首页> 外文期刊>Biochimica et Biophysica Acta. Molecular and cell biology of Lipids >Influence of dietary fatty acids on endocannabinoid and N-acylethanolamine levels in rat brain, liver and small intestine
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Influence of dietary fatty acids on endocannabinoid and N-acylethanolamine levels in rat brain, liver and small intestine

机译:饮食脂肪酸对大鼠脑,肝和小肠内大麻素和N-酰基乙醇胺水平的影响

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Endocannabinoids and N-acylethanolamines are lipid mediators regulating a wide range of biological functions including food intake. We investigated short-term effects of feeding rats five different dietary fats (palm oil (PO), olive oil (OA), safflower oil (LA), fish oil (170) and arachidonic acid (AA)) on tissue levels of 2-arachidonoylglycerol, anandamide, oleoylethanolamide, palmitoylethanolamide, stearoylethanolamide, linoleoylethanolamide, eicosapentaenoylethanolamide, docosahexaenoylethanolamide and tissue fatty acid composition. The LA-diet increased linoleoylethanolamide and linoleic acid in brain, jejunum and liver. The OA-diet increased brain levels of anandamide and oleoylethanolamide (not 2-arachidonoylglycerol) without changing tissue fatty acid composition. The same diet increased oleoylethanolamide in liver. All five dietary fats decreased oleoylethanolamide in jejunum without changing levels of anandamide, suggesting that dietary fat may have an orexigenic effect. The AA-diet increased anandamide and 2-arachidonoylglycerol in jejunum without effect on liver. The FO-diet decreased liver levels of all N-acylethanolamines (except eicosapentaenoylethanolamide and docosahexaenoylethanolamide) with similar changes in precursor lipids. The AA-diet and FO-diet had no effect on N-acylethanolamines, endocannabinoids or precursor lipids in brain. All N-acylethanolamines activated PPAR-alpha. In conclusion, short-term feeding of diets resembling human diets (Mediterranean diet high in monounsaturated fat, diet high in saturated fat, or diet high in polyunsaturated fat) can affect tissue levels of endocannabinoids and N-acylethanolamines. (C) 2008 Elsevier B.V. All rights reserved.
机译:内源性大麻素和N-酰基乙醇胺是调节多种生物学功能(包括食物摄入)的脂质介质。我们调查了喂养大鼠五种不同饮食脂肪(棕榈油(PO),橄榄油(OA),红花油(LA),鱼油(170)和花生四烯酸(AA))对组织中2-水平的短期影响花生四烯酰基甘油,阿南酰胺,油酰基乙醇酰胺,棕榈酰基乙醇酰胺,硬脂酰基乙醇酰胺,亚油酰基乙醇酰胺,二十碳五烯酰基乙醇酰胺,二十二碳六烯酰基乙醇酰胺和组织脂肪酸组成。 LA饮食增加脑,空肠和肝脏中的亚油酰基乙醇酰胺和亚油酸。 OA饮食增加了大脑中的anandamide和油酰乙醇酰胺(而不是2-arachidonoylglycerol)的大脑水平,而没有改变组织脂肪酸的组成。相同的饮食会增加肝脏中的油酰乙醇酰胺。所有这五种饮食脂肪都降低了空肠中的油酰乙醇酰胺含量,而不变的是anandamide水平,这表明饮食脂肪可能具有致癌作用。 AA饮食增加空肠中的anandamide和2-arachidonoylglycerol,对肝脏没有影响。 FO饮食降低了所有N-酰基乙醇胺(二十碳五烯基乙醇酰胺和二十二碳六烯基乙醇酰胺除外)的肝脏水平,并且前体脂质的变化相似。 AA饮食和FO饮食对脑中的N-酰基乙醇胺,内源性大麻素或前体脂质没有影响。所有N-酰基乙醇胺均活化了PPAR-α。总之,类似于人类饮食(单不饱和脂肪含量高的地中海饮食,饱和脂肪含量高的饮食或多不饱和脂肪含量高的饮食)的短期喂养会影响内源性大麻素和N-酰基乙醇胺的组织水平。 (C)2008 Elsevier B.V.保留所有权利。

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