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The Programming of Cardiac Hypertrophy in the Offspring by Maternal Obesity Is Associated with Hyperinsulinemia, AKT, ERK, and mTOR Activation
Open accessAbstract
Human and animal studies suggest that suboptimal early nutrition during critical developmental periods impacts long-term health. For example, maternal overnutrition during pregnancy and lactation in mice programs insulin resistance, obesity, and endothelial dysfunction in the offspring. Here we investigated the effects of diet-induced maternal obesity on the offspring cardiac phenotype and explored potential underlying molecular mechanisms. Dams fed the obesogenic diet were heavier (P < 0.01) and fatter (P < 0.0001) than controls throughout pregnancy and lactation. There was no effect of maternal obesity on offspring body weight or body composition up to 8 wk of age. However, maternal obesity resulted in increased offspring cardiac mass (P < 0.05), increased heart-body weight (P < 0.01), heart weight-tibia length (P < 0.05), increased left ventricular free wall thickness and area (P < 0.01 and P < 0.05, respectively), and increased myocyte width (P < 0.001). Consistent with these structural changes, the expression of molecular markers of cardiac hypertrophy were also increased [Nppb(BNP), Myh7-Myh6(βMHC-αMHC) (both P < 0.05) and mir-133a (P < 0.01)]. Offspring were hyperinsulinemic and displayed increased insulin action through AKT (P < 0.01), ERK (P < 0.05), and mammalian target of rapamycin (P < 0.05). p38MAPK phosphorylation was also increased (P < 0.05), suggesting pathological remodeling. Increased Ncf2(p67(phox)) expression (P < 0.05) and impaired manganese superoxide dismutase levels (P < 0.01) suggested oxidative stress, which was consistent with an increase in levels of 4-hydroxy-2-trans-nonenal (a measure of lipid peroxidation). We propose that maternal diet-induced obesity leads to offspring cardiac hypertrophy, which is independent of offspring obesity but is associated with hyperinsulinemia-induced activation of AKT, mammalian target of rapamycin, ERK, and oxidative stress.
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![Fig. 2. A, Combined left ventricular wall width (includes both the intraventricular septum and left ventricular free wall), left ventricular free wall only, and intraventricular septum only. Left ventricular free wall data were log transformed and an unpaired Student t test was performed. B, Frozen sections (5 μm) of cardiac tissue were stained with wheat germ agglutinin and imaged for measurements of myocyte width. Consecutive sections of the same representative images were then stained for hematoxylin-and-eosin-stained sections. Scale bar, 50 μm for all images. Only myocytes in longitudinal axis cross-section were measured and widths measured from a total of 80–100 cells from two separate images per sample. Open bars [control (Ctrl)] and filled bars (Mat-Ob). Data are expressed as means ± sem. RNA from ventricular tissue of control and Mat-Ob males at 8 wk of age (n = 7 and 9, respectively, in which one offspring represents one litter) was isolated, purified, and cDNA obtained by reverse transcription. C, Gene expression of Nppb, Nppa, Myh7, and Myh6 was quantified by real-time PCR using primers shown in Supplemental Table 1. All data were normalized to Gapdh as described in Materials and Methods. The ratio of Mhy7 to Myh6 was analyzed by a Mann-Whitney U test and presented as means ± interquartile ranges (n = 7 control and n = 9 Mat-Ob for all analyses). ***, P < 0.001; **, P < 0.01; *, P < 0.05.](/paper-figures/e757bfbffaa4411eb5c0bc1a86871bfe/the-programming-of-cardiac-hypertrophy-in-the-offspring-by-maternal-obesity-is-figure-2.jpg)
![Fig. 3. Gene expression was quantified by real-time PCR using primers shown in Supplemental Table 1, and all data were normalized to Gapdh. A–D, mir-133a, mir-1, p300, and Gata-4 expression. E, Gene expression of Srf and myocardin. F, Western blotting of SRF. G, Crossed-linked chromatin from ventricular tissue of control and Mat-Ob males was immunoprecipitated with anti-SRF, and enrichment of mir-133a SRF cis elements was quantified by quantitative PCR amplification of an approximately 100 bp amplicon around the two cis-elements. Open bars [control (Ctrl)] and filled bars (Mat-Ob). Data expressed as means ± sem (n = 7 control and n = 9 Mat-Ob for all analyses). **, P < 0.01; *, P < 0.05.](/paper-figures/25fe94ed50594c3ea71c4a40fe2bdc13/the-programming-of-cardiac-hypertrophy-in-the-offspring-by-maternal-obesity-is-figure-3.jpg)
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“the Ozanne group showed that young adult male offspring (at 3 and 8 weeks of age) from obese dams have increased heart weight, LV wall thickness and increased heart weight to body weight ratio, compared to offspring from control dams [93,112].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
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“In line with cardiac hypertrophy, increased expression of Nppb, Acta1 and the ratio of Myh7:Myh6 gene expression were observed in the offspring of obese dams [93,112].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Moreover, the effect of maternal obesity on cellular cardiomyocyte hypertrophy were only observed in the 3- and 8-week-old offspring [93,112] and not 12-week-old offspring [112].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Interestingly, phosphorylation of Akt at the activating Ser-473 site was elevated in hearts of offspring from obese dams, although this appeared to be mediated by increased p38-Mitogen-activated protein kinase signalling through Erk and mTOR [93]”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
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“Interestingly, phosphorylation of Akt at the activating Ser-473 site was elevated in hearts of offspring from obese dams, although this appeared to be mediated by increased p38-Mitogen-activated protein kinase signalling through Erk and mTOR [93]”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
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In the citing paper
“Reduced levels of mitochondrial localized superoxide dismutase-2 in the hearts of offspring of obese dams [93] suggest that maternal obesity increases the sensitivity of the offspring myocardium to oxidative damage.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
The cited source says what the claim attributes to it.
