Habitual food intake and polyunsaturated fatty acid deficiency in liver cirrhosis

Okita, Misako; Sasagawa, Takayo; Tomioka, Kayoko; Hasuda, Kaori; Ota, Yasuko; Suzuki, Kazuhiko; Watanabe, Akïharu

doi:10.1016/s0899-9007(01)00756-0

Cited by 17 publications

(14 citation statements)

References 14 publications

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“…However, the possibility that significant changes may occur with increased severity of hepatic lesions cannot be ruled out. In agreement with this suggestion, low plasma contents of LCPUFA were observed in patients with end-stage liver disease [37] or in cirrhotic patients with hepatitis B and C viruses [38]. Low contents of LCPUFA in plasma were also found in rats with carbon tetrachloride-induced liver damage, which correlates with the depletion of LCPUFA in the liver [39].…”

Section: Discussionsupporting

confidence: 68%

Increase in long-chain polyunsaturated fatty acid n−6/n−3 ratio in relation to hepatic steatosis in patients with non-alcoholic fatty liver disease

et al. 2004

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Hepatic steatosis is a major feature associated with NAFLD (non-alcoholic fatty liver disease). The aims of the present study were to assess the levels of PUFA (polyunsaturated fatty acids) in liver total lipids, triacylglycerols (triglycerides) and phospholipids of NAFLD patients in relation to those in adipose tissue and hepatic indexes related to oxidative stress as factors contributing to hepatic steatosis. Eleven control subjects and 19 patients with NAFLD were studied. Analysis of liver and abdominal adipose tissue fatty acids was carried out by GLC. The liver content of protein carbonyl groups and malondialdehyde were taken as indexes related to oxidative stress. NAFLD patients had a depletion in LCPUFA (long-chain PUFA) of the n -6 and n -3 series in liver triacylglycerols, with decreased 20:4, n -6/18:2, n -6 and (20:5, n -3+22:6, n -3)/18:3, n -3 ratios, whereas liver phospholipids contained higher n -6 and lower n -3 LCPUFA. These findings were accompanied by an enhancement of (i) n -6/ n -3 ratio in liver and adipose tissue, (ii) 18:1, n -9 trans levels in adipose tissue, and (iii) hepatic lipid peroxidation and protein oxidation indexes. It is concluded that a marked enhancement in LCPUFA n -6/ n -3 ratio occurs in the liver of NAFLD patients, a condition that may favour lipid synthesis over oxidation and secretion, thereby leading to steatosis. Depletion of hepatic LCPUFA may result from both defective desaturation of PUFA, due to inadequate intake of precursors, such as 18:3, n -3, and higher intake of the 18:1, n -9 trans isomer leading to desaturase inhibition, and from an increased peroxidation of LCPUFA due to oxidative stress.

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Section: Discussionsupporting

confidence: 68%

Increase in long-chain polyunsaturated fatty acid n−6/n−3 ratio in relation to hepatic steatosis in patients with non-alcoholic fatty liver disease

et al. 2004

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“…(53,54) Generally, the habitual diet of Serbian adults is characterized by a high intake of energy derived from dietary fats, combined with a lower protein and complex carbohydrate intake. (27,28) Dietary n -6/ n -3 PUFA ratio should be maintained between 2.8 and 3.2 in chronic liver disease, (55,56) but this ratio in the patients in our study was 12.2 (10.7 in well-nourished and 14.8 in malnourished patients). Consequently, it is important to emphasize that patients have dietary habits to consume (sunflower-oil based) n -6 PUFA cooking oil as a part of their usual diet with low fish intake.…”

Section: Discussionmentioning

confidence: 64%

“…(52) It is important to note that lower levels of LA found in our malnutrition patients could be to an impaired fat absorption related to decrease levels of bile salt and to lymphangiectasia, (5) frequently observed in cirrhosis. The derangement of the serum phospholipids fatty acid profile in patients with an acceptable nutritional status depends mainly on hepatocellular insufficiency (2,11,55) which led to low n -6/ n -3 ratio in this cirrhotic patients. The clinical significance of low PUFA status is still unknown, although abnormal FA profile may contribute to clinical problems such as itching, pruritus, abnormal perspiration, susceptibility to infection, delayed wound healing, anemia, thrombocytopenia, diminished platelet aggregation, dysfunction in eicosanoid synthesis and diminished immune system status as seen in patients with cirrhosis.…”

Section: Discussionmentioning

confidence: 94%

Abnormalities in the serum phospholipids fatty acid profile in patients with alcoholic liver cirrhosis - a pilot study

