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Updated: Jul 5, 2025
The Use of Gas Chromatography to Analyze Compositional Changes of Fatty Acids in Rat Liver Tissue during Pregnancy
Published on: March 13, 2014
Maternal Diet High in Linoleic Acid Alters Offspring Lipids and Hepatic Regulators of Lipid Metabolism in an
Nirajan Shrestha1, Simone L Sleep1, Olivia J Holland1,2
1School of Pharmacy and Medical Science, Griffith University, Southport, QLD 4222, Australia.
Insights
Maternal high linoleic acid (LA) diets negatively impact offspring liver health. Avoiding high LA intake during and after pregnancy is crucial for reducing offspring disease risk.
Area of Science:
- Nutritional science
- Developmental biology
- Metabolic research
Background:
- Linoleic acid (LA), an omega-6 polyunsaturated fatty acid (PUFA), is vital for fetal development.
- Maternal high LA (HLA) diets are known to affect offspring cardiovascular and hepatic development in a sex-specific manner.
Purpose of the Study:
- To investigate the effects of maternal and postnatal high LA (HLA) diets on adolescent offspring hepatic lipids and gene expression.
- To determine if postnatal diet can modify the effects of maternal HLA diet.
Main Methods:
- Female Wistar Kyoto rats were fed either low LA (LLA) or high LA (HLA) diets during gestation and lactation.
- Offspring were weaned onto LLA or HLA diets and euthanized at postnatal day 40.
- Hepatic lipids and gene expression (Pparg, Srebf1, Hmgcr, Lpl, Cpt1a) were analyzed.
Main Results:
- Maternal HLA diet altered hepatic cholesterol, uric acid, and gene expression (Pparg, Srebf1, Hmgcr) in a sex-specific manner.
- Postnatal HLA diet affected liver weight and hepatic triglycerides, also with sex-specific effects.
- Significant interactions between maternal and postnatal HLA diets were observed for Lpl, Cpt1a, and Pparg in females.
Conclusions:
- Maternal and postnatal high LA (HLA) diets independently and interactively impact offspring hepatic lipid metabolism.
- Avoiding high LA intake throughout pregnancy and early life is recommended to mitigate potential long-term health risks in offspring.
Abstract:
Linoleic acid (LA), an n-6 polyunsaturated fatty acid (PUFA), is essential for fetal growth and development. A maternal high LA (HLA) diet alters cardiovascular development in adolescent rats and hepatic function in adult rats in a sex-specific manner. We investigated the effects of an HLA diet on adolescent offspring hepatic lipids and hepatic lipid metabolism gene expression, and the ability of the postnatal diet to alter these effects. Female Wistar Kyoto rats were fed low LA (LLA; 1.44% energy from LA) or high LA (HLA; 6.21% energy from LA) diets during pregnancy and gestation/lactation. Offspring, weaned at postnatal day (PN) 25, were fed LLA or HLA and euthanised at PN40 (n = 6-8). Maternal HLA increased circulating uric acid, decreased hepatic cholesterol and increased hepatic Pparg in males, whereas only hepatic Srebf1 and Hmgcr increased in females. Postnatal (post-weaning) HLA decreased liver weight (% body weight) and increased hepatic Hmgcr in males, and decreased hepatic triglycerides in females. Maternal and postnatal HLA had an interaction effect on Lpl, Cpt1a and Pparg in females. These findings suggest that an HLA diet both during and after pregnancy should be avoided to improve offspring disease risk.