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“In 8-week-old offspring of obese dams, the expression of insulin receptor-β, a key component for mediating insulin signalling in the heart, was reduced [93].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
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“Fernandez-Twinn et al. [93] discovered that exposure of the offspring to maternal obesity increased the cardiac expression of miR-133 and reduced the mRNA expression of one of its putative targets, Gata-4, which is upregulated in cardiac hypertrophy.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
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“Fernandez-Twinn et al. [93] discovered that exposure of the offspring to maternal obesity increased the cardiac expression of miR-133 and reduced the mRNA expression of one of its putative targets, Gata-4, which is upregulated in cardiac hypertrophy.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
The cited source says what the claim attributes to it.
In the citing paper
“Fernandez-Twinn et al. [93] discovered that exposure of the offspring to maternal obesity increased the cardiac expression of miR-133 and reduced the mRNA expression of one of its putative targets, Gata-4, which is upregulated in cardiac hypertrophy.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
The cited source says what the claim attributes to it.
In the citing paper
“Reduced levels of mitochondrial localized superoxide dismutase-2 in the hearts of offspring of obese dams [93] suggest that maternal obesity increases the sensitivity of the offspring myocardium to oxidative damage.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
The cited source says what the claim attributes to it.
In the citing paper
“suggesting that protein translation supporting pathologic cardiac hypertrophy was activated.”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [93]
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Metadata
- Authors
- Fernandez-Twinn, D. S., Blackmore, H. L., Siggens, L., Giussani, D. A., Cross, C. M., Foo, R., & Ozanne, S. E.
- Affiliations
- Metabolic Research Laboratories (D.S.F.-T., H.L.B., S.E.O.), University of Cambridge, Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge CB2 0QQ, United Kingdom
- University of Cambridge (GB)
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2012-12-01
- Volume
- 153
- Issue
- 12
- Pages
- 5961-5971
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC3568261
- OpenAlex
- W2075074527
- Cited by
- 141
- References
- 43
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 5 · 2023: 8 · 2022: 17 · 2021: 7 · 2020: 10 · 2019: 7 · 2018: 18 · 2017: 9 · 2016: 14 · 2015: 11 · 2014: 13 · 2013: 10
- FWCI
- 9.53
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Endocrinology (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust (EU-FP7-, 086797, 086797/Z/08/Z)
- British Heart Foundation (FS/09/050, FS/09/029/27902)
- European Commission (289346)
- Directorate for Biological Sciences
- Medical Research Council (EU FP7)
- Biotechnology and Biological Sciences Research Council (BB/F015364/1)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- maternal obesity, diet-induced obesity, cardiac hypertrophy, hyperinsulinemia, Akt signaling, ERK signaling, mTOR signaling, p38 MAPK, oxidative stress, manganese superoxide dismutase, lipid peroxidation, cardiomyocyte hypertrophy, developmental programming, cardiac remodeling
- MeSH terms
- Animals, Body Composition, Body Weight, Female, Cardiomegaly, Hyperinsulinism, Male, Mice, Inbred C57BL, Mothers, Obesity, Phenotype, Pregnancy, Pregnancy, Animal, Prenatal Exposure Delayed Effects, Lipid Peroxidation, Oxidative Stress, Maternal Nutritional Physiological Phenomena, Extracellular Signal-Regulated MAP Kinases, Proto-Oncogene Proteins c-akt, Mice, TOR Serine-Threonine Kinases
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