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Cited by 22Birth, Development, and HealthFatty Acid Research and HealthPrenatal Substance Exposure Effects

Postnatal Dietary Omega-3 Fatty Acid Supplementation Rescues Glucocorticoid-Programmed Adiposity, Hypertension, and Hyperlipidemia in Male Rat Offspring Raised on a High-Fat Diet

Zulkafli, Intan S., Waddell, Brendan J., Mark, Peter J.·2013·Endocrinology
DOI 10.1210/en.2013-1153
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Abstract

Fetal glucocorticoid excess programs several adverse outcomes in adult offspring, many of which can be prevented by postnatal, dietary omega-3 (n-3) fatty acids. Here we tested 2 separate hypotheses: 1) a postnatal high-fat diet exacerbates the glucocorticoid-programmed phenotype; and 2) postnatal, dietary n-3 fatty acids rescue programmed outcomes, even in the presence of a high-fat diet challenge. Pregnant Wistar rat dams were either untreated or administered dexamethasone acetate (Dex; 0.5 μg/mL drinking water) from day 13 of pregnancy. Offspring were cross-fostered to untreated mothers and males were weaned onto a standard (Std), high-fat, low n-3 (HF), or high-fat, high n-3 (HFHn-3) diet. Prenatal Dex reduced birth weight (26%) and delayed puberty onset by 1.2 days, irrespective of postnatal diet. Prenatal Dex programmed increased blood pressure in adult offspring, an effect worsened by the postnatal HF diet. Supplementation with high n-3 fatty acids, however, prevented both the Dex and HF-induced increases in blood pressure. Prenatal Dex also programmed increased adiposity, plasma cholesterol, and plasma triglyceride levels at 6 months of age, particularly in those offspring raised on the HF diet. But again, each of these adverse outcomes was rescued by supplementation of the HF diet with n-3 fatty acids. In conclusion, the capacity of n-3 fatty acids to overcome adverse programming outcomes remains evident, even in the presence of a HF diet challenge.

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  • In animal studies, excess glucocorticoid exposure in utero consistently programmes the offspring for increased adiposity.

    “In animal studies, excess glucocorticoid exposure in utero was consistently shown to programme the offspring for increased adiposity (Table 6 and [119–123]).”

    From Developmental programming of offspring adipose tissue biology and obesity risk (2021) · cites this paper as [121]

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Authors
Zulkafli, I. S., Waddell, B. J., & Mark, P. J.
Affiliations
The University of Western Australia (AU)
Corresponding author
Mark, Peter J.
ORCID
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2013-06-19
Volume
154
Issue
9
Pages
3110-3117
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2013-1153
OpenAlex
W2093422222
Cited by
22
References
47
Citations by year
2025: 1 · 2021: 2 · 2020: 2 · 2019: 7 · 2017: 1 · 2016: 3 · 2015: 1 · 2014: 2 · 2013: 3
FWCI
2.79
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • UWA Profiles and Research Repository (UWA) (submittedVersion)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
Keywords
omega-3 fatty acids, prenatal dexamethasone, high-fat diet, postnatal diet, offspring programming, hypertension, adiposity, hyperlipidemia, puberty onset, birth weight, serum cholesterol, plasma triglycerides, developmental origins of health and disease
MeSH terms
Animals, Anti-Inflammatory Agents, Non-Steroidal, Disease Models, Animal, Female, Glucocorticoids, Hyperlipidemias, Hypertension, Male, Maternal-Fetal Exchange, Pregnancy, Pregnancy Complications, Random Allocation, Stress, Physiological, Stress, Psychological, Fatty Acids, Omega-3, Rats, Wistar, Dietary Supplements, Fetal Development, Adiposity, Rats, Diet, High-Fat

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