Interaction between maternal and postnatal high fat diet leads to a greater risk of myocardial dysfunction in offspring via enhanced lipotoxicity, IRS-1 serine phosphorylation and mitochondrial defects

Turdi, Subat; Ge, Wei; Hu, Nan; Bradley, Katherine M.; Wang, Xiaoming; Ren, Jun

doi:10.1016/j.yjmcc.2012.12.007

Cited by 88Birth, Development, and HealthCardiovascular Function and Risk FactorsDiet, Metabolism, and Disease

Interaction between maternal and postnatal high fat diet leads to a greater risk of myocardial dysfunction in offspring via enhanced lipotoxicity, IRS-1 serine phosphorylation and mitochondrial defects

Turdi, Subat, Ge, Wei, Hu, Nan, Bradley, Katherine M., Wang, Xiaoming, Ren, Jun·2013·Journal of Molecular and Cellular Cardiology

DOI 10.1016/j.yjmcc.2012.12.007

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Abstract

Maternal overnutrition is associated with heart diseases in adult offspring. However, combined effect of maternal and postnatal fat intake on cardiac function is unknown. This study was designed to examine the impact of maternal and postnatal fat intake on metabolic, myocardial, insulin and mitochondrial responses in adult offspring. Pregnant FVB mice were fed a low fat (LF) or high fat (HF) diet during gestation and lactation. Weaning male offspring were placed on either LF or HF (calorie-restricted HF-fed mice used as weight control) for 4 months prior to assessment of metabolic indices, myocardial histology, cardiac function, insulin signaling, mitochondrial integrity and reactive oxygen species (ROS) generation. Compared with LF- and HF-fed weight-control mice, postnatal HF intake resulted in obesity, adiposity, dyslipidemia, insulin resistance, cardiac hypertrophy, interrupted cardiac contractile, intracellular Ca(2+) and mitochondrial properties, all of which were significantly accentuated by prenatal fat exposure. Despite the preserved cardiac contractile function, LF offspring from HF-fed dams displayed higher body weights, increased adiposity and glucose intolerance. HF-fed mice with prenatal HF exposure displayed upregulated serine phosphorylation of IRS-1, PTP1B, the rate-limiting fatty acid synthesis enzyme stearoyl-CoA desaturase (SCD1) and hypertrophic markers (calcineurin A, GATA4, ANP, β-MHC and skeletal α-actin), while suppressing AMP-dependent protein kinase, glucose uptake and PGC-1α levels. Importantly, myocardial and mitochondrial ultrastructural abnormalities were more pronounced in HF-fed offspring with prenatal fat exposure, shown as loss of mitochondrial density and membrane potential, increased ROS generation and apoptosis. Our data suggest that prenatal dietary fat exposure predisposes offspring to postnatal dietary fat-induced cardiac hypertrophy and contractile defect possibly via lipotoxicity, glucose intolerance and mitochondrial dysfunction. This article is part of a Special Issue entitled "Focus on Cardiac Metabolism".

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Elevated fibrosis was observed in the offspring of obese dams.
“This was also consistent with elevated fibrosis observed in the offspring of obese dams [113].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [113]

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Abstract 18063: Maternal and Postnatal High-Fat Diet Interaction Leads to Greater Risk of Myocardial Dysfunction in Offspring via Obesity-Induced Lipotoxicity, IRS-1 Serine Phosphorylation and Mitochondrial Defects
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Maternal exposure to high-fat diet induces long-term mitochondrial alterations in the offspring heart
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Maternal obesity causes fetal cardiac hypertrophy and alters adult offspring myocardial metabolism in mice
Vaughan, O. R., Rosario, F. J., Chan, J., Cox, L. A., Ferchaud‐Roucher, V., Berry, K. A. Z., Reusch, J. E. B., Keller, A. C., Powell, T. L., & Jansson, T. (2022) · The Journal of Physiology · doi:10.1113/jp282462 · Cited by 44 · see citing works

Authors: Turdi, S., Ge, W., Hu, N., Bradley, K. M., Wang, X., & Ren, J.
Affiliations: University of Wyoming (US)
Air Force Medical University (CN)
Corresponding author: Ren, Jun
ORCID: Ge, Wei
Hu, Nan
Wang, Xiaoming
Ren, Jun
Venue: Journal of Molecular and Cellular Cardiology
Publisher: Elsevier BV
Published: 2013-02
Volume: 55
Pages: 117-129
ISSN: 0022-2828 (ISSN-L)
DOI: 10.1016/j.yjmcc.2012.12.007
OpenAlex: W2102009292
Cited by: 88
References: 66
Citations by year: 2026: 6 · 2025: 7 · 2024: 4 · 2023: 6 · 2022: 11 · 2021: 7 · 2020: 7 · 2019: 5 · 2018: 6 · 2017: 5 · 2016: 5 · 2015: 9 · 2014: 6 · 2013: 4
FWCI: 5.30
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Journal of Molecular and Cellular Cardiology (publishedVersion)
PubMed (publishedVersion)
Funders: American Heart Association (0355521Z)
American Diabetes Association (7-0-RA-21)
Topics: Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords: maternal high-fat diet, cardiac dysfunction, cardiac hypertrophy, lipotoxicity, IRS-1 serine phosphorylation, insulin resistance, mitochondrial dysfunction, reactive oxygen species, impaired glucose tolerance, adiposity, dyslipidemia, stearoyl-CoA desaturase, PGC-1α, AMPK, PTP1B, cardiomyocyte apoptosis
MeSH terms: Phospholamban, Adult, Animals, Calcium, Calcium-Binding Proteins, Echocardiography, Female, Glucose, Glucose Tolerance Test, Heart, Cardiomegaly, Humans, Hypertrophy, Male, Mitochondria, Myocardial Contraction, Myocardium, Organ Size, Phosphorylation, Pregnancy, Prenatal Exposure Delayed Effects, Biomarkers, Apoptosis, Reactive Oxygen Species, Adipocytes, Sodium-Calcium Exchanger, Maternal Nutritional Physiological Phenomena, Lipid Metabolism, Proto-Oncogene Proteins c-akt, Mice, Membrane Potential, Mitochondrial, Sarcoplasmic Reticulum Calcium-Transporting ATPases, AMP-Activated Protein Kinases, Insulin Receptor Substrate Proteins, Diet, High-Fat

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Interaction between maternal and postnatal high fat diet leads to a greater risk of myocardial dysfunction in offspring via enhanced lipotoxicity, IRS-1 serine phosphorylation and mitochondrial defects

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