Impact of perinatal α-linolenic acid deficiency combined with high-fat diet consumption on tissue-specific fatty acid profiles in rats: Maternal and offspring analysis.

BACKGROUND

An imbalance in the dietary ratio of omega-6 (n-6) to omega-3 (n-3) polyunsaturated fatty acids (PUFAs) and/or a high-fat diet (HFD) may disrupt the metabolic conversion of essential PUFAs, such as linoleic acid (LA) and α-linolenic acid (ALA), into their long-chain derivatives (LC-PUFAs), thereby altering their accumulation in various tissues. To determine the effects of low maternal intake of ALA and/or an HFD on FA composition in maternal tissues (liver, adipose tissue, and erythrocytes) and offspring tissues (liver, erythrocytes, adipose tissue, heart, kidney, intestine, muscle, brain, eye, lung, and stomach contents) in rats.

METHODS

A prospective, randomized, controlled experimental study was conducted in Sprague-Dawley rats. Animals were assigned to one of four dietary intervention groups: CD-<1%-ALA, CD-2%-ALA, HFD-<1%-ALA, and HFD-2%-ALA. The diets were administered throughout the pregestational, gestational, and postnatal periods. Following euthanasia, tissue samples were collected and analyzed for FA composition using gas chromatography.

RESULTS

The accumulation of n-3 PUFAs varied across the analyzed tissues, suggesting tissue-specific uptake or incorporation of ALA. The liver exhibited the highest capacity for PUFA biosynthesis in rats, whereas extrahepatic tissues showed limited activity. Moreover, maternal diet did not consistently correlate with PUFA concentrations in the offspring.

CONCLUSIONS

The increase in ALA is tissue-specific, reflecting differential incorporation among tissue types. Maternal n-3 PUFA stores become a critical source for the transfer of these FAs to the offspring, particularly under dietary stress conditions such as low ALA intake or HFDs.