The effects of different high-fat (lard, soybean oil, corn oil or olive oil) diets supplemented with fructo-oligosaccharides on colonic alkaline phosphatase activity in rats.

PURPOSE: We recently reported that fermentable non-digestible carbohydrates including fructo-oligosaccharides (FOS) commonly elevate colonic alkaline phosphatase (ALP) activity and the expression of IAP-I, an ALP gene, in rats fed a high-fat (HF) diet, and also elevate gut mucins and modulate gut microbiota. This study aims to investigate whether dietary fat types influence the effect of FOS on colonic ALP activity and the luminal environment in HF-fed rats. METHODS: Male Sprague-Dawley rats were fed a diet containing 30% soybean oil, corn oil, olive oil or lard with or without 4% FOS for 2 weeks. Colon ALP activity, gene expression, and gut luminal variables including mucins and microbiota were measured. RESULTS: In the lard diet groups, dietary FOS significantly elevated colonic ALP activity and the expression of IAP-I. The elevating effect of FOS on colonic ALP activity was also observed in the olive oil diet groups, although here the IAP-I expression was not changed. However, the soybean oil and corn oil diet groups did not exhibit the elevating effect of FOS on colon ALP. Fecal ALP and mucins were significantly elevated by dietary FOS regardless of dietary fat types, and the effect of FOS was prominent in the lard diet groups. The number of Lactobacillus spp. observed in fecal matter was significantly increased by dietary FOS in the lard and olive oil diet groups, but not in the soybean oil and corn oil diets groups. CONCLUSION: This study suggests that dietary fat types may change the effect of FOS on the colonic luminal environment including the ALP activity in rats fed a high-fat diet.

Consumption of non-digestible oligosaccharides elevates colonic alkaline phosphatase activity by up-regulating the expression of IAP-I, with increased mucins and microbial fermentation in rats fed a high-fat diet.

We have recently reported that soluble dietary fibre, glucomannan, increased colonic alkaline phosphatase (ALP) activity and the gene expression without affecting the small-intestinal activity and that colonic ALP was correlated with gut mucins (index of intestinal barrier function). We speculated that dietary fermentable carbohydrates including oligosaccharides commonly elevate colonic ALP and gene expression as well as increase mucin secretion and microbial fermentation. To test this hypothesis, male Sprague-Dawley rats were fed a diet containing 30 % lard with or without 4 % fructo-oligosaccharides (FOS), galacto-oligosaccharides (GOS), raffinose (RAF) and lactulose (LAC), which are non-digestible oligosaccharides or isomalto-oligosaccharides (IMOS; some digestible oligosaccharides) for 2 weeks. Colon ALP activity, the gene expression and gut luminal variables including mucins, organic acids and microbiota were measured. Colonic ALP was significantly elevated in the FOS, RAF and LAC groups, and a similar trend was observed in the GOS group. Colonic expression of intestinal alkaline phosphatase (IAP -I), an ALP gene, was significantly elevated in the FOS, GOS and RAF groups and tended to be increased in the LAC group. Dietary FOS, GOS, RAF and LAC significantly elevated faecal mucins, caecal n-butyrate and faecal ratio of Bifidobacterium spp. Dietary IMOS had no effect on colonic ALP, mucins, organic acids and microbiota. Colon ALP was correlated with mucins, caecal n-butyrate and faecal Bifidobacterium spp. This study demonstrated that non-digestible and fermentable oligosaccharides commonly elevate colonic ALP activity and the expression of IAP-I, with increasing mucins and microbial fermentation, which might be important for protection of gut epithelial homoeostasis.

High-fat diet promotes the effect of fructo-oligosaccharides on the colonic luminal environment, including alkaline phosphatase activity in rats.

We recently reported that fermentable nondigestible carbohydrates such as oligosaccharides, commonly increase colonic alkaline phosphatase (ALP) activity and the gene expression of Alpi-1, coding for rat intestinal alkaline phosphatase-I isozyme in rats and that the effect of oligosaccharides on colonic ALP activity is affected by the quality of dietary fats. We hypothesized that the amount of dietary fat would modulate the effect of oligosaccharides on colonic ALP and luminal environment in rats. In experiment 1, male Sprague-Dawley rats were fed a low-fat (LF, 5% lard) or high-fat (HF, 30% lard) diet with or without 4% fructo-oligosaccharides (FOS). In experiment 2, they were fed a 2.5%, 7%, 20%, or 40% fat (lard) diet with 4% FOS for 2 weeks. Dietary FOS in the HF diet (HF-FOS) significantly increased ALP activity in the colon and cecal digesta and colonic expression of Alpi-1, but not in the LF diet with FOS groups (LF-FOS). In comparison to the LF-FOS group, the increases in fecal mucins, Lactobacillus ratio, as well as cecal n-butyrate, and the decrease in fecal Clostridium coccoides, were more pronounced in the HF-FOS group. Compared with the 2.5% or 7% fat + FOS diet, the 20% fat + FOS diet significantly increased colonic ALP activity, Alpi-1 expression, and fecal mucins. These factors did not differ significantly between 20% and 40% fat + FOS diets. To exert the maximum effect of FOS on the colonic luminal environment, including ALP activity in rats, significantly more fat may be required than that contained present a LF diet.

