![]() ![]() ![]() ![]() It is well established now that host physiology, metabolism and behavior may be affected by the gut microbiota. However, the microbiota may also be involved. ![]() Epigenetic mechanisms have been shown to play a major role in neonatal programming by imprinting gene expression. The mechanisms underlying the potential programming effect of n-6 PUFA status on adiposity are not all yet established. Interestingly, in several studies, maternal dietary n-3 PUFA supplementation did not affect offspring adiposity, suggesting that lowering n-6 PUFA content may be more effective in reducing the risk of metabolic disease in offspring. Breast milk PUFA levels have also been correlated to adiposity in two studies reporting higher fat mass at 4 months of age in the quartile with the greater ARA/ n-3 long chain (LC)-PUFA ratio in breast milk, and a negative correlation has been reported between fat mass at 7 years of age and breast milk docosahexaenoic acid (DHA) content. However, this effect does not seem to be long-lasting, since no such correlation was found when offspring were 23 years old in the MEFAB cohort, or at 5 years in the GUSO cohort. In epidemiological studies, the level of LA, of its derivatives, or of the n-6/ n-3 ratio in maternal or cord plasma was positively correlated to adiposity immediately at birth (Growing up towards Healthy Outcomes (GUSTO) cohort ), or in childhood at 6 or 7 years of age (Generation R cohort, Maastrich Essential Fatty Acid Birth (MEFAB) cohort, Southampton Women’s Survey (SWS) cohort, US pregnant cohort ). reported that a low perinatal n-6/ n-3 PUFA ratio exposure predisposed adult offspring to a phenotype of resistance to diet-induced obesity. A high intake of n-6 PUFA during this critical window of development results in a progressive accumulation of body fat across generations. Specifically, LA, and especially its derivative, arachidonic acid (ARA), display pro-adipogenic properties that are related to a greater risk of obesity and related metabolic conditions. Strong evidence indicates that maternal nutrition during gestation and lactation can profoundly affect offspring health and disease risk later in life. Consequently, the levels of linoleic acid (LA), an essential n-6 fatty acid, of women’s milk also increased from 6% to a plateau at around 16% of total fatty acids. In the past three decades, the overconsumption of vegetable oils rich in n-6 polyunsaturated fatty acids (PUFA) and the lower intake of n-3 PUFA has resulted in an imbalance in the n-6/ n-3 ratio, rising from 1:1 to 20:1 nowadays. This programming effect of a maternal LA-diet may be related to the alteration of offspring gut microbiota. Our study suggests that perinatal exposure to high LA levels induces a differential metabolic response to weaning diet exposure in adult life. The maternal LA-diet impacted offspring cecal microbiota diversity and composition at 3 months of age, but had only few remnant effects upon cecal microbiota composition at 6 months of age. At 3 months of age, the maternal LA-diet favored low-grade inflammation and greater adiposity, while at 6 months of age, offspring intestinal barrier function, adipose tissue physiology and hepatic conjugated linoleic acids were strongly influenced by the weaning diet. At weaning, offspring were either maintained on the maternal diet or fed the other diet for 3 or 6 months. Pregnant rats were fed a control diet (2% LA) or an LA-rich diet (12% LA) during gestation and lactation. Herein, we investigated the effects of maternal and weaning linoleic acid (LA)-rich diet interactions on gut intestinal and adipose tissue physiology in young (3-month-old) and older (6-month-old) adult offspring. However, the mechanisms underlying the potential programming effect of n-6 PUFA upon offspring physiology are not yet all established. Maternal n-6 polyunsaturated fatty acids (PUFA) consumption during gestation and lactation can predispose offspring to the development of metabolic diseases such as obesity later in life. ![]()
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