Tetsuyuki Katayama

Oxalic acid is available as a natural antioxidant in some systems

Oxalic acid is found in a wide variety of plants. This study showed that oxalic acid suppressed in vitro lipid peroxidation in a concentration-dependent manner. Furthermore, oxalic acid reduced the rate of ascorbic acid oxidation in the presence of hydrogen peroxide and Cu(2+). These results suggest that oxalic acid is available as a natural antioxidant.

Effect of dietary level of phytic acid on hepatic and serum lipid status in rats fed a high-sucrose diet.

The effect of dietary 0.02–10% sodium phytate on the hepatic and serum lipid status of rats fed a high-sucrose diet for 14 d was investigated. Hepatic levels of triglyceride and cholesterol and lipogenic enzymes activity were reduced with increasing dietary phytate level. The addition of 10% sodium phytate drastically depressed growth, food intake, and serum triglyceride and cholesterol levels.

Effects of dietary myo-inositol or phytic acid on hepatic concentrations of lipids and hepatic activities of lipogenic enzymes in rats fed on corn starch or sucrose

This study was undertaken with growing rats to compare the effects of dietary 0.1% myo-inositol or 0.5% sodium phytate on the changes in the metabolism of hepatic lipids due to sucrose feeding. Liver weight, hepatic concentrations of total lipids and triglyceride, and hepatic activities of glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49), malic enzyme (ME, EC 1.1.1.40), fatty acid synthetase (FAS, EC 2.3.1.85), citrate cleavage enzyme (CCE, EC 4.1.3.8) and acetyl-CoA carboxylase (CBX, EC 6.4.1.2) were remarkably higher in rats fed on sucrose than in rats fed on corn starch for 12 or 13 days. Dietary myo-inositol and phytate significantly depressed the rises in liver weight, hepatic concentrations of total lipids and triglyceride, and hepatic activities of G6PD, ME, FAS and CCE due to sucrose feeding. These results suggested that dietary myo-inositol and phytate both can protect sucrose-fed animals against an accumulation of hepatic lipids, which might be at least in part ascribed to the depression in the hepatic lipogenesis.

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.

Elevated concentrations of α-tocopherol, ascorbic acid, and serum lipids in rats fed polychlorinated biphenyls, chlorobutanol, or phenobarbital

Abstract Experiments were conducted with growing rats to investigate the effects of dietary 0.05% polychlorinated biphenyls (PCB), 0.3% chlorobutanol (Chloretone), and 0.2% phenobarbital sodium on intestinal absorption of α-tocopherol and serum and tissue lipids. and the influence of dietary 5% pectin and 0.2% ethyl p-chlorophenoxyisobutyrate (clofibrate) on the changes in these lipids due to dietary 0.4% Chloretone. Dietary addition of PCB increased serum concentrations of α-tocopherol, cholesterol, and phospholipids. These were mainly attributed to the increments in the fraction of high-density lipoproteins. PCB intake increased tissue α-tocopherol and apparent absorption of α-tocopherol from intestine. Similar changes in serum and tissue lipids and in intestinal absorption of α-tocopherol were observed with dietary Chloretone and phenobarbital. Dietary clofibrate and pectin depressed the increase in serum concentrations of these lipids by Chloretone. Changes in serum levels of α-tocopherol, cholesterol, and phospholipids correlated with those in apparent absorption of α-tocopherol. These results suggest that the increase in serum cholesterol and phospholipids due to xenobiotics relates to the increase in serum and tissue α-tocopherol.

Dietary phytic acid modulates characteristics of the colonic luminal environment and reduces serum levels of proinflammatory cytokines in rats fed a high-fat diet

Dietary phytic acid (PA; myo-inositol [MI] hexaphosphate) is known to inhibit colon carcinogenesis in rodents. Dietary fiber, which is a negative risk factor of colon cancer, improves characteristics of the colonic environment, such as the content of organic acids and microflora. We hypothesized that dietary PA would improve the colonic luminal environment in rats fed a high-fat diet. To test this hypothesis, rats were fed diets containing 30% beef tallow with 2.04% sodium PA, 0.4% MI, or 1.02% sodium PA + 0.2% MI for 3 weeks. Compared with the control diet, the sodium PA diet up-regulated cecal organic acids, including acetate, propionate, and n-butyrate; this effect was especially prominent for cecal butyrate. The sodium PA + MI diet also significantly increased cecal butyrate, although this effect was less pronounced when compared with the sodium PA diet. The cecal ratio of Lactobacillales, cecal and fecal mucins (an index of intestinal barrier function), and fecal β-glucosidase activity were higher in rats fed the sodium PA diet than in those fed the control diet. The sodium PA, MI, and sodium PA + MI diets decreased levels of serum tumor necrosis factor α, which is a proinflammatory cytokine. Another proinflammatory cytokine, serum interleukin-6, was also down-regulated by the sodium PA and sodium PA + MI diets. These data showed that PA may improve the composition of cecal organic acids, microflora, and mucins, and it may decrease the levels of serum proinflammatory cytokines in rats fed a high-fat, mineral-sufficient diet.

Effects of dietary myo-inositol, D-chiro-inositol and L-chiro-inositol on hepatic lipids with reference to the hepatic myo-inositol status in rats fed on 1,1,1 -trichloro -2,2 -bis (p-chlorophenyl) ethane

The effects of dietary 0.2% inositol stereoisomers on the hepatic lipids and myo-inositol (MI) status in rats fed with 1,1,1-trichloro-2,2-bis (p-chlorophenyl) ethane (DDT) were investigated. Dietary MI reduced the hepatic lipids in the rats fed with DDT. Dietary D-chiro-inositol (DCI) and L-chiro-inositol (LCI) both had a promoting effect on the increase in hepatic lipids due to DDT feeding. Dietary MI enhanced the hepatic free MI level and the phosphatidylinositol/phosphatidylcholine ratio, but dietary DCI reduced the level and ratio.

Effect of Dietary Phytic Acid on Hepatic Activities of Lipogenic and Drug-Metabolizing Enzymes in Rats Fed 1,1,1-trichloro-2,2-bis (P-chlorophenyl) Ethane (DDT)

This study was conducted to examine the influence of dietary sodium phytate (10.2g/kg diet) on hepatic activities of lipogenic and drug-metabolizing enzymes in rats fed 1,1,1-trichloro-2,2-bis (P-chlorophenyl) ethane (DDT) (0.7g/kg diet). Dietary DDT enhanced hepatic lipids, elevated hepatic activities of lipogenic enzymes, increased serum levels of cholesterol and phospholipid, and raised hepatic activities of drug-metabolizing enzymes. Dietary phytate significantly decreased the rises in hepatic lipids and the activities of lipogenic enzymes due to DDT feeding. The enhancement in hepatic activity of phase II drug-metabolizing enzyme, glutathione S-transferase, that had been caused by DDT feeding was significantly enhanced with dietary phytate. These results suggest that dietary phytate can protect DDT-fed animals against an accumulation of hepatic lipids, by depressing of hepatic lipogenesis. The present study also implies that dietary phytate might improve the function of drug-metabolizing enzymes exposed to DDT.

Effect of dietary addition of myo-inositol on lipid metabolism in rats fed sucrose or corn starch

Abstract The effect of dietary addition of myo-inositol on lipid metabolism was examined in rats fed diets containing either sucrose or corn starch for 16–17 days. Sucrose-fed rats showed significant increases in hepatic weight, total lipids, triglyceride, cholesterol and serum triglyceride, accompanied by the activities of hepatic glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49) and malic enzyme (ME, EC 1.1.1.40), compared to rats fed corn starch diet. The increases in these parameters due to sucrose feeding were clearly depressed by dietary myo-inositol. Sucrose intake also increased serum level of phospholipid, but the effect was not influenced by dietary myo-inositol. In the animals fed corn starch, dietary myo-inositol had no apparent effect on lipid metabolic parameters mentioned above. These results suggest that an exogenous source of myo-inositol may be of importance to animals fed sucrose when compared to rats fed corn starch.

Effects of dietary myo-inositol related compounds on sucrose-mediated hepatic lipid accumulation in rats

We have previously shown that dietary myo-inositol and phytic acid depress elevations of hepatic lipids and of hepatic lipogenic enzymes activities in rats fed a high-sucrose diet. In the present study, we examined whether dietary phytin (Calcium magnesium phytate) normalizes the enhancements of hepatic lipid parameters caused by sucrose feeding as well as dietary myo-inositol or phytate (sodium phytate), and whether this normalizing effect of phytate is caused by a mechanism involving reduced intestinal sucrase activity. Male Wistar rats were fed a sucrose-based diet (650g/kg diet) with supplementation of myo-inositol (1g/kg diet), phytate (sodium phytate, 5.13g/kg diet) or phytin (Calcium Magnesium phytate, 4.23g/kg diet). Phytin feeding reduced liver weight, hepatic concentrations of total lipids and triglyceride, and hepatic activities of glucose-6-phosphate dehydrogenase (G6PD, EC 1.1.1.49), malic enzyme (ME, EC 1.1.1.40) and fatty acid synthetase (FAS, EC 2.3.1.85) in rats fed the sucrose-based diet as well as myo-inositol or phytate. Dietary phytate had no influence on intestinal activities of enzymes including sucrase (EC 3.2.1.48). We speculated that the ameliorative effect of dietary myo-inositol, phytate or phytin on sucrose-induced fatty liver is not mediated through altering intestinal absorption of sucrose.