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.

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.

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.

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.

Increased intestinal ethanol following consumption of fructooligosaccharides in rats.

Previous studies have suggested that ethanol is a fermentation product of microflora. However, it is unknown whether this ethanol production is elevated by intake of prebiotics. Prebiotics are considered to enhance the production of short-chain fatty acids (SCFAs) as a fermentation product of beneficial bacteria. In the present study, the effect of fructooligosaccharides (FOS) consumption on intestinal ethanol levels was investigated. Rats were fed a diet with or without 10% FOS for two weeks. Consequently, FOS intake significantly increased ethanol levels per gram of ileum and cecum digesta of the rats (3.5-fold and 1.9-fold, respectively, P<0.01). The numbers of cecum Bifidobacterium (producer of ethanol and lactate) were significantly increased by FOS intake (P<0.05) and correlated with the cecum ethanol levels per gram of cecum (r=0.626, P<0.05). FOS intake also led to a significant increase in the cecum levels of SCFAs, namely lactate, propionate and n-butyrate (P<0.05). Furthermore, ethanol levels were