Tags

Type your tag names separated by a space and hit enter

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.
J Mol Cell Cardiol. 2013 Feb; 55:117-29.JM

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".

Authors+Show Affiliations

Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23266593

Citation

Turdi, Subat, et al. "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." Journal of Molecular and Cellular Cardiology, vol. 55, 2013, pp. 117-29.
Turdi S, Ge W, Hu N, et al. 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. J Mol Cell Cardiol. 2013;55:117-29.
Turdi, S., Ge, W., Hu, N., Bradley, K. M., Wang, X., & Ren, J. (2013). 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. Journal of Molecular and Cellular Cardiology, 55, 117-29. https://doi.org/10.1016/j.yjmcc.2012.12.007
Turdi S, et al. 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. J Mol Cell Cardiol. 2013;55:117-29. PubMed PMID: 23266593.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Turdi,Subat, AU - Ge,Wei, AU - Hu,Nan, AU - Bradley,Katherine M, AU - Wang,Xiaoming, AU - Ren,Jun, Y1 - 2012/12/22/ PY - 2012/09/23/received PY - 2012/12/01/revised PY - 2012/12/04/accepted PY - 2012/12/26/entrez PY - 2012/12/26/pubmed PY - 2013/7/5/medline SP - 117 EP - 29 JF - Journal of molecular and cellular cardiology JO - J. Mol. Cell. Cardiol. VL - 55 N2 - 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". SN - 1095-8584 UR - https://www.unboundmedicine.com/medline/citation/23266593/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_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2828(12)00435-X DB - PRIME DP - Unbound Medicine ER -