Abstract
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. However, the mechanisms underlying the potential programming effect of n-6 PUFA upon offspring physiology are not yet all established. 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. Pregnant rats were fed a control diet (2% LA) or an LA-rich diet (12% LA) during gestation and lactation. At weaning, offspring were either maintained on the maternal diet or fed the other diet for 3 or 6 months. 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. 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. Our study suggests that perinatal exposure to high LA levels induces a differential metabolic response to weaning diet exposure in adult life. This programming effect of a maternal LA-diet may be related to the alteration of offspring gut microbiota.
Highlights
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 [1]
Breast milk PUFA levels have been correlated to adiposity in two studies reporting higher fat mass at 4 months of age in the quartile with the greater arachidonic acid (ARA)/n-3 long chain (LC)-PUFA ratio in breast milk [8], and a negative correlation has been reported between fat mass at 7 years of age and breast milk docosahexaenoic acid (DHA) content [15]
At weaning, offspring tissue fatty acid composition was profoundly impacted by the maternal diet with greater proportions of n-6 PUFA and a lower proportion of MUFA in the liver and epididymal adipose tissue (Table S3) despite similar body weights
Summary
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 [1]. 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 [9]), or in childhood at 6 or 7 years of age (Generation R cohort [10], Maastrich Essential Fatty Acid Birth (MEFAB) cohort [11], Southampton Women’s Survey (SWS) cohort [12], US pregnant cohort [13]) 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 [14], or at 5 years in the GUSO cohort [9]. Breast milk PUFA levels have 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 [8], and a negative correlation has been reported between fat mass at 7 years of age and breast milk docosahexaenoic acid (DHA) content [15]
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