Effect of five cysteine-containing compounds on three lipogenic enzymes in Balb/cA mice consuming a high saturated fat diet.
The in vivo effects of N-acetyl cysteine (NAC), S-allyl cysteine, S-ethyl cysteine (SEC), S-methyl cysteine (SMC), and S-propyl cysteine (SPC) against hyperlipidemia development and oxidation stress in Balb/cA mice consuming a high saturated fat diet were examined. The influence of these agents on plasma levels of glucose, insulin, uric acid, TG, cholesterol, and the activity of three lipogenic enzymes--glucose-6-phosphate dehydrogenase, malic enzyme, and FA synthase--was determined. All mice consumed the coconut oil-basd, high saturated fat diet, water, and cysteine or one of the five cysteine-containing compounds for 4 wk. The diet with 18% saturated fat significantly elevated the activity of three lipogenic enzymes and significantly increased TG and cholesterol biosynthesis in plasma and liver (P < 0.05). When compared with the water and cysteine groups, the treatments from five cysteine-containing agents significantly reduced high saturated fat diet-increased malic enzyme and FA synthase activities, and significantly lowered TG levels in plasma and liver (P< 0.05); however, only NAC, SAC, and SMC treatments significantly reduced cholesterol levels in plasma and liver (P < 0.05). The five cysteine-containing agents significantly restored high saturated fat diet-decreased glutathione peroxidase (GPX) activity in liver (P< 0.05); however, only SMC and SPC significantly restored GPX activity in heart and kidney (P< 0.05). These agents also significantly improved high saturated fat diet-related hyperglycemia, hyperuricemia, and oxidation stress (P < 0.05). These data support the hypothesis that these compounds are potential multiply-protective agents for hyperlipidemia prevention or therapy.
Lin
Chun-che
CC
Department of Internal Medicine, Chungshan Medical University Hospital, Taiwan, Republic of China.
Yin
Mei-chin
MC
Hsu
Cheng-chin
CC
Lin
Meng-pei
MP
D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003545:Cysteine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D004032:Diet; D004041:Dietary Fats / Q000494:pharmacology; D064429:Fatty Acid Synthases / Q000187:drug effects* / Q000378:metabolism; D005227:Fatty Acids / Q000494:pharmacology; D005954:Glucosephosphate Dehydrogenase / Q000187:drug effects* / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000187:drug effects / Q000378:metabolism; D006949:Hyperlipidemias / Q000188:drug therapy / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007668:Kidney / Q000187:drug effects / Q000201:enzymology; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008291:Malate Dehydrogenase / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009206:Myocardium / Q000201:enzymology; D014527:Uric Acid / Q000097:blood
D001786:Blood Glucose; D004041:Dietary Fats; D005227:Fatty Acids; D007328:Insulin; D014527:Uric Acid; C028742:S-propylcysteine; C065299:S-allylcysteine; C008425:S-methylcysteine; C026826:S-ethylcysteine; D008291:Malate Dehydrogenase; C031917:malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+); D005954:Glucosephosphate Dehydrogenase; D005979:Glutathione Peroxidase; D064429:Fatty Acid Synthases; D003545:Cysteine; D000111:Acetylcysteine