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Previously, we noted that the dietary restriction of α-linolenic acid (ALA, n-3) for 4 weeks after weaning brought about significant decreases in the BDNF content and p38 MAPK activity in the striatum of mice, but not in the other regions of the brain, compared with an ALA-and linoleic acid (LNA, n-6)-adequate diet. In this study, we examined whether a prolonged dietary manipulation induces biochemical changes in other regions of the brain as well. Mice were fed a safflower oil (SAF) diet (ALA-restricted, LNA-adequate) or a perilla oil (PER) diet (containing adequate amounts of ALA and LNA) for 8 weeks from weaning. The docosahexaenoic acid (DHA, 22:6n-3) contents and p38 MAPK activities in the cerebral cortex, striatum and hippocampus were significantly lower in the SAF group. The BDNF contents and protein kinase C (PKC) activities in the cerebral cortex as well as in the striatum, but not in the hippocampus, were significantly lower in the SAF group. These data indicate that the biochemical changes induced by the dietary restriction of ALA have a time lag in the striatum and cortex, suggesting that the signal is transmitted through decreased p38 MAPK activity and BDNF content and ultimately decreased PKC activity.Highly unsaturated fatty acids (HUFAs, ≧ 20 carbons and ≧ 3 double bonds), mainly arachidonic acid (ARA, 20:4n-6) and docosahexaenoic acid (DHA,, are essential components of membrane lipids in the mammalian brain; they are synthesized from dietary essential fatty acids, namely, linoleic acid (LNA, 18:2n-6) and α-linolenic acid (ALA, 18:3n-3), respectively, by sequential desaturation, elongation, and/or chain shortening. Various studies have reported that the behavioral and biochemical parameters of mammalian brains are affected by long-term dietary manipulations, e.g., n-3 polyunsaturated fatty acid (PUFA) such as ALA and/or DHA, which is required for neuronal development, behavioral performance, neuroprotection, synaptic plasticity and several other functions (3,6,7,11,15,19,28,30). Long-term dietary manipulations using linoleic acid (LNA)-adequate but α-linolenic acid (ALA)-restricted diets, e.g., over the course of two generations, have been shown to modify membrane phospholipid acyl chains, learning ability and general behavior in rodents compared with diets containing adequate amounts of LNA and ALA (14,36). The nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are members of the neurotrophin family that normally plays a crucial role in neuronal development, function, survival, and plasticity. NGF is a prototype of members of the neurotrophin family that have approximately 50% amino acid sequence homologies with each other. NGF regulates neuronal survival and stimulates neural differentiation via the TrkA receptor (1,16,33). BDNF, a 27-kDa protein, regulates the survival, growth, and differentiation of new neurons during early neural development, maintaining neuro-
Previously, we noted that the dietary restriction of α-linolenic acid (ALA, n-3) for 4 weeks after weaning brought about significant decreases in the BDNF content and p38 MAPK activity in the striatum of mice, but not in the other regions of the brain, compared with an ALA-and linoleic acid (LNA, n-6)-adequate diet. In this study, we examined whether a prolonged dietary manipulation induces biochemical changes in other regions of the brain as well. Mice were fed a safflower oil (SAF) diet (ALA-restricted, LNA-adequate) or a perilla oil (PER) diet (containing adequate amounts of ALA and LNA) for 8 weeks from weaning. The docosahexaenoic acid (DHA, 22:6n-3) contents and p38 MAPK activities in the cerebral cortex, striatum and hippocampus were significantly lower in the SAF group. The BDNF contents and protein kinase C (PKC) activities in the cerebral cortex as well as in the striatum, but not in the hippocampus, were significantly lower in the SAF group. These data indicate that the biochemical changes induced by the dietary restriction of ALA have a time lag in the striatum and cortex, suggesting that the signal is transmitted through decreased p38 MAPK activity and BDNF content and ultimately decreased PKC activity.Highly unsaturated fatty acids (HUFAs, ≧ 20 carbons and ≧ 3 double bonds), mainly arachidonic