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Cited by 127Birth, Development, and HealthCardiovascular Function and Risk FactorsGestational Diabetes Research and Management

Maternal diet-induced obesity programs cardiovascular dysfunction in adult male mouse offspring independent of current body weight

Open access
Blackmore, Heather L., Niu, Youguo, Fernandez-Twinn, Denise S., Tarry-Adkins, Jane L., Giussani, Dino A., Ozanne, Susan E.·2014·Endocrinology
DOI 10.1210/en.2014-1383PMC PMC4255219
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Abstract

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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  • The effect of maternal obesity on cellular cardiomyocyte hypertrophy was only observed in the 3- and 8-week-old offspring and not 12-week-old offspring.

    “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]

    The Results section reports that cardiomyocyte cell enlargement in male mouse offspring was most pronounced at 3 and 8 weeks and was no longer apparent at 12 weeks. It does not establish the claim’s stronger wording that the effect was observed only at 3 and 8 weeks; the study also measured cell area at 5 weeks. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Maternal obesity reduced left ventricular developed pressure and increased left ventricular end diastolic volume using Langendorff heart perfusion, revealing the presence of diastolic dysfunction in the offspring.

    “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]

    The Results section reports that Langendorff perfusion showed reduced LV developed pressure and increased LV end-diastolic pressure in offspring of obese dams; it identifies the latter as a marker of diastolic dysfunction. The claim substitutes end-diastolic volume for pressure. Although a separate Results section reports increased LV volume, that was assessed by stereology, not Langendorff perfusion. (LLM, conf=0.90)

    Experimental — accuracy not yet measured

  • Young adult male offspring at 3 and 8 weeks of age from obese dams have increased heart weight, left ventricular wall thickness and increased heart weight to body weight ratio, compared to offspring from control dams.

    “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]

    The Results section (page unavailable) reports increased absolute and relative heart weight in male offspring of obese dams, most pronounced at 3 and 8 weeks; Table 2 confirms a higher heart-weight-to-body-weight ratio at both ages. It also describes evidence of LV wall thickening, but does not establish increased LV wall thickness at both specified ages: the measured LV wall volume differs significantly at 3 weeks, not at 8 weeks. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • At 12 weeks of age, heart weights were not different, consistent with no differences in body weight, adiposity or circulating lipids.

    “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]

    The Results state that heart weights were similar between groups by 12 weeks, with no difference in growth trajectory or fat-pad weights at that age. They also report no overall maternal-diet effect on circulating lipids, but Table 1 contains lipid measurements only at 3, 5, and 8 weeks; it does not establish no lipid difference at 12 weeks. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Maternal obesity increased the expression of β1-adrenergic receptors and reduced the expression of troponin and sarcoplasmic/endoplasmic reticulum calcium transporter-2a.

    “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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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.
ORCID
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2014-10-01
Volume
155
Issue
10
Pages
3970-3980
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2014-1383
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
Licence
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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