Ristić‐Medić

Takić

Vučić

et al. 2013

J. Clin. Biochem. Nutr.

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The fatty acid composition of serum phospholipids were analyzed in 20 patients with alcoholic liver cirrhosis (11 with malnutrition and 9 with acceptable nutritional status); 25 healthy age and sex-matched adults were used as controls. Cirrhotic patients showed higher levels of palmitic acid and total saturated fatty acids than healthy subjects. Total n-6 and n-3 polyunsaturated fatty acids (PUFA), and levels of linoleic, dihomo-gama linolenic, arachidonic, and docosahexaenoic acid were significantly lower (p<0.001) in patients with alcoholic cirrhosis compared to healthy controls. Significant changes were also found between patients stratified according to nutritional status. In particular, the sum of n-3 PUFA was significantly lower (p<0.001) and ratio of n-6/n-3 fatty acids was higher (p<0.01) in malnourished patients when compared to the patients with acceptable nutritional status. Furthermore, important changes in the levels of saturated fatty acids, palmitoleic and oleic acid and long-chain PUFA were found in well-nourished patients with alcoholic cirrhosis as well. Our present data confirmed evidence that malnutrition is one of the factors that led to lower levels of polyunsaturated fatty acids in patients with alcoholic liver cirrhosis. PUFA supplementation in the latter needs further investigation.

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“…The spots corresponding to phospholipid were scraped from the plates and transmethylated using acetylchloride/methanol (5 : 50, v/v). The fatty acid methyl esters were analyzed by gas-liquid chromatography (Model GC-14A: Shimadzu, Kyoto, Japan) as described previously ( 18 ). Statistical analyses.…”

Section: Subjects After Approval From Okayama Saiseikaimentioning

confidence: 99%

Serum Cytokeratin 18 M30 Antigen Level and Its Correlation with Nutritional Parameters in Middle-Aged Japanese Males with Nonalcoholic Fatty Liver Disease (NAFLD)

Tabuchi

Tomioka

Kawakami

et al. 2010

J Nutr Sci Vitaminol

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Summary Cytokeratin (CK) 18 M30 antigen has been proposed as a diagnostic marker of nonalcoholic fatty liver disease (NAFLD). We studied serum CK18 M30 antigen level and examined the correlations among CK18 and biological data, dietary intake, and plasma fatty acid composition in middle-aged Japanese males with (NAFLD; n ϭ 42) and without NAFLD (control; n ϭ 35). NAFLD was diagnosed if subjects showed fatty liver on abdominal ultrasonography and their alcohol consumption was Ͻ 20 g/d. They were also confirmed to have negative serological results for tests of autoimmune liver disease and hepatitis B and C. In the NAFLD group, body mass index, waist circumference, serum M30 antigen, alanine transaminase (ALT), cholinesterase, triacylglycerol, LDL-cholesterol, and HbA1c were significantly higher than in the control group. In the fatty acid analysis of plasma phospholipids, significantly higher dihomo-␥ -linolenic acid (DGLA), total saturated fatty acids (SFA), and palmitic/linoleic acid ratio as well as lower arachidonic acid/DGLA ratio were observed in the NAFLD group compared with the control group. In the NAFLD group, M30 antigen was correlated positively with serum ALT, plasma DGLA, dietary SFA, and serum TNF-␣ as determined by partial correlation analysis controlled for BMI. On the basis of multivariate regression analysis using a stepwise method, M30 antigen was significantly associated with ALT and plasma DGLA. Regarding the determinants of NAFLD as revealed by logistic regression analysis, a high odds ratio was observed for plasma DGLA. In conclusion, members of the NAFLD group showed higher levels of serum CK18 M30 antigen and M30 antigen was strongly associated with serum ALT and plasma DGLA. Abnormal fatty acid metabolism may be a factor that causes aggravation of NAFLD.

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Habitual food intake and polyunsaturated fatty acid deficiency in liver cirrhosis

Cited by 17 publications

References 14 publications

Increase in long-chain polyunsaturated fatty acid n−6/n−3 ratio in relation to hepatic steatosis in patients with non-alcoholic fatty liver disease

Increase in long-chain polyunsaturated fatty acid n−6/n−3 ratio in relation to hepatic steatosis in patients with non-alcoholic fatty liver disease

Abnormalities in the serum phospholipids fatty acid profile in patients with alcoholic liver cirrhosis - a pilot study

Serum Cytokeratin 18 M30 Antigen Level and Its Correlation with Nutritional Parameters in Middle-Aged Japanese Males with Nonalcoholic Fatty Liver Disease (NAFLD)

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