Phytic acid actions on hepatic lipids and gut microbiota in rats fed a diet high in sucrose is influenced by dietary fat level.

Phytic acid (PA) or myoinositol intake was recently reported by our group to suppress hepatic lipogenic gene expression and modulate gut microbiota in rats fed a high-sucrose diet (HSC). The aim of this study was to investigate the effect of PA and dietary fat level on fatty liver and gut microbiota in rats fed an HSC diet. Male Sprague-Dawley rats were fed a high-fat (HF), HSC diet or a low-fat (LF), HSC diet with or without 1.02% sodium PA for 12 days. Hepatic lipid levels, hepatic enzyme activity, and expression of the enzymes and transcriptional factors related to lipid metabolism, cecal organic acids, and fecal microbiota were evaluated. PA intake depressed hepatic total lipid and triglyceride levels; reduced hepatic activity and expression of lipogenic enzymes; elevated fecal proportion of Lactobacillus spp; and increased cecal succinate level in rats fed the LF diet. The HF diet, when compared with the LF diet, depressed hepatic total lipid and triglyceride levels; reduced hepatic activity and expression of lipogenic enzymes; increased hepatic expression of carnitine palmitoyl-transferase 1a and cAMP-responsive element binding protein 3-like 3; and elevated fecal proportions of Lactobacillus spp and Bifidobacterium spp. In the HF diet groups, PA intake did not affect the factors associated with hepatic lipid metabolism and gut microbiota. In conclusion, dietary fat level could change the effect of PA on hepatic lipid metabolism and gut microbiota and, in turn, could alter the degree of nutritional importance of PA in rats fed an HSC diet.

Intake of phytic acid and myo-inositol lowers hepatic lipogenic gene expression and modulates gut microbiota in rats fed a high-sucrose diet.

Dietary phytic acid (PA) was recently reported by our group to suppress hepatic lipogenic gene expression and modulate gut microbiota in rats fed a high-sucrose (HSC) diet. The present study aimed to investigate whether the modulatory effects of PA depend on the dietary carbohydrate source and are attributed to the myo-inositol (MI) ring of PA. Male Sprague-Dawley rats were fed an HSC or a high-starch (HSR) diet with or without 1.02% sodium PA for 12 days. Subsequently, the rats were fed the HSC diet, the HSC diet containing 1.02% sodium PA or an HSC diet containing 0.2% MI for 12 days. The HSC diet significantly increased the hepatic triglyceride (TG) concentration as well as the activity and expression of hepatic lipogenic enzymes compared with the HSR diet. The increases were generally suppressed by dietary PA with a concomitant increase in the fecal and cecal ratios of Lactobacillus spp. In rats fed the HSR diet, PA intake did not substantially affect the factors associated with hepatic lipid metabolism or gut microbiota composition. The effects of MI intake were similar to that of PA intake on hepatic lipogenesis and gut microbiota in rats fed the HSC diet. These results suggest that dietary PA downregulates hepatic lipogenic gene expression and modulates gut microbiota composition in rats fed an HSC diet but not in rats fed an HSR diet. The MI ring of PA may be responsible for the effects of PA intake on hepatic lipogenic gene expression and gut microbiota.

Glucomannan consumption elevates colonic alkaline phosphatase activity by up-regulating the expression of IAP-I, which is associated with increased production of protective factors for gut epithelial homeostasis in high-fat diet-fed rats.

We previously reported that consumption of glucomannan-containing food (lily bulb) modulates gut microbiota and increases gut immunoglobulin A (IgA, index of intestinal immune function), mucins (index of intestinal barrier function), and colonic alkaline phosphatase (ALP) activity in rats fed a high-fat (HF) diet. Small intestinal ALP has an established protective effect in inflammatory diseases, whereas little is known about the function of colonic ALP activity. We hypothesized that dietary glucomannan would increase colonic ALP activity and the gene expression in rats fed an HF diet. To test this hypothesis, male Sprague-Dawley rats were fed a diet containing 30% lard with or without 4% high or low viscous glucomannan (HGM or LGM) for 2 weeks. Dietary HGM and LGM significantly increased colonic ALP activity without affecting ALP activity in the small intestine. The colonic expression of IAP-I, an ALP gene expressed throughout the intestine, was significantly higher in the HGM and LGM groups when compared with the control group. The colonic expression of Akp3 and Alpl, other ALP genes, were not affected by HGM and LGM. Dietary HGM and LGM significantly elevated fecal levels of IgA and mucins and cecal organic acids, including n-butyrate, propionate, and lactate. Colon ALP correlated with fecal IgA, mucins, and cecal organic acids. The present study showed that dietary glucomannan elevates colonic ALP activity by up-regulation of the expression of IAP-I, which might be important for protection of gut epithelial homeostasis.

Dietary phytic acid prevents fatty liver by reducing expression of hepatic lipogenic enzymes and modulates gut microflora in rats fed a high-sucrose diet.

OBJECTIVES: The aim of this study was to investigate the effect of phytic acid (PA) on fatty liver and gut microflora in rats fed a high-sucrose (HSC) diet. METHODS: Three groups of rats were fed a high-starch (HSR) diet or an HSC diet with or without 1.02% sodium PA for 12 d. We evaluated hepatic weight, total lipids, and triacylglycerol (TG) levels, the activities and expression of hepatic lipogenic enzymes (glucose-6-phosphate dehydrogenase, malic enzyme 1, and fatty acid synthetase), and fecal microflora. RESULTS: The HSC diet significantly increased hepatic total lipids and TG levels, and the activities and expression of the hepatic lipogenic enzymes compared with the HSR diet. These upregulations were clearly suppressed by dietary PA. Consumption of PA elevated the fecal ratio of Lactobacillus spp. and depressed the ratio of Clostridium cocoides, and suppressed the elevation in the ratio of C. leptum induced by the HSC diet. CONCLUSION: This work showed that dietary PA ameliorates sucrose-induced fatty liver through reducing the expression of hepatic lipogenesis genes and modulates gut microflora in rats.

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.

Dietary lectin lowers serum cholesterol and raises fecal neutral sterols in cholesterol-fed rats.

This study examined the influence of a low level of dietary lectin (0.34%), at a dose that did not affect body weight or food intake, on the concentration of serum cholesterol and fecal excretion of neutral sterols in rats fed a diet containing 0.50% cholesterol and 0.13% sodium cholate for 12 d. In experiment 1, rats fed a diet with 0.34% lectin, concanavalin A, had significantly lower concentrations of serum total cholesterol and hepatic cholesterol, a higher ratio of HDL-cholesterol to total cholesterol, enhanced excretion of fecal neutral sterols and reduced apparent cholesterol absorption or digestibility as compared with rats fed a diet without lectin. Fecal excretion of acidic sterols was unaffected by dietary lectin. In contrast, dietary 0.34% lectin had no significant effect on concentrations of serum total protein or glucose. In experiment 2, we examined whether the cholesterol-lowering activity of the lectin was responsibility for its carbohydrate-binding activity. The effect of dietary lectin on concentrations of serum and hepatic cholesterol and excretion of fecal neutral sterols was prevented by simultaneous administration of methyl-alpha-D-mannopyranoside with specific affinity for the carbohydrate-binding sites of the lectin. These results suggest that dietary lectins might reduce concentrations of serum and hepatic cholesterol by a mechanism involving higher excretion of neutral sterols and that these alterations might be associated with the carbohydrate-binding activity of lectin.

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 ß-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.

Dietary inositol hexakisphosphate, but not myo-inositol, clearly improves hypercholesterolemia in rats fed casein-type amino acid mixtures and 1,1,1-trichloro-2,2-bis (p-chlorophenyl) ethane.

We have previously shown that dietary inositol hexakisphosphate (IP6) and myo-inositol prevent fatty liver in rats fed a casein-based diet containing 1,1,1-trichloro-2,2-bis (p-chlorophenyl) ethane (DDT). This study was performed to examine the comparative effects of dietary equimolar amounts of sodium IP6 (1.02%) and myo-inositol (0.2%) on the development of DDT-induced fatty liver and hypercholesterolemia in rats fed 20% casein-type amino acid mixtures designed to exclude a possible myo-inositol contaminant in casein. Thirty-six male Wistar rats were divided into 6 groups of 6 rats each for: a control group, myo-inositol-supplemented group, IP6-supplemented group, DDT-treated group, DDT + myo-inositol-supplemented group, and a DDT + IP6-supplemented group. Dietary IP6 clearly suppressed the rises in serum concentrations of cholesterol and phospholipids because of DDT feeding, but myo-inositol had no significant influence on such elevations. Dietary IP6, but not myo-inositol, caused significant body weight gain with or without DDT intake. Supplemental IP6 and myo-inositol significantly increased hepatic-free myo-inositol regardless of DDT intake and prevented fatty liver in rats fed DDT. In conclusion, dietary IP6 and myo-inositol exert similar effects on DDT-induced fatty liver and myo-inositol status but distinct effects on DDT-induced hypercholesterolemia and growth rate in rats fed casein-type amino acid mixtures.

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 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.