Yukako Okazaki

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.

Consumption of Some Polyphenols Reduces Fecal Deoxycholic Acid and Lithocholic Acid, the Secondary Bile Acids of Risk Factors of Colon Cancer

This study was performed to examine the effect of dietary polyphenols on fecal secondary bile acids, such as deoxycholic acid and lithocholic acid, the risk factors of colon cancer, in rats fed a high-fat diet. In experiment 1, rats were fed a 30% beef tallow diet containing 0.5% polyphenols for 3 weeks. Dietary curcumin and caffeic acid significantly reduced the fecal concentration of deoxycholic acid. Dietary caffeic acid, catechin, rutin, and ellagic acid significantly reduced fecal lithocholic acid. Fecal hyodeoxycholic acid, a metabolite of lithocholic acid, was markedly lowered by dietary curcumin, caffeic acid, catechin, and rutin. In experiment 2, rats were fed a 30 or 5% beef tallow diet with or without the addition of 0.5% curcumin. In the rats without receiving curcumin, the fecal level of deoxycholic acid was significantly higher in the high-fat diet group than in the low-fat diet group. Fecal deoxycholic acid was significantly reduced by dietary curcumin in the high-fat diets but not in the low-fat diets. The results suggest novel effects of some polyphenols favorable for colon health by reducing secondary bile acids in animals fed a high-fat diet.

Consumption of a Resistant Protein, Sericin, Elevates Fecal Immunoglobulin A, Mucins, and Cecal Organic Acids in Rats Fed a High-Fat Diet

We previously reported that consumption of a resistant protein, sericin, reduces colon tumorigenesis, constipation, and serum TG in rodents. The present study was conducted to elucidate the effects of dietary sericin on the intestinal luminal environment in rats fed a high-fat (HF) diet. Rats were fed 300 or 50 g/kg of beef tallow with or without 40 g/kg sericin, a protein purified from cocoons of Bombix mori, for 3 wk. Intestinal luminal variables, including IgA (index of intestinal immune function), mucins (index of barrier function), organic acids, microflora, and secondary bile acids, were measured. Dietary sericin markedly elevated fecal IgA in the HF diet group (3-fold, P < 0.05) but not in the low-fat (LF) diet group. Fecal mucin levels were elevated by sericin intake in the HF diet group (P < 0.05). Cecal organic acids, including acetate, propionate, n-butyrate, and succinate, were significantly lower in the HF diet group compared with the LF diet group. Dietary sericin significantly elevated cecal acetate and n-butyrate in the HF diet group but not in the LF diet group. Compared with the LF diet, the HF diet significantly increased serum TG in the untreated group but not in those fed sericin. The HF diet increased lower density lipoprotein (VLDL + IDL + LDL) cholesterol and it was reduced by sericin intake (P < 0.05). There was an inverse correlation between serum TG and cecal acetate (Spearman rank correlation coefficient = -0.63; P < 0.001). The profile of microflora in cecal digesta and fecal secondary bile acids (a risk factor for colon cancer) did not differ between the HF diet and HF diet with sericin groups. These results suggest a novel and favorable effect of sericin on colon health by modulating intestinal immune and barrier functions and fermentation in rats fed a HF diet.

Consumption of Sericin Reduces Serum Lipids, Ameliorates Glucose Tolerance and Elevates Serum Adiponectin in Rats Fed a High-Fat Diet

The effect was examined of dietary sericin on the lipid and carbohydrate metabolism in rats fed with a high-fat diet. The rats were fed with a 20% beef tallow diet with or without sericin at the level of 4% for 5 weeks. The final body weight and white adipose tissue weight were unaffected by dietary manipulation. The consumption of sericin significantly reduced the serum levels of triglyceride, cholesterol, phospholipids and free fatty acids. Serum very-low-density lipoprotein (VLDL)-triglyceride, VLDL-cholesterol, low-density lipoprotein (LDL)-cholesterol and LDL-phospholipids were also significantly reduced by the sericin intake. Liver triglyceride and the activities of glucose 6-phosphate dehydrogenase and malic enzyme, the lipogenic enzymes, were also reduced by the sericin intake. Dietary sericin caused a marked elevation in serum adiponectin. The consumption of sericin suppressed the increases in plasma glucose and insulin levels after an intraperitoneal glucose injection. These results imply the usefulness of sericin for improving the lipid and carbohydrate metabolism in rats fed on a high-fat diet.

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.

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.

Burdock Fermented by Aspergillus awamori Elevates Cecal Bifidobacterium, and Reduces Fecal Deoxycholic Acid and Adipose Tissue Weight in Rats Fed a High-Fat Diet

This study investigated the effects of dietary supplementation with burdock powder and Aspergillus awamori-fermented burdock powder at 5% on the intestinal luminal environment and body fat in rats fed a high-fat (HF) diet. Food intake and growth were unaffected by dietary manipulation. Consumption of the burdock and fermented burdock diets significantly elevated fecal IgA and mucins (indices of intestinal immune and barrier functions) and reduced fecal lithocholic acid (a risk factor for colon cancer) (p<0.05). The fermented burdock diet markedly elevated cecal Bifidobacterium and organic acids, including lactate, acetate, propionate, and butyrate, and reduced fecal deoxycholic acid (a risk factor for colon cancer) and perirenal adipose tissue weight (p<0.05), but the burdock diet did not. These results suggest that consumption of fermented burdock improves the intestinal luminal environment and suppresses obesity in rats fed a HF diet.

Cecal Succinate Elevated by Some Dietary Polyphenols May Inhibit Colon Cancer Cell Proliferation and Angiogenesis

This study demonstrated that 0.5% dietary rutin, ellagic acid, or curcumin markedly increased cecal succinate levels in rats fed a high-fat diet, whereas catechin, caffeic acid, and quercetin did not. Other organic acids were modestly or hardly affected by polyphenols. To clarify the effects of succinate levels increased by polyphenols, this study examined the effects of succinate on the growth and proliferation of colon cancer cells and angiogenesis. The growth and proliferation of HT29 human colon cancer cells and angiogenesis in an ex vivo model were significantly inhibited by succinate at a dose close to that in the cecum of rats fed polyphenols. Furthermore, succinate inhibited the migration of human umbilical vein endothelial cells. These findings suggest that the consumption of some polyphenols affects the health and diseases of the large intestine by elevating succinate.

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.