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Maternal Diet-induced Obesity Programs Cardiovascular Dysfunction in Adult Male Mouse Offspring Independent of Current Body Weight
Open accessAbstract
Obese pregnancies are not only associated with adverse consequences for the mother but also the long-term health of her child. Human studies have shown that individuals from obese mothers are at increased risk of premature death from cardiovascular disease (CVD), but are unable to define causality. This study aimed to determine causality using a mouse model of maternal diet–induced obesity. Obesity was induced in female C57BL/6 mice by feeding a diet rich in simple sugars and saturated fat 6 weeks prior to pregnancy and throughout pregnancy and lactation. Control females were fed laboratory chow. Male offspring from both groups were weaned onto chow and studied at 3, 5, 8, and 12 weeks of age for gross cardiac morphometry using stereology, cardiomyocyte cell area by histology, and cardiac fetal gene expression using qRT-PCR. Cardiac function was assessed by isolated Langendorff technology at 12 weeks of age and hearts were analyzed at the protein level for the expression of the β1 adrenergic receptor, muscarinic type-2 acetylcholine receptor, and proteins involved in cardiac contraction. Offspring from obese mothers develop pathologic cardiac hypertrophy associated with re-expression of cardiac fetal genes. By young adulthood these offspring developed severe systolic and diastolic dysfunction and cardiac sympathetic dominance. Importantly, cardiac dysfunction occurred in the absence of any change in corresponding body weight and despite the offspring eating a healthy low-fat diet. These findings provide a causal link to explain human observations relating maternal obesity with premature death from CVD in her offspring.
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“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 [112]
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“Maternal obesity reduced LV-developed pressure and increased LV end diastolic volume using Langendorff heart perfusion, revealing the presence of diastolic dysfunction in the offspring [112].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [112]
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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 [112]
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“Interestingly, at 12 weeks of age, heart weights were not different, consistent with no differences in body weight, adiposity or circulating lipids [112].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [112]
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“Examination of proteins that regulate the contractile properties of the heart revealed that maternal obesity increased the expression of β1-adrenergic receptors and reduced the expression of troponin and sarcoplasmic/endoplasmic reticulum calcium transporter-2a (SERCA2a) [112].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [112]
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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 [112]
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Metadata
- Authors
- Blackmore, H. L., Niu, Y., Fernandez-Twinn, D. S., Tarry-Adkins, J. L., Giussani, D. A., & Ozanne, S. E.
- Affiliations
- University of Cambridge (GB)
- University of Cambridge, Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science (H.L.B., D.S.F.-T., J.L.T.-A., S.E.O.), Addenbrookes Hospital, Cambridge CB2 0QQ, United Kingdom
- Corresponding author
- Blackmore, Heather L.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2014-10-01
- Volume
- 155
- Issue
- 10
- Pages
- 3970-3980
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- PMC
- PMC4255219
- OpenAlex
- W2100072681
- Cited by
- 127
- References
- 59
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 11 · 2023: 9 · 2022: 12 · 2021: 16 · 2020: 10 · 2019: 11 · 2018: 16 · 2017: 5 · 2016: 15 · 2015: 8 · 2014: 3
- FWCI
- 9.72
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Endocrinology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Apollo (University of Cambridge) (submittedVersion, cc-by)
- Funders
- British Heart Foundation (PG/14/5/30547, PG/13/46/30329, PG/09/037/27387, FS/09/029/27902)
- Lister Institute of Preventive Medicine
- Medical Research Council
- Biotechnology and Biological Sciences Research Council (BB/E002668/1)
- 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 › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Keywords
- maternal obesity, diet-induced obesity, cardiovascular dysfunction, cardiac hypertrophy, cardiac remodeling, cardiac function, beta1-adrenergic receptor, muscarinic receptors, saturated fat, high-sugar diet, lactation, C57BL/6 mice
- MeSH terms
- Animals, Body Weight, Cardiovascular Diseases, Cells, Cultured, Diet, Female, Mice, Inbred C57BL, Obesity, Pregnancy, Pregnancy Complications, Prenatal Exposure Delayed Effects, Maternal Nutritional Physiological Phenomena, Embryonic Development, Mice
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