acid (ARA, 20:4n-6) and docosahexaenoic acid (DHA,, are essential components of membrane lipids in the mammalian brain; they are synthesized from dietary essential fatty acids, namely, linoleic acid (LNA, 18:2n-6) and α-linolenic acid (ALA, 18:3n-3), respectively, by sequential desaturation, elongation, and/or chain shortening. Various studies have reported that the behavioral and biochemical parameters of mammalian brains are affected by long-term dietary manipulations, e.g., n-3 polyunsaturated fatty acid (PUFA) such as ALA and/or DHA, which is required for neuronal development, behavioral performance, neuroprotection, synaptic plasticity and several other functions (3,6,7,11,15,19,28,30). Long-term dietary manipulations using linoleic acid (LNA)-adequate but α-linolenic acid (ALA)-restricted diets, e.g., over the course of two generations, have been shown to modify membrane phospholipid acyl chains, learning ability and general behavior in rodents compared with diets containing adequate amounts of LNA and ALA (14,36). The nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are members of the neurotrophin family that normally plays a crucial role in neuronal development, function, survival, and plasticity. NGF is a prototype of members of the neurotrophin family that have approximately 50% amino acid sequence homologies with each other. NGF regulates neuronal survival and stimulates neural differentiation via the TrkA receptor (1,16,33). BDNF, a 27-kDa protein, regulates the survival, growth, and differentiation of new neurons during early neural development, maintaining neuro-
BACKGROUND Egg yolks contain large amounts of cholesterol and are suspected to be harmful after long‐term consumption. In this experiment, 63 rats were used to evaluate the effect of egg white (EW) and egg yolk (EY) supplementation on serum lipids and brain cognition. The feeding time lasted 4 weeks after a 1‐week acclimation. RESULTS Body weight was significantly higher in rats fed 132.0 g kg−1 EW and significantly lower when fed 40 g kg−1 EY (P < 0.05). Total cholesterol and low‐density lipoprotein increased in rats fed 72.0 g kg−1 EW compared with rats from NC and EY groups (P < 0.05). High‐density lipoprotein (HDL) was higher in rats fed 40 g kg−1 EY and decreased when fed 72.0 g kg−1 EW (P < 0.05). Rats fed a diet with EY exhibited abundant neurons in the CA1 hippocampus and complete subcellular structures. Rats fed 132 g kg−1 EW exhibited shrunken cells and swollen mitochondria. Brain‐derived neurotrophic factor had constitutively low expression among groups, while tyrosine kinase B (TrkB) exhibited higher expression levels in rats fed a diet containing EY compared with other groups (P < 0.05). CONCLUSION EY consumption reduced body weight and increased HDL levels. Diet containing EY could improve cognition through enhanced trkB expression. © 2019 Society of Chemical Industry
α‐linolenic acid (ALA, 18:3n‐3) is a carboxylic acid composed of 18 carbon atoms and three cis double bonds, and is an essential fatty acid indispensable to the human body. This study aims to systematically review related studies on the dietary sources, metabolism, and pharmacological effects of ALA. Information on ALA was collected from the internet database PubMed, Elsevier, ResearchGate, Web of Science, Wiley Online Library, and Europe PMC using a combination of keywords including “pharmacology,” “metabolism,” “sources.” The following findings are mainly contained. (a) ALA can only be ingested from food and then converted into eicosapentaenoic acid and docosahexaenoic acid in the body. (b) This conversion process is relatively limited and affected by many factors such as dose, gender, and disease. (c) Pharmacological research shows that ALA has the anti‐metabolic syndrome, anticancer, antiinflammatory, anti‐oxidant, anti‐obesity, neuroprotection, and regulation of the intestinal flora properties. (d) There are the most studies that prove ALA has anti‐metabolic syndrome effects, including experimental studies and clinical trials. (e) The therapeutic effect of ALA will be affected by the dosage. In short, ALA is expected to treat many diseases, but further high quality studies are needed to firmly establish the clinical efficacy of ALA.
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