ABSTRACT
AIM To investigate the effect of fenofibrate and simvastatin on the serum free fatty acids of alcoholic fatty liver in rats. METHODS The rat model of alcoholic fatty liver was reproduced by chronic ethanol ingestion plus olive oil diet. The model rats were divided into three groups as follows: finofibrate treatment group(finofibrate 80 mg?kg -1 po, once a day),simvastatin treatment group (simvastatin 4 mg?kg -1 po, once a day)and control group without either above-mentioned treatment. Experimental rats were treated for four weeks and then sacrificed for blood sampling. Serum free fatty acids were analyzed by gas chromatography. RESULTS Fenofibrate significantly ameliorated the decrease in polyunsaturated fatty acids induced by ethanol [oleic acid:(38.212?7.788) ?g?L -1 vs (31.620?6.142) ?g?L -1,linoleic acid:(37.269?8.065) ?g?L -1 vs (30.254?9.063) ?g?L -1,arachidonic acid:(11.646?2.601) ?g?L -1 vs (9.012?1.236) ?g?L -1] accompanied by the improvement of the fat infiltration of the liver, but demonstrated no effect on the increase in serum saturated fatty acids by ethanol. In the contrast, simvastatin can aggravate the decrease in polyunsatrurated fatty acids and significantly increase the levels of satrurated fatty acids in serum induced by ethanol along with the pathological aggravation of alcoholic fatty liver. CONCLUSION The results of present study revealed that fenofibrate and simvastatin exerted different effect on the serum free fatty acids of alcoholic fatty liver. Polyunsatrurated fatty acids in the serum play an important role in the pathogenesis and treatment response of alcoholic fatty liver.
ABSTRACT
<p><b>OBJECTIVE</b>To study the relationship between aldehyde dehydrogenase (ALDH) gene polymorphism and alcoholic liver disease, and investigate the genetic pathogenesis of alcoholic liver disease (ALD).</p><p><b>METHODS</b>PCR, restriction endonuclease and electrophoresis were used, to detect the genotypes and alleles frequencies of ALDH gene in patients in the control group, alcohol dependent group and ALD group, and each group contained 20 patients.</p><p><b>RESULTS</b>The frequencies of ALDH2*1 and ALDH2*2 allele had statistic significance between control group and ALD group (x2=4.80, P<0.05), and no statistic significance between control group and alcohol dependent group. ALDH2*1/*1 was predominant in alcohol dependent group and ALD group, while ALDH2*2/*2 was not detected.</p><p><b>CONCLUSIONS</b>The gene polymorphism of ALDH is close to ALD. The allele of ALDH2*2 may be a negative risk factor for the developing of ALD</p>
Subject(s)
Adult , Humans , Male , Aldehyde Dehydrogenase , Genetics , Alleles , Gene Frequency , Liver Diseases, Alcoholic , Genetics , Polymorphism, Genetic , Risk FactorsABSTRACT
<p><b>OBJECTIVE</b>To investigate the fat decreasing effects of fenofibrate on alcoholic fatty liver and drug-induced fatty liver in rats.</p><p><b>METHODS</b>Alcoholic fatty liver and drug-induced fatty liver rats models were established. The two kinds of rats with fatty liver were seperatedly divided into fenofibrate treatment group (80 mg/kg daily) and control group without treatment. Rats were killed after four weeks, then the levels of serum triglycerides (TG), total cholesterol (TC), high density lipoprotein (HDL) and malondialdehyde (MDA), hepatic lipase (HL), lipoprotein lipase (LPL) both in serum and liver tissue were measured according to the Test Kits. Histopathological changes in liver was dyed with HE and observed under light microscope.</p><p><b>RESULTS</b>After treatment by fenofibrate, in the serum of rats with alcoholic fatty liver, the level of TG decreased significantly (1.07 mmol/L 0.06 mmol/L vs 1.56 mmol/L 0.29 mmol/L, t=5.115, p<0.001), while the level of TC had no alteration. The levels of MDA both in serum and liver tissue decreased (1.10 nmol/L 0.22 nmol/L vs 1.26 nmol/L 0.21 nmol/L, t=0.592, p<0.05; 5.92 nmol/g 1.24 nmol/g vs 7.42 nmol/g 1.22 nmol/g, t=3.477, p<0.05, respectively), while the levels of HL, LPL in serum and liver tissue increased significantly (Serum: 0.053muEq/ml/h 0.006muEq/ml/h vs 0.037 muEq/ml/h 0.006muEq/ml/h, t=-5.086, p<0.001; 0.018 muEq/ml/h 0.004 muEq/ml/h vs 0.014muEq/ml/h 0.004muEq/ml/h, t=-2.485, p<0.05. Liver tissue: 0.075muEq/ml/h 0.010muEq/ml/h vs 0.065muEq/ml/h 0.007muEq/ml/h, t=-2.437, p<0.05; 0.022 muEq/ml/h 0.014 muEq/ml/h vs 0.008 muEq/ml/h 0.002 muEq/ml/h, t=-2.876, p<0.05). Fat content in liver decreased (26.01 mg/g 1.69 mg/g vs 71.45 mg/g 2.66 mg/g, t=-43.224, p<0.001). The pathological changes of liver in fenofibrate-treated rats with alcoholic fatty liver were improved. For the drug-induced fatty liver rats, fenofibrate treatment group had no difference from the untreated control group.</p><p><b>CONCLUSION</b>Fenofibrate can significantly decrease the fat content in liver tissue of rats with alcoholic fatty liver, as well as ameliorating liver pathological changes. But fenofibrate has no effect on drug-induced fatty liver.</p>