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Updated: Apr 14, 2026
The Use of Gas Chromatography to Analyze Compositional Changes of Fatty Acids in Rat Liver Tissue during Pregnancy
Published on: March 13, 2014
Maternal high-fat-diet programs rat offspring liver fatty acid metabolism
Emily L Seet1, Jennifer K Yee, Juanita K Jellyman
1Department of Obstetrics and Gynecology, Perinatal Research Laboratories, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, 1124 West Carson Street Box 446, RB-1 Bldg., Torrance, CA, 90502, USA.
Insights
A maternal high-fat diet programs offspring for obesity by increasing liver fat synthesis. This diet alters fatty acid metabolism and increases stearoyl-CoA desaturase-1 (SCD-1) in adult offspring, contributing to adiposity.
Area of Science:
- Metabolic programming
- Developmental origins of health and disease (DOHaD)
- Nutritional science
Background:
- Maternal high-fat (HF) diet is linked to offspring obesity and metabolic dysfunction.
- Previous studies showed HF offspring have higher body weight, adiposity, and triacylglycerol (TAG) levels.
- The underlying mechanisms involving programmed changes in liver fatty acid metabolism remain unclear.
Purpose of the Study:
- To investigate if a maternal HF diet programs offspring for adiposity through increased liver monounsaturated fatty acid synthesis.
- To determine if programmed changes in liver fatty acid metabolism are associated with increased stearoyl-CoA desaturase-1 (SCD-1) expression.
- To analyze the impact of maternal HF diet on offspring liver fatty acid desaturation indices and SCD-1 protein abundance.
Main Methods:
- Female rats were fed a HF diet rich in monounsaturated fatty acids (MUFA) during gestation and lactation.
- Offspring were analyzed for plasma and liver fatty acid composition using gas chromatography/mass spectrometry.
- Liver protein abundance of SCD-1 was quantified in newborns and adult offspring.
Main Results:
- Maternal HF diet led to decreased C16 desaturation indices in HF newborns.
- Adult HF offspring exhibited increased C16 desaturation indices in plasma and liver.
- Liver SCD-1 protein abundance was significantly elevated in adult HF offspring.
Conclusions:
- Maternal HF diet during pregnancy and lactation programs offspring for increased adiposity.
- This programming involves increased liver SCD-1 protein abundance and altered C16 desaturation pathways in adult offspring.
- These metabolic alterations contribute to the development of obesity and related metabolic issues in offspring.
Abstract:
In offspring exposed in utero to a maternal diet high in fat (HF), we have previously demonstrated that despite similar birth weights, HF adult offspring at 6 months of age had significantly higher body weights, greater adiposity, and increased triacylglycerol (TAG) levels as compared to controls. We hypothesized that a maternal HF diet predisposes to offspring adiposity via a programmed increase in the synthesis of monounsaturated fatty acids in the liver and hence increased substrate availability for liver TAG synthesis. We further hypothesized that programmed changes in offspring liver fatty acid metabolism are associated with increased liver expression of the lipogenic enzyme stearoyl-CoA desaturase-1 (SCD-1). Female rats were maintained on a HF diet rich in monounsaturated fatty acids (MUFA) prior to and throughout pregnancy and lactation. After birth, newborns were nursed by the same dam, and all offspring were weaned to control diet. Plasma and liver fatty acid compositions were determined using gas chromatography/mass spectrometry. Fatty acid C16 desaturation indices of palmitoleic/palmitic and (vaccenic + palmitoleic)/palmitic and the C18 desaturation index of oleic/stearic were calculated. Liver protein abundance of SCD-1 was analyzed in newborns and adult offspring. Plasma and liver C16 desaturation indices were decreased in HF newborns, but increased in the adult offspring. Liver SCD-1 expression was increased in the HF adult offspring. These data show that the maternal HF diet during pregnancy and lactation increases offspring liver SCD-1 protein abundance and alters the liver C16 desaturase pathway.
