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Objectives: Ceramide (Cer), known as apoptotic markers, increases with prenatal ethanol (EtOH) exposure, resulting in neuroapoptosis. Whether maternal nutrition can impact Cer concentrations in brain, via altering plasma and brain fatty acid compositions have not been examined. This study compared a standard chow with a formulated semi-purified energy dense (E-dense) diet on fatty acid composition, Cer concentrations, and apoptosis in plasma and brain regions (cortex, cerebellum, and hippocampus) of pups exposed to EtOH during gestation. Methods: Pregnant Sprague–Dawley rats were randomized into four groups: chow (n = 6), chow + EtOH (20% v/v) (n = 7), E-dense (n = 6), and E-dense + EtOH (n = 8). At postnatal day 7, representing the peak brain growth spurt in rats, lipids, and apoptosis were analyzed by gas chromatography and a fluorometric caspase-3 assay kit, respectively. Results: Maternal E-dense diet increased total fatty acid concentrations (p < 0.0001), including docosahexaenoic acid (DHA) (p < 0.0001) in plasma, whereas DHA concentrations were decreased in the cerebellum (p < 0.03) of pups than those from chow-fed dams. EtOH-induced Cer elevations in the hippocampus of pups born to dams fed chow were reduced by an E-dense diet (p < 0.02). No significant effects of maternal diet quality and EtOH were observed on caspase-3 activity. No significant correlations existed between plasma/brain fatty acids and Cer concentrations. Discussions: Maternal diet quality affected fatty acid compositions and Cer concentrations of pups with prenatal EtOH exposure, differently. Maternal nutrition has the potential to prevent or alleviate some of the adverse effects of prenatal EtOH exposure. [ABSTRACT FROM AUTHOR]

Maternal nutrition status plays an important role in the development of fetal alcohol spectrum disorders (FASD), but its direct evidence is lacking. This study compared a standard chow with a semi-purified energy-dense (E-dense) diet on birth and metabolic outcomes in rats after ethanol (EtOH) consumption during pregnancy. Pregnant Sprague–Dawley rats were randomised into four groups: chow (n 6), chow + EtOH (20 %, v/v) (n 7), E-dense (n 6) and E-dense + EtOH (n 8). Birth outcomes including litter size, body and organ weights were collected. Metabolic parameters were measured in dams and pups at postnatal day (PD) 7. Maternal EtOH consumption decreased body weights (P < 0·0001) and litter sizes (P < 0·05) in chow-fed dams. At PD7, pups born to dams fed the E-dense diet had higher body (P < 0·002) and liver weights (P < 0·0001). These pups also had higher plasma total cholesterol (P < 0·0001), TAG (P < 0·003) and alanine aminotransferase (P < 0·03) compared with those from chow-fed dams. Dams fed the E-dense diet had higher plasma total (P < 0·0001) and HDL-cholesterol (P < 0·0001) and lower glucose (P < 0·0001). EtOH increased total cholesterol (P < 0·03) and glucose (P < 0·05) only in dams fed the E-dense diet. Maternal exposure to the E-dense diet attenuated prenatal EtOH-induced weight loss and produced different metabolic outcomes in both dams and pups. While the long-lasting effects of these outcomes are unknown, this study highlights the importance of maternal diet quality for maternal health and infant growth and suggests that maternal nutrition intervention may be a potential target for alleviating FASD. [ABSTRACT FROM AUTHOR]

• DHA is more predominate fatty acids in immature testis than mature rat testis. • The major transition from n-3 to n-6 fatty acid environment in testis occurs at weaning and pre-puberty. • Immature testes are more responsive to maternal DHA diet during gestation and lactation. • Dietary DHA did not reduce n-6 DPA in mature testis. • Testes fatty acids are insensitive to prenatal ethanol exposure in our experimental diet regime. Ethanol (EtOH) exposure impairs, but docosahexaenoic acid (DHA) supports testis functions. This study investigated whether dietary DHA and prenatal EtOH exposure affected fatty acid profiles equally in immature and mature testis during developmental stages. Female rats were exposed to ± EtOH (3g/kg BW, twice a day via gavage) throughout pregnancy, while consuming a diet supplemented ± DHA (1.4%, w/w). Pups were continued on their mother's diet after weaning with testes collected for fatty acid analysis at different stages of reproductive development, at gestational day 20 (GD20) and postnatal day (PD) 4, 21, 49, and 90, to present fetal, neonatal, weaning, prepubertal and adult stages, respectively. Regardless of EtOH exposure, dietary DHA significantly increased in testis DHA at all ages, with testis at weaning and prepuberty being more responsive to the diet (p<0.0002). Immature testis at GD20 and PD4 contained more DHA than n-6 docosapentaenoic acid (n-6 DPA) compared to mature testis while being well responsive to the maternal DHA diet through gestation and lactation. The level of n-6 very long chain fatty acids and (VLCFA) and n-6 DPA, distinctively increased from weaning and prepuberty, respectively, and were not reduced by the DHA diet at prepuberty and adulthood. Prenatal EtOH minimally affected testis fatty acids during development. Immature and mature testis responds differently to dietary DHA. The age around sexual maturity might be a critical time for dietary intervention as testis was more responsive to diet at this time point. The increase in DPA and n-6 VLCFA in matured testis while not affected by dietary DHA, indicates their critical roles in male reproductive function in rodents. [ABSTRACT FROM AUTHOR]