Effects of N-acetylcysteine on sucrose-rich diet-induced hyperglycaemia, dyslipidemia and oxidative stress in rats.
This study examined whether sucrose-rich diet (SRD)-induced hyperglycaemia, dyslipidemia and oxidative stress may be inhibited by N-acetylcysteine (C(5)H(9)-NO(3)S), an organosulfur from Allium plants. Male Wistar 40 rats were divided into four groups (n=10): (C) given standard chow and water; (N) receiving standard chow and 2 mg/l N-acetylcysteine in its drinking water; (SRD) given standard chow and 30% sucrose in its drinking water; and (SRD-N) receiving standard chow, 30% sucrose and N-acetylcysteine in its drinking water. After 30 days of treatment, SRD rats had obesity with increased abdominal circumference, hyperglycaemia, dyslipidemia and hepatic triacylglycerol accumulation. These adverse effects were associated with oxidative stress and depressed lipid degradation in hepatic tissue. The SRD adverse effects were not observed in SDR-N rats. N-Acetylcysteine reduced the oxidative stress, enhancing glutathione-peroxidase activity, and normalizing lipid hydroperoxyde, reduced glutathione and superoxide dismutase in hepatic tissue of SRD-N rats. The beta-hydroxyacyl coenzyme-A dehydrogenase and citrate-synthase activities were increased in SRD-N rats, indicating enhanced lipid degradation in hepatic tissue as compared to SRD. SRD-N rats had reduced serum oxidative stress and diminished glucose, triacylglycerol, very-low-density lipoprotein (VLDL), oxidized low-density lipoprotein (ox-LDL) and cholesterol/high-density lipoprotein (HDL) ratio in relation to SRD. In conclusion, NAC offers promising therapeutic values in prevention of dyslipidemic profile and alleviation of hyperglycaemia in high-sucrose intake condition by improving antioxidant defences. N-Acetylcysteine had also effects preventing metabolic shifting in hepatic tissue, thus enhancing fat degradation and reducing body weight gain in conditions of excess sucrose intake. The application of this agent in food system via exogenous addition may be feasible and beneficial for antioxidant protection.
Diniz
Yeda S
YS
Department of Chemistry and Biochemistry, Institute of Biological Sciences, São Paulo State University, UNESP, 18618-000, Botucatu, São Paulo, Brazil.
Rocha
Katiucha K H R
KK
Souza
Gisele A
GA
Galhardi
Cristiano M
CM
Ebaid
Geovana M X
GM
Rodrigues
Hosana G
HG
Novelli Filho
José Luiz V B
JL
Cicogna
Antonio C
AC
Novelli
Ethel L B
EL
D000111:Acetylcysteine / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D019422:Dietary Sucrose / Q000008:administration & dosage; D050171:Dyslipidemias / Q000097:blood / Q000378:metabolism / Q000517:prevention & control*; D005978:Glutathione / Q000097:blood / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000097:blood / Q000378:metabolism; D006943:Hyperglycemia / Q000097:blood / Q000378:metabolism / Q000517:prevention & control*; D050356:Lipid Metabolism / Q000187:drug effects; D008054:Lipid Peroxides / Q000097:blood / Q000378:metabolism; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000097:blood / Q000378:metabolism
D000975:Antioxidants; D001786:Blood Glucose; D019422:Dietary Sucrose; D008054:Lipid Peroxides; D008055:Lipids; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D000111:Acetylcysteine