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J M Bourre - One of the best experts on this subject based on the ideXlab platform.
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roles of unsaturated Fatty Acids especially omega 3 Fatty Acids in the brain at various ages and during ageing
Journal of Nutrition Health & Aging, 2004Co-Authors: J M BourreAbstract:: Among various organs, in the brain, the Fatty Acids most extensively studied are omega-3 Fatty Acids. Alpha-linolenic Acid (18:3omega3) deficiency alters the structure and function of membranes and induces minor cerebral dysfunctions, as demonstrated in animal models and subsequently in human infants. Even though the brain is materially an organ like any other, that is to say elaborated from substances present in the diet (sometimes exclusively), for long it was not accepted that food can have an influence on brain structure, and thus on its function. Lipids, and especially omega-3 Fatty Acids, provided the first coherent experimental demonstration of the effect of diet (nutrients) on the structure and function of the brain. In fact the brain, after adipose tissue, is the organ richest in lipids, whose only role is to participate in membrane structure. First it was shown that the differentiation and functioning of cultured brain cells requires not only alpha-linolenic Acid (the major component of the omega-3, omega3 family), but also the very long omega-3 and omega-6 carbon chains (1). It was then demonstrated that alpha-linolenic Acid deficiency alters the course of brain development, perturbs the composition and physicochemical properties of brain cell membranes, neurones, oligodendrocytes, and astrocytes (2). This leads to physicochemical modifications, induces biochemical and physiological perturbations, and results in neurosensory and behavioural upset (3). Consequently, the nature of polyunsaturated Fatty Acids (in particular omega-3) present in formula milks for infants (premature and term) conditions the visual and cerebral abilities, including intellectual. Moreover, dietary omega-3 Fatty Acids are certainly involved in the prevention of some aspects of cardiovascular disease (including at the level of cerebral vascularization), and in some neuropsychiatric disorders, particularly depression, as well as in dementia, notably Alzheimer's disease. Recent results have shown that dietary alpha-linolenic Acid deficiency induces more marked abnormalities in certain cerebral structures than in others, as the frontal cortex and pituitary gland are more severely affected. These selective lesions are accompanied by behavioural disorders more particularly affecting certain tests (habituation, adaptation to new situations). Biochemical and behavioural abnormalities are partially reversed by a dietary phospholipid supplement, especially omega-3-rich egg yolk extracts or pig brain. A dose-effect study showed that animal phospholipids are more effective than plant phospholipids to reverse the consequences of alpha-linolenic Acid deficiency, partly because they provide very long preformed chains. Alpha-linolenic Acid deficiency decreases the perception of pleasure, by slightly altering the efficacy of sensory organs and by affecting certain cerebral structures. Age-related impairment of hearing, vision and smell is due to both decreased efficacy of the parts of the brain concerned and disorders of sensory receptors, particularly of the inner ear or retina. For example, a given level of perception of a sweet taste requires a larger quantity of sugar in subjects with alpha-linolenic Acid deficiency. In view of occidental eating habits, as omega-6 Fatty Acid deficiency has never been observed, its impact on the brain has not been studied. In contrast, Omega-9 Fatty Acid deficiency, specifically oleic Acid deficiency, induces a reduction of this Fatty Acid in many tissues, except the brain (but the sciatic nerve is affected). This Fatty Acid is therefore not synthesized in sufficient quantities, at least during pregnancy-lactation, implying a need for dietary intake. It must be remembered that organization of the neurons is almost complete several weeks before birth, and that these neurons remain for the subject's life time. Consequently, any disturbance of these neurons, an alteration of their connections, and impaired turnover of their constituents at any stage of life, will tend to accelerate ageing. The enzymatic activities of sytivities of synthesis of long-chain polyunsaturated Fatty Acids from linoleic and alpha-linolenic Acids are very limited in the brain: this organ therefore depends on an exogenous supply. Consequently, Fatty Acids that are essential for the brain are arachidonic Acid and cervonic Acid, derived from the diet, unless they are synthesized by the liver from linoleic Acid and alpha-linolenic Acid. The age-related reduction of hepatic desaturase activities (which participate in the synthesis of long chains, together with elongases) can impair turnover of cerebral membranes. In many structures, especially in the frontal cortex, a reduction of cervonic and arachidonic Acids is observed during ageing, predominantly associated with a reduction of phosphatidylethanolamines (mainly in the form of plasmalogens). Peroxisomal oxidation of polyunsaturated Fatty Acids decreases in the brain during ageing, participating in decreased turnover of membrane Fatty Acids, which are also less effectively protected against peroxidation by free radicals.
Jong Hoon Ryu - One of the best experts on this subject based on the ideXlab platform.
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The memory-enhancing effect of erucic Acid on scopolamine-induced cognitive impairment in mice.
Pharmacology biochemistry and behavior, 2016Co-Authors: Eunji Kim, Jin Jeon, Sunhee Lee, Hyung Eun Lee, Ha Neul Kim, Eun-rhan Woo, Jong Hoon RyuAbstract:Erucic Acid is a monounsaturated Omega-9 Fatty Acid isolated from the seed of Raphanus sativus L. that is known to normalize the accumulation of very long chain Fatty Acids in the brains of patients suffering from X-linked adrenoleukodystrophy. Here, we investigated whether erucic Acid enhanced cognitive function or ameliorated scopolamine-induced memory impairment using the passive avoidance, Y-maze and Morris water maze tasks. Erucic Acid (3mg/kg, p.o.) enhanced memory performance in normal naive mice. In addition, erucic Acid (3mg/kg, p.o.) ameliorated scopolamine-induced memory impairment, as assessed via the behavioral tasks. We then investigated the underlying mechanism of the memory-enhancing effect of erucic Acid. The administration of erucic Acid increased the phosphorylation levels of phosphatidylinositide 3-kinase (PI3K), protein kinase C zeta (PKCζ), extracellular signal-regulated kinase (ERK), cAMP response element-binding protein (CREB) and additional protein kinase B (Akt) in the hippocampus. These results suggest that erucic Acid has an ameliorative effect in mice with scopolamine-induced memory deficits and that the effect of erucic Acid is partially due to the activation of PI3K-PKCζ-ERK-CREB signaling as well as an increase in phosphorylated Akt in the hippocampus. Therefore, erucic Acid may be a novel therapeutic agent for diseases associated with cognitive deficits, such as Alzheimer's disease.
Eunji Kim - One of the best experts on this subject based on the ideXlab platform.
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The memory-enhancing effect of erucic Acid on scopolamine-induced cognitive impairment in mice.
Pharmacology biochemistry and behavior, 2016Co-Authors: Eunji Kim, Jin Jeon, Sunhee Lee, Hyung Eun Lee, Ha Neul Kim, Eun-rhan Woo, Jong Hoon RyuAbstract:Erucic Acid is a monounsaturated Omega-9 Fatty Acid isolated from the seed of Raphanus sativus L. that is known to normalize the accumulation of very long chain Fatty Acids in the brains of patients suffering from X-linked adrenoleukodystrophy. Here, we investigated whether erucic Acid enhanced cognitive function or ameliorated scopolamine-induced memory impairment using the passive avoidance, Y-maze and Morris water maze tasks. Erucic Acid (3mg/kg, p.o.) enhanced memory performance in normal naive mice. In addition, erucic Acid (3mg/kg, p.o.) ameliorated scopolamine-induced memory impairment, as assessed via the behavioral tasks. We then investigated the underlying mechanism of the memory-enhancing effect of erucic Acid. The administration of erucic Acid increased the phosphorylation levels of phosphatidylinositide 3-kinase (PI3K), protein kinase C zeta (PKCζ), extracellular signal-regulated kinase (ERK), cAMP response element-binding protein (CREB) and additional protein kinase B (Akt) in the hippocampus. These results suggest that erucic Acid has an ameliorative effect in mice with scopolamine-induced memory deficits and that the effect of erucic Acid is partially due to the activation of PI3K-PKCζ-ERK-CREB signaling as well as an increase in phosphorylated Akt in the hippocampus. Therefore, erucic Acid may be a novel therapeutic agent for diseases associated with cognitive deficits, such as Alzheimer's disease.
Pere Puigserver - One of the best experts on this subject based on the ideXlab platform.
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oleic Acid stimulates complete oxidation of Fatty Acids through protein kinase a dependent activation of sirt1 pgc1α complex
Journal of Biological Chemistry, 2013Co-Authors: Zachary Gerharthines, John E Dominy, Mitsuhisa Tabata, Yang Kevin Xiang, Pere PuigserverAbstract:Fatty Acids are essential components of the dynamic lipid metabolism in cells. Fatty Acids can also signal to intracellular pathways to trigger a broad range of cellular responses. Oleic Acid is an abundant monounsaturated Omega-9 Fatty Acid that impinges on different biological processes, but the mechanisms of action are not completely understood. Here, we report that oleic Acid stimulates the cAMP/protein kinase A pathway and activates the SIRT1-PGC1α transcriptional complex to modulate rates of Fatty Acid oxidation. In skeletal muscle cells, oleic Acid treatment increased intracellular levels of cyclic adenosine monophosphate (cAMP) that turned on protein kinase A activity. This resulted in SIRT1 phosphorylation at Ser-434 and elevation of its catalytic deacetylase activity. A direct SIRT1 substrate is the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator 1-α (PGC1α), which became deacetylated and hyperactive after oleic Acid treatment. Importantly, oleic Acid, but not other long chain Fatty Acids such as palmitate, increased the expression of genes linked to Fatty Acid oxidation pathway in a SIRT1-PGC1α-dependent mechanism. As a result, oleic Acid potently accelerated rates of complete Fatty Acid oxidation in skeletal muscle cells. These results illustrate how a single long chain Fatty Acid specifically controls lipid oxidation through a signaling/transcriptional pathway. Pharmacological manipulation of this lipid signaling pathway might provide therapeutic possibilities to treat metabolic diseases associated with lipid dysregulation.
Carina C Clingman - One of the best experts on this subject based on the ideXlab platform.
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a feedback loop couples musashi 1 activity to omega 9 Fatty Acid biosynthesis a dissertation
2014Co-Authors: Carina C ClingmanAbstract:All living creatures change their gene expression program in response to nutrient availability and metabolic demands. Nutrients and metabolites can directly control transcription and activate second-‐messenger systems. In bacteria, metabolites also affect post-‐transcriptional regulatory mechanisms, but there are only a few isolated examples of this regulation in eukaryotes. Here, I present evidence that RNA-‐binding by the stem cell translation regulator Musashi-‐1 (MSI1) is allosterically inhibited by 18-‐22 carbon ω-‐9 monounsaturated Fatty Acids. The Fatty Acid binds to the N-‐terminal RNA Recognition Motif (RRM) and induces a conformational change that prevents RNA association. Musashi proteins are critical for development of the brain, blood, and epithelium. I identify stearoyl-‐CoA desaturase-‐1 as a MSI1 target, revealing a feedback loop between ω-‐9 Fatty Acid biosynthesis and MSI1 activity. To my knowledge, this is the first example of an RNA-‐binding protein directly regulated by Fatty Acid. This finding may represent one of the first examples of a potentially broad network connecting metabolism with post-‐transcriptional regulation.
