Abstract
Linoleic acid (LA), an n-6 polyunsaturated fatty acid (PUFA), is essential for fetal growth and development. We aimed to investigate the effect of maternal and postnatal high LA (HLA) diet on plasma FA composition, plasma and hepatic lipids and genes involved in lipid metabolism in the liver of adult offspring. Female rats were fed with low LA (LLA; 1.44% LA) or HLA (6.21% LA) diets for 10 weeks before pregnancy, and during gestation/lactation. Offspring were weaned at postnatal day 25 (PN25), fed either LLA or HLA diets and sacrificed at PN180. Postnatal HLA diet decreased circulating total n-3 PUFA and alpha-linolenic acid (ALA), while increased total n-6 PUFA, LA and arachidonic acid (AA) in both male and female offspring. Maternal HLA diet increased circulating leptin in female offspring, but not in males. Maternal HLA diet decreased circulating adiponectin in males. Postnatal HLA diet significantly decreased aspartate transaminase (AST) in females and downregulated total cholesterol, HDL-cholesterol and triglycerides in the plasma of males. Maternal HLA diet downregulated the hepatic mRNA expression of Hmgcr in both male and female offspring and decreased the hepatic mRNA expression of Cpt1a and Acox1 in females. Both maternal and postnatal HLA diet decreased hepatic mRNA expression of Cyp27a1 in females. Postnatal diet significantly altered circulating fatty acid concentrations, with sex-specific differences in genes that control lipid metabolism in the adult offspring following exposure to high LA diet in utero.
Highlights
We aimed to investigate the effects of a maternal high Linoleic acid (LA) (HLA) diet on adiposity, blood pressure, glucose tolerance and parameters associated with lipid metabolism in the liver of adult rat offspring
Data are presented as mean ± standard error of the mean (SEM)
A human study has previously shown that the n-6/n-3 FA ratio increases in non-alcoholic steatohepatitis, suggesting that increased LA in the diet may contribute to liver injury [19]
Summary
Given that fetal programming describes how the fetus adapts to the dietary factors it has been exposed, changing the postnatal environment that is different from that experience in utero may contribute to adult-onset of disease At this time, we do not know if the impact of an elevated maternal LA diet on offspring health could be reversed by a postnatal diet with recommended concentrations of LA or if this may instead exacerbate negative outcomes. We aimed to investigate the effects of a maternal high LA (HLA) diet on adiposity, blood pressure, glucose tolerance and parameters associated with lipid metabolism in the liver of adult rat offspring. It is well accepted that developmental programming of metabolic diseases occurs in sex-specific manner [17,18], we separately analysed both male and female adult offspring in the present study
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