| Incidence of non-alcoholic fatty liver disease (NAFLD) increases, with similarmain risk factors as Metabolic Syndrome, closely correlated with serum lipid andinsulin resistance. Dietary factors, especially maladjustment of dietary fatty acidpattern, are the main causes of fat metabolism related diseases. However, it isimpossible to accurately calculate the content of dietary lipids and fatty acids.Short-term dietary influences the plasma/serum membrane fatty acid, while long-termdietary influences the platelet membrane fatty acid. Therefore, we applied plasma andplatelet membrane phospholipids (PL) fatty acid compositions as biomarkers of thedietary fat intake in this study. By measuring plasma and platelet membrane PL fattyacid compositions of NAFLD subjects and control subjects, we analyzed therelationship between NAFLD and dietary fatty acid intake.101 NAFLD subjects aged between 22～78 and 108 control subjects agedbetween 20～76 were recruited from Zhejiang Hospital. Diagnosis criteria of NAFLDwas applied from Society of Liver Diseases, CMA. The exclusion criteria for thisstudy were: evidence of renal disease, cardiovascular disease, diseases of thyroid glandand adrenal gland, diabetes mellitus, hypothyroid antilipidic therapy, weight losing therapy,intense physical activity. The subjects'sex, age, height, weight, blood pressure, dietaryhabits, smoking & alcohol history, drug therapy history, and heart, brain, liver, kidneydisease history and family disease history were questioned. After limosis venousblood collection, blood biochemical parameters were tested by the standard methods,plasma and platelet membrane PL fatty acid compositions were analyzed by GC.Results: age, height, weight, BMI, blood pressure were significantly higher inNAFLD subjects than in control subjects. Biochemical parameters ALB,ALP,LDL-C,FINS,HOMA-IR mean value in NAFLD subjects were also significantlyhigher in NAFLD subjects than in control subjects, but HDL-C lower in NAFLDsubjects than in control subjects. Multifactor logistic stepwise regression analysisshowed, smoking, BMI, TG and HOME-IR were independent risk factors ofNAFLD, while HDL-C was a protective factor of NAFLD. Plasma total saturatedfatty acids were significantly higher in NAFLD subjects than in control subjects,while polyunsaturated fatty acids lower in NAFLD subjects than in control subjects. Plasma membrane PL fatty acid was positively correlated with NAFLD independentrisk factor BMI. Plasma membrane PL C 14: 1, C 18: 1 n-7, C20: 0, C22: 4 n-6, C22:2 n-6 and Total PUFA percentage were significantly lower in NAFLD subjects than incontrol subjects. HOMA-IR was negatively correlated with plasma PL C20:4 n-6,C22: 5 n-3 and n-3 PUFA, n-6 PUFA concentration, positively correlated with C22: 2n-6, negatively correlated with PUFA. Plasma PL total fatty acids were 113.6mg/100ml in control subjects, 128.9 mg/100ml in NAFLD subjects. Platelet PL n-3PUFA were significantly lower in NAFLD subjects than in control subjects, while n-6PUFA and n-6/ n-3 PUFA were significantly higher in NAFLD subjects than incontrol subjects.Conclusions: ALP,ALT,GGT are significantly higher in NAFLD subjects thanin control subjects. Liver cell fat denaturalizes in NAFLD subjects, thus liver cells areharmed, and liver functions are influenced, smoking, BMI, TG and HOME-IR areindependent risk factors of NAFLD, while HDL-C is a protective factor of NAFLD;NAFLD is closely correlated with metabolic syndrome.N-3 PUFA prevents liver cells from denaturalization, but high n-6/n-3 PUFAinduces NAFLD. Plasma and platelet membrane PL fatty acid composition differencesbetween NAFLD subjects and control subjects indicate that incidence of NAFLD iscorrelated with maladjustment of dietary fatty acid.
|
PDF Full Text Request