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Cited by 98Birth, Development, and HealthNitric Oxide and Endothelin EffectsDiet, Metabolism, and Disease

Maternal high-fat diet impacts endothelial function in nonhuman primate offspring

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Fan, L, Lindsley, S R, Comstock, S M, Takahashi, D L, Evans, A E, He, G-W, Thornburg, K L, Grove, K L·2013·International Journal of Obesity
DOI 10.1038/ijo.2012.42PMC PMC3468685
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Abstract

OBJECTIVE: The link between maternal under-nutrition and cardiovascular disease (CVD) in the offspring later in life is well recognized, but the impact of maternal over-nutrition on the offspring's cardiovascular function and subsequent risk for CVD later in life remains unclear. Here, we investigated the impact of maternal exposure to a high-fat/calorie diet (HFD) during pregnancy and early postnatal period on endothelial function of the offspring in a nonhuman primate model. METHODS: Offspring, naturally born to either a control (CTR) diet (14% fat calories) or a HFD (36% fat calories) consumption dam, were breast-fed until weaning at about 8 months of age. After weaning, the offspring were either maintained on the same diet (CTR/CTR, HFD/HFD), or underwent a diet switch (CTR/HFD, HFD/CTR). Blood samples and arterial tissues were collected at necropsy when the animals were about 13 months of age. RESULTS: HFD/HFD juveniles displayed an increased plasma insulin level and glucose-stimulated insulin secretion in comparison with CTR/CTR. In abdominal aorta, but not the renal artery, acetylcholine-induced vasorelaxation was decreased remarkably for HFD/HFD juveniles compared with CTR/CTR. HFD/HFD animals also showed a thicker intima wall and an abnormal vascular-morphology, concurrent with elevated expression levels of several markers related to vascular inflammation and fibrinolytic function. Diet-switching animals (HFD/CTR and CTR/HFD) displayed modest damage on the abdominal vessel. CONCLUSION: Our data indicate that maternal HFD exposure impairs offspring's endothelial function. Both early programming events and postweaning diet contribute to the abnormalities that could be reversed partially by diet intervention.

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  • In macaques, maternal high-fat diet followed by a post-weaning high-fat diet induced greater inflammation than postnatal high-fat feeding of the offspring on its own.

    “Moreover, in macaques, maternal high-fat diet, followed by a post-weaning high-fat diet, induced greater vascular remodeling and inflammation than postnatal high-fat feeding of the offspring on its own [128].”

    From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [128]

    The Results (Pro-inflammation; page unavailable) report elevated aortic proinflammatory markers in offspring exposed to high-fat diets both maternally and after weaning (H/H), while offspring exposed only after weaning (C/H) had normal TNFα and ICAM-1 levels and a modest VEGF increase. This supports a greater proinflammatory response in H/H animals, but the paper says overt inflammation with histiocytic infiltration was not detected; the claim's unqualified reference to greater inflammation overstates that finding. (LLM, conf=0.82)

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  • In macaques, maternal high-fat diet followed by a post-weaning high-fat diet induced greater vascular remodeling than postnatal high-fat feeding of the offspring on its own.

    “Moreover, in macaques, maternal high-fat diet, followed by a post-weaning high-fat diet, induced greater vascular remodeling and inflammation than postnatal high-fat feeding of the offspring on its own [128].”

    From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [128]

    The Results (Intima thickness; page unavailable) report a nearly 90% thicker abdominal-aorta intima in offspring exposed to both maternal and postweaning high-fat diets than in controls, but also report thickening in offspring exposed only after weaning. They do not establish that structural remodeling was greater in the former group than in the postweaning-only group. The Results (Pro-inflammation; page unavailable) do show a broader increase in inflammatory markers in the former group. (LLM, conf=0.81)

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Research works printed but not linked: 1

  1. Meyers MR Gokce N Endothelial dysfunction in obesity: etiological role in atherosclerosis Curr Opin Endocrinol Diabetes Obes 2007 14 365 369 17940464

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Authors
Fan, L., Lindsley, S. R., Comstock, S. M., Takahashi, D. L., Evans, A. E., He, G.-W., Thornburg, K. L., & Grove, K. L.
Affiliations
  • Oregon National Primate Research Center (US)
  • Oregon Health & Science University (US)
Corresponding author
Grove, K L
ORCID
Venue
International Journal of Obesity
Publisher
Springer Science and Business Media LLC
Published
2012-03-27
Volume
37
Issue
2
Pages
254-262
ISSN
  • 0307-0565 (ISSN-L)
  • 1476-5497
DOI
10.1038/ijo.2012.42
PMC
PMC3468685
OpenAlex
W2092805406
Cited by
98
References
51
Citations by year
2026: 2 · 2024: 7 · 2023: 2 · 2022: 5 · 2021: 4 · 2020: 9 · 2019: 7 · 2018: 9 · 2017: 4 · 2016: 12 · 2015: 15 · 2014: 13 · 2013: 7 · 2012: 2
FWCI
10.40
Type
journal article
Language
en
Open access
Licence
Locations
  • International Journal of Obesity (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (P51OD011092)
  • Oregon National Primate Research Center (P51OD011092)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R24DK090964, R01DK079194, P30DK020593)
  • National Center for Research Resources (P51RR000163)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (P01HD034430)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords
maternal high-fat diet, endothelial function, maternal overnutrition, developmental programming, cardiovascular risk, insulin resistance, glucose-stimulated insulin secretion, acetylcholine-induced vasodilation, abdominal aorta, intimal thickening, vascular inflammation, fibrinolysis, diet switching, post-weaning diet
MeSH terms
Animals, Animals, Newborn, Disease Models, Animal, Endothelium, Vascular, Fasting, Female, Fetal Growth Retardation, Liver, Macaca, Male, Maternal-Fetal Exchange, Obesity, Placental Insufficiency, Pregnancy, Prenatal Exposure Delayed Effects, Primates, Weaning, Gene Expression Regulation, Developmental, Maternal Nutritional Physiological Phenomena, Overnutrition, Carotid Intima-Media Thickness, Diet, High-Fat, Real-Time Polymerase Chain Reaction

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