Relation of plasma polyunsaturated fatty acids (PUFA) with the mortality in liver cirrhosis (LC). Multivariate analysis

Polyunsaturated fatty acid deficiency reverses effects of alcohol on mitochondrial energy metabolism

“…On the one hand, PUFA deficiency may have deleterious functional repercussions, because PUFA enclose important biological functions such as cell membrane components, which regulate membrane fluidity and protein activities, and as precursors of biologically active compounds. Such detrimental effect is suggested by the finding that PUFA deficiency is an independent predictive factor of mortality in patients with alcoholic cirrhosis [1]. On the other hand, PUFA deficiency could be viewed as an adaptive phenomenon having beneficial effects.…”

“…Polyunsaturated fatty acids (PUFA) deficiency is a common finding in patients with alcoholic liver disease [1][2][3]. Its role in pathogenesis of liver disease is unclear and the suitability of reversing such PUFA deficiency remains controversial [4,5].…”

Effects of dietary supplementation with arachidonic acid on platelet and renal function in patients with cirrhosis

“…cholesterol and phosphatidylcholine, in different cell types such as platelets, red blood cells (RBCs) and kidney brush-border membranes [7][8][9][10][11][12][13][14]. Changes in membrane fatty acids consist of elevation of monounsaturated fatty acids at the expense of saturated fatty acids and AA [7,8,[14][15][16]. AA, a minor component of the normal diet, is mostly synthesized from linoleic acid (18:2ω6) provided by the diet, which is therefore a major determinant in the overall availability of AA.…”

Reduced Brain Content of Arachidonic Acid and Docosahexaenoic Acid Is Related to the Severity of Liver Fibrosis

“…Many studies had stated that 18 carbon essential fatty acids in the diets of ESLD patients should have been sufficient to prevent classical essential fatty acid deficiency [18]. However, it was noted that acute supplementation with fats high in linoleic acid and alpha linolenic acid content through IV feeding, along with adequate protein and calories, were not able to change the diminished level of AA, EPA, and DHA in plasma phospholipids in ESLD, suggesting that the conversion of 18 carbon essential fatty acids to their elongated and desaturated forms was impaired [19][20][21]. Besides the decreasing content of AA, EPA, and DHA in plasma phospholipid in ESLD, our study demonstrated that the degree of liver cirrhosis affects significantly the level of AA and DHA in brain membrane phospholipid as well.…”