4.5 Article

Maternal consumption of o3 attenuates metabolic disruption elicited by saturated fatty acids-enriched diet in offspring rats

Journal

NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES
Volume 32, Issue 1, Pages 279-289

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.numecd.2021.09.010

Keywords

Phenotypic plasticity; High-fat diet; Alpha-linolenic; Transmissible chronic diseases

Funding

  1. Fundacao de Amparo a Ciencia e Tecnologia de Pernambuco e PE, Brazil [PRONEM 0797e4.05/14, IBPG-1478-4.05/16, IBPG-03134.05/19]
  2. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico -Brazil [311386/2019-9]

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The study found that maternal consumption of a high-fat diet enriched with omega-3 can prevent metabolic disruptions caused by HFD in offspring until early adulthood, but the long-term effects are limited.
Background and aims: High-fat diet (HFD) intake during gestation and lactation has been associated with an increased risk of developing cardiometabolic disorders in adult offspring. We investigated whether metabolic alterations resulting from the maternal consumption of HFD are prevented by the addition of omega-3 (o3) in the diet. Methods and results: Wistar rat dams were fed a control (C: 19% of lipids and o6:o3 = 12), HF (HF: 33% lipids and o6:o3 = 21), or HF enriched with o3 (HFu3: 33% lipids and o6:o3 = 9) diet during gestation and lactation, and their offspring food consumption, murinometric measurements, serum levels of metabolic markers, insulin and pyruvate sensitivity tests were evaluated. The maternal HFD increased body weight at birth, dyslipidemia, and elevated fasting glucose levels in the HF group. The enrichment of o3 in the maternal HFD led to lower birth weight and improved lipid, glycemic, and transaminase biochemical profile of the HFu3 group until the beginning of adulthood. However, at later adulthood of the offspring, there was no improvement in these biochemical parameters. Conclusion: Our findings show the maternal consumption of high-fat o3-rich diet is able to attenuate or prevent metabolic disruption elicited by HFD in offspring until 90 days old, but not in the long term, as observed at 300 days old of the offspring. (c) 2021 Published by Elsevier B.V. on behalf of The Italian Diabetes Society, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition and the Department of Clinical Medicine and Surgery, Federico II University.

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