The objective of this study was to examine the benefits of different n6/n3 polyunsaturated fatty acid ratios on the lipid metabolism, insulin resistance, and oxidative stress in the adipose tissue of rats fed a high-fructose diet. Male and female rats were divided into four groups: a control group (CON) (n6/n3 ratio ~7), a high-fructose group (HF) (n6/n3 ratio ~7), an N6-HF group (n6/n3 ratio ~50), and the DHA-HF group (n6/n3 ratio ~1, with the addition of docosahexaenoic (DHA) and eicosapentaenoic (EPA) acid). The CON group received plain water and the HF group received 15% fructose in their drinking water. Fructose induced an increase in the content of serum triglycerides, serum cholesterol, and HOMA-IR index. Among the fatty acids, elevated proportions of C18:1n9 and C16:1n7, as well as an increase in total monounsaturated fatty acid (MUFA), were found in the adipose tissue of the HF group. Fructose treatment also changed oxidative parameters, including a marked increase in the serum malondialdehyde (MDA) content. Meanwhile, DHA supplementation caused a significant decrease in the serum MDA concentration in comparison with the HF group. In addition, DHA/EPA supplementation attenuated oxidative stress by increasing NRF 2 gene expression. Fructose treatment also significantly decreased the adiponectin level, while DHA supplementation ameliorated it. The changes observed in this trial, including the decrease in the content of DHA and EPA, the decreased EPA/ARA ratio, and the increase in the expression of inflammatory genes, are characteristics of the low-grade inflammation caused by fructose treatment. These changes in the rat adipose tissue could be prevented by dietary intervention consisting of DHA supplementation and a low n6/n3 ratio.

Background/Objectives: This study investigated the effects of maternal metabolic syndrome during pregnancy on hepatic fatty acid metabolism and betacellulin expression in rat offspring. A rat model of maternal metabolic syndrome was created with a high-fructose diet (15% fructose in drinking water for six months). Methods: The females with metabolic syndrome were divided into the CON group, the HF group, which received fructose in drinking water, and the HF-DHA group, which received fructose in water and increased amounts of DHA (docosahexaenoic acid) and EPA (eicosapentaenoic acid) in the diet (2.5% fish oil in the diet). The male and female offspring were killed at birth and their liver tissue was analyzed for the fatty acid profile and expression of Δ-9-desaturase and betacellulin. Results: When the rat offspring were exposed in utero to maternal fatty acids altered by the high-fructose diet, this resulted in a similarly altered fatty acid profile in the liver, with the most significant changes being Δ-9 desaturation and a dramatic increase in monounsaturated fatty acids. The offspring also showed an overexpression of hepatic betacellulin. Supplementation with DHA and EPA increased the DHA content and normalized the fatty acid composition of oleic acid, saturated fatty acids, linoleic acid and n3-docosapentaenoic acid in the offspring of mothers on a high-fructose diet. In addition, the DHA/EPA supplementation of fructose-fed mothers normalized hepatic Δ-9-desaturase and betacellulin overexpression in the offspring, suggesting that DHA/EPA supplementation affects not only the fatty acid content but also the liver function. Conclusions: The changes observed in this study suggest that DHA/EPA supplementation may modulate the effects of maternal programming on disorders of the lipid metabolism in the offspring.