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Influence of the nutritional status and oxidative stress in the desaturation and elongation of n-3 and n-6 polyunsaturated fatty acids: Impact on non-alcoholic fatty liver disease

多不饱和脂肪酸 氧化应激 非酒精性脂肪肝 脂肪变性 脂肪肝 生物化学 生物 内分泌学 内科学 脂肪酸 化学 医学 疾病
作者
Luis A. Videla,María Catalina Hernández-Rodas,Adam H. Metherel,Rodrigo Valenzuela
出处
期刊:Prostaglandins Leukotrienes and Essential Fatty Acids [Elsevier]
卷期号:181: 102441-102441 被引量:66
标识
DOI:10.1016/j.plefa.2022.102441
摘要

Polyunsaturated fatty acids (PUFA) play essential roles in cell membrane structure and physiological processes including signal transduction, cellular metabolism and tissue homeostasis to combat diseases. PUFA are either consumed from food or synthesized by enzymatic desaturation, elongation and peroxisomal β-oxidation. The nutritionally essential precursors α-linolenic acid (C18:3n-3; ALA) and linoleic acid (C18:2n-6; LA) are subjected to desaturation by Δ6D/Δ5D desaturases and elongation by elongases 2/5, enzymes that are induced by insulin and repressed by PUFA. Maintaining an optimally low n-6/n-3 PUFA ratio is linked to prevention of the development of several diseases, including nonalcoholic fatty liver disease (NAFLD) that is characterized by depletion of PUFA promoting hepatic steatosis and inflammation. In this context, supplementation with n-3 PUFA revealed significant lowering of hepatic steatosis in obese patients, whereas prevention of fatty liver by high-fat diet in mice is observed in n-3 PUFA and hydroxytyrosol co-administration. The aim of this work is to review the role of nutritional status and nutrient availability on markers of PUFA biosynthesis. In addition, the impact of oxidative stress developed as a result of NAFLD, a redox imbalance that may alter the expression and activity of the enzymes involved, and diminished n-3 PUFA levels by free-radical dependent peroxidation processes will be discussed.
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