Effects of dietary carbohydrate and myo-inositol on metabolic changes in rats fed 1,1,1-trichloro-2,2-bis (p-chlorophenyl) ethane (DDT).
This study was conducted to examine the effects of dietary carbohydrate [starch or sucrose (500 g/kg diet)] and myo-inositol (2 g/kg diet) on metabolic changes in rats fed 1,1,1-trichloro-2,2-bis (p-chlorophenyl) ethane (DDT) (0.7 g/kg diet). Dietary DDT enhanced serum and hepatic lipids and hepatic thiobarbituric acid reactive substances (TBA-RS), elevated hepatic activities of lipogenic enzymes such as malic enzyme (ME), glucose-6-phosphate dehydrogenase (G6PD) and fatty acid synthetase (FAS), increased hepatic cytochrome P-450 content and the activities of drug-metabolizing enzymes such as aminopyrine N-demethylase, glutathione S-transferase and 4-nitrophenol-UDP glucuronosyltransferase (4NP-UDPGT) and raised hepatic ascorbic acid and serum copper. Dietary sucrose promoted the increases in hepatic concentrations of total lipids, triglyceride and cholesterol, hepatic activity of ME, hepatic TBA-RS, cytochrome P-450 content and serum copper due to DDT feeding when compared to DDT administered in a starch based diet. Dietary myo-inositol significantly depressed the rises in hepatic concentrations of total lipids, triglyceride and cholesterol and the activities of ME and G6PD due to DDT feeding regardless of dietary carbohydrate quality. Dietary starch supplemented with myo-inositol potentiated the enhancements in hepatic activities of Phase II drug-metabolizing enzymes such as glutathione S-transferase and 4NP-UDPGT due to DDT feeding. These results suggest that dietary starch and myo-inositol can protect DDT fed rats against an accumulation of hepatic lipids, which might be mainly ascribed to the depression of hepatic lipogenesis. In addition, the present study implies that the supplementation of myo-inositol to high starch diet might improve the function of drug-metabolizing enzymes exposed to DDT.
Okazaki
Yukako
Y
Department of Human Life Sciences Education, Graduate School of Education, Hiroshima University, Higashi-Hiroshima 739-8524, Japan.
Katayama
Tetsuyuki
T
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D003300:Copper / Q000097:blood; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D003634:DDT / Q000008:administration & dosage*; D004032:Diet; D004040:Dietary Carbohydrates / Q000494:pharmacology*; D019422:Dietary Sucrose / Q000494:pharmacology; D064429:Fatty Acid Synthases / Q000378:metabolism; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D014453:Glucuronosyltransferase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D007294:Inositol / Q000494:pharmacology*; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects* / Q000378:metabolism*; D008291:Malate Dehydrogenase / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013213:Starch / Q000008:administration & dosage; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014280:Triglycerides / Q000097:blood
D004040:Dietary Carbohydrates; D019422:Dietary Sucrose; D008055:Lipids; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D007294:Inositol; D003300:Copper; D013213:Starch; D003577:Cytochrome P-450 Enzyme System; D002784:Cholesterol; D003634:DDT; D008291:Malate Dehydrogenase; D005954:Glucosephosphate Dehydrogenase; D064429:Fatty Acid Synthases; D014453:Glucuronosyltransferase; D005982:Glutathione Transferase; D001205:Ascorbic Acid