Omega-6:Omega-3 Fatty Acid Ratio and Total Fat Content of the Maternal Diet Alter Offspring Growth and Fat Deposition in the Rat

Abstract

Omega-3 long-chain polyunsaturated fatty acids (LCPUFA) have been shown to inhibit lipogenesis and adipogenesis in adult rats. Their possible early life effects on offspring fat deposition, however, remain to be established. To investigate this, female Wistar rats (n = 6–9 per group) were fed either a 9:1 ratio of linoleic acid (LA) to alpha-linolenic acid (ALA) or a lower 1:1.5 ratio during pregnancy and lactation. Each ratio was fed at two total fat levels (18% vs. 36% fat w/w) and offspring were weaned onto standard laboratory chow. Offspring exposed to a 36% fat diet, irrespective of maternal dietary LA:ALA ratio, were lighter (male, 27 g lighter; female 19 g lighter; p < 0.0001) than those exposed to an 18% fat diet between 3 and 8 weeks of age. Offspring exposed to a low LA (18% fat) diet had higher proportions of circulating omega-3 LCPUFA and increased gonadal fat mass at 4 weeks of age (p < 0.05). Reduced Srebf1 mRNA expression of hepatic (p < 0.01), gonadal fat (p < 0.05) and retroperitoneal fat (p < 0.05) tissue was observed at 4 weeks of age in male and female offspring exposed to a 36% fat diet, and hepatic Srebf1 mRNA was also reduced in male offspring at 8 weeks of age (p < 0.05). Thus, while offspring fat deposition appeared to be sensitive to both maternal dietary LA:ALA ratio and total fat content, offspring growth and lipogenic capacity of tissues appeared to be more sensitive to maternal dietary fat content.

Maternal and Postnatal High Linoleic Acid Diet Impacts Lipid Metabolism in Adult Rat Offspring in a Sex-Specific Manner

“…However, the direct role of LA in metabolic health is still controversial [ 25 ]. The effect of LA on liver health is poorly understood, and only a few studies have investigated the impact of maternal LA directly on offspring fatty acid composition and hepatic lipid metabolism [ 26 , 27 ].…”

“…Studies have shown that maternal overnutrition increases the risk of offspring weight gain; [ 16 , 28 ] however, there are conflicting data as to whether the maternal dietary LA concentration contributes to this. A recent study has demonstrated that maternal HFD reduces offspring body weight independent of changes in the ratio of dietary LA/ALA [ 26 ]. Furthermore, in this study, maternal or postnatal diet did not affect offspring body weight in adulthood, which may be due to matched fat content in both LLA and HLA diets.…”

“…Interestingly, in this study, a postnatal HLA diet decreased total n-3 and ALA in the plasma of both male and female offspring irrespective of maternal diet, while DPA in male offspring and EPA in female offspring were decreased by both maternal and postnatal HLA diet. Recently, a study showed that a high maternal LA diet decreased whole blood total n-3 fatty acid in 8-week-old offspring of both sexes, despite the offspring no longer being directly treated with HLA diet [ 26 ]. A meta-analysis has shown that higher circulating n-3 PUFA are associated with a lower metabolic syndrome risk [ 48 ] suggesting that lower n-3 PUFA may increase risk of disease.…”

“…We further investigated the effect of a maternal or postnatal HLA diet on lipids and expression of genes related to lipid metabolism in the liver of adult offspring. A previous study in a rat model has shown that exposure to a high LA (36% fat) diet during pregnancy results in reduced liver triglyceride in 8-week-old male offspring but not in female offspring [ 26 ] While there are multiple randomized controlled trials that studied effects of LA on plasma cholesterol, [ 55 ] there is a paucity of data showing effect on liver lipids, probably due to lack of feasibility in humans. In our study, a maternal or postnatal HLA diet did not affect cholesterol or triglyceride in the liver of adult offspring.…”

Maternal omega-3 fatty acid deficiency affects fetal thermogenic development and postnatal musculoskeletal growth in mice

“…Inadequate n-3 PUFA leads to docosahexaenoic acid (DHA) deficiency that could affect fetal and postnatal neurodevelopment [33], feto-placental changes in epigenetics [34], offspring growth and lipogenic capacity [35], and others. PUFA and its metabolites also regulate bone formation and resorption [17].…”