Effects of cysteine-containing compounds on biosynthesis of triacylglycerol and cholesterol and anti-oxidative protection in liver from mice consuming a high-fat diet.
Effects of n-acetyl cysteine (NAC), s-ethyl cysteine (SEC), s-propyl cysteine (SPC) and cysteine on enzymes participating in biosynthesis of TAG and cholesterol, and antioxidant protection in liver from mice consuming a high-saturated fat diet was examined. The high-fat diet provided 70 % fat energy, in which saturated fat was 55 % of total fat. NAC, SEC, SPC or cysteine, each agent at 1 g/l, was directly added into the drinking water as a supplement for 4 weeks. Results showed high saturated fat significantly increased hepatic TAG and total cholesterol contents (P < 0.05) via enhancing the activity and mRNA expression of malic enzyme, fatty acid synthase and 3-hydroxy-3-methylglutaryl coenzyme A reductase (P < 0.05). The intake of NAC, SEC or SPC significantly decreased TAG and total cholesterol levels (P < 0.05) via lowering the activity and mRNA expression of these three lipogenic-related enzymes (P < 0.05). NAC, SEC or SPC treatment also significantly suppressed high saturated fat-induced hepatic mRNA expression of sterol regulatory element-binding protein (SREBP)-1c and SREBP-2 (P < 0.05). High saturated fat decreased hepatic content of glutathione, and the activity of catalase and glutathione peroxidase (P < 0.05). The intake of NAC, SEC or SPC significantly increased hepatic glutathione content (P < 0.05), restored the activity and mRNA expression of glutathione peroxidase, and alleviated the high saturated fat-induced oxidative stress (P < 0.05). These results support that NAC, SEC and SPC are potent agents for affecting hepatic biosynthesis of TAG and cholesterol, and protecting liver against high saturated fat-associated oxidative damage.
Lin
Chun-Che
CC
Department of Internal Medicine, Chung Shan Medical University Hospital, 110, Sec.1, Chien-Ku N Rd., Taichung City, Taiwan, ROC.
Yin
Mei-Chin
MC
D000111:Acetylcysteine / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000378:metabolism; D002784:Cholesterol / Q000032:analysis / Q000096:biosynthesis*; D003545:Cysteine / Q000031:analogs & derivatives / Q000378:metabolism* / Q000494:pharmacology; D004041:Dietary Fats / Q000008:administration & dosage* / Q000378:metabolism; D064429:Fatty Acid Synthases / Q000235:genetics / Q000378:metabolism; D005978:Glutathione / Q000032:analysis / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006903:Hydroxymethylglutaryl CoA Reductases / Q000235:genetics / Q000378:metabolism; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism*; D008291:Malate Dehydrogenase / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051780:Sterol Regulatory Element Binding Protein 1 / Q000378:metabolism; D051782:Sterol Regulatory Element Binding Protein 2 / Q000378:metabolism; D051779:Sterol Regulatory Element Binding Proteins / Q000235:genetics / Q000378:metabolism; D014280:Triglycerides / Q000032:analysis / Q000096:biosynthesis*
D000975:Antioxidants; D004041:Dietary Fats; D012333:RNA, Messenger; C497390:SREBF2 protein, human; D051780:Sterol Regulatory Element Binding Protein 1; D051782:Sterol Regulatory Element Binding Protein 2; D051779:Sterol Regulatory Element Binding Proteins; D014280:Triglycerides; C028742:S-propylcysteine; D002784:Cholesterol; C026826:S-ethylcysteine; D006903:Hydroxymethylglutaryl CoA Reductases; D008291:Malate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D064429:Fatty Acid Synthases; D005978:Glutathione; D003545:Cysteine; D000111:Acetylcysteine