMed Central (London )

ISSN (Electronic): 2042-6410

Publication date (Electronic): 15 September 2022

Publication date PMC-release: 15 September 2022

Publication date Collection: 2022

Volume: 13

Electronic Location Identifier: 48

Affiliations

[1 ]GRID grid.411701.2, ISNI 0000 0004 0417 4622, Cellular and Molecular Research Center, Department of Anatomical Sciences, , Birjand University of Medical Sciences, ; Birjand, Iran

[2 ]GRID grid.411701.2, ISNI 0000 0004 0417 4622, Department of Pathology, Faculty of Medicine, , Birjand University of Medical Sciences, ; Birjand, Iran

[3 ]GRID grid.411701.2, ISNI 0000 0004 0417 4622, Faculty of Medicine, , Birjand University of Medical Sciences, ; Birjand, Iran

Author information

Mehran Hosseini http://orcid.org/0000-0002-6793-2035

Article

Publisher ID: 458

DOI: 10.1186/s13293-022-00458-8

PMC ID: 9479437

PubMed ID: 36109770

SO-VID: 6ed7e93d-dd95-4912-8007-0cbe2704491a

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 4 November 2021

Date accepted : 31 August 2022

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100005117, Birjand University of Medical Sciences;

Award ID: 456205

Award Recipient : Mehran Hosseini

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ScienceOpen disciplines: Human biology

Keywords: preeclampsia,offspring,growth disorders,metabolic dysfunction,diabetes,ghrelin

Data availability:

ScienceOpen disciplines: Human biology

Keywords: preeclampsia, offspring, growth disorders, metabolic dysfunction, diabetes, ghrelin

The maternal reduced uteroplacental perfusion model of preeclampsia induces sexually dimorphic metabolic responses in rat offspring

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Abstract

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Most cited references 52

The hypertensive disorders of pregnancy: ISSHP classification, diagnosis & management recommendations for international practice

Influence of maternal obesity on the long-term health of offspring.

Intrauterine programming of obesity and type 2 diabetes

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