Maternal and Early Dietary Fatty Acid Intake: Changes in Lipid Metabolism and Liver Enzymes in Adult Rats

Abstract

Over the last decade, much evidence has emerged to suggest that alterations in maternal nutrition during pregnancy may irreversibly affect aspects of physiological and biochemical functions in the fetus. This study was designed to determine the mechanisms involved in these alterations. Our hypothesis was that the type of maternal dietary fat received in early life could determine the level of lipoprotein lipase (LPL; EC 3.1.1.34) activity and gene expression which would be maintained into later life. A diet high in (n-3) polyunsaturated fatty acids was predicted to be associated with higher levels of lipoprotein lipase (LPL) activity and expression and lower levels of plasma triglyceride after a high fat meal challenge. Using a 2x2 factorial design, Wistar Albino rats were pair-fed either a fish oil diet (50 g/kg) or a mixed oil diet (50 g/kg) for the last 2 wk of gestation, during lactation and pups were fed these diets until 5 wk of age. After 5 wk, the rats were fed nonpurified diet. The rats were killed at 5 wk (young) or 10 wk (adult) of age after a mixed oil (50 g/kg) test meal. There were significant age effects on plasma triglyceride (P<0.02), cholesterol (P<0.001), glucose-dependent insulinotrophic polypeptide (GIP) (P<0.001) and liver glutathione reductase activity (P<0.05) which were all higher in the young rats compared to the adults. There were significant effects of diet on triglyceride (P<0.001), cholesterol (P<0.001) and LPL mRNA levels (P<0.001). GIP and triglyceride levels were significantly correlated (r = 0.66; P<0.001). Omental adipose tissue LPL activity as significantly higher in the fish-oil fed groups compared to the other groups (P<0.001), whereas Epididymal adipose tissue LPL mRNA was significantly higher in the mixed oil-fed adults compared to the other groups (P<0.001). The latter result suggested an imprinting effect of fatty acid composition in early life on LPL gene expression. Liver superoxide dismutase activity was affected by age and diet and was higher in the young than in the adults and higher in the fish oil-fed young than in those fed the mixed oil-fed (P<0.005). Catalase activity was also affected by age (P<0.001) and diet (P<0.001), and there was a significant interaction between age and diet (P<0.001). Catalase activity was higher in rats fed fish oils at both stages of development, suggesting that feeding fish oils to rats in early life raises oxidative stress throughout life. The majority of the significant differences shown were between the age groups and not between the two dietary groups, suggesting that postprandial handling of a standard fat meal is affected more by age than by early dietary fatty acid composition. However, the mechanisms of biological imprinting of fatty acids on LPL expression and on enzymes related to oxidative stress requires more investigation.

Healthy effect of different proportions of marine ω-3 PUFAs EPA and DHA supplementation in Wistar rats: Lipidomic biomarkers of oxidative stress and inflammation

“…the antioxidant response after ω-3 EPA and DHA supplementation: enhance of SOD [34], and CAT activities [35], and genes related to endogenous antioxidant system [36]; although the different aptitude of EPA vs DHA have not been described yet.…”

Effects of n–3 Supplementation on Plasma and Liver Phospholipid Fatty Acids Profile in Aged Wistar Rats

“…9 Fish oils which are rich in n-3 PUFAs have been postulated to be beneficial in several disease states including atherosclerosis, hypertension and arthritis. 11,12 The major n-3 FAs found in fish oil are EPA [20:5 (n-3)] and DHA (22:6, n-3). Fish oils have been shown to reduce hepatic lipogenesis and VLDL secretion and increase post-heparin plasma LPL activity.…”

Nutrigenomics of hepatic steatosis in a feline model: effect of monosodium glutamate, fructose, and Trans-fat feeding

“…Animal models which more closely resembled human pathology with respect to NA-FLD and NASH would be desirable, particularly in relation to gene expression modulation (nutrigenomics), which could become targets for therapeutic intervention in hepatic fibrosis and tissue damage. Since maternal nutrition during pregnancy affects many aspects of physiology and development of the offspring, including liver function (Chapman et al 2000), our model of diet-induced hepatic steatosis involved life-time exposure to the diets beginning in utero in order to mimic more closely the human situation. This manuscript describes a novel model using four different diet regimens that produced significant changes in the extent of hepatic steatosis and markers of fibrosis and liver damage between the study groups, together with significant changes in the expression of hepatic genes involved in lipid metabolism, fibrosis, inflammation, and tissue damage/ remodeling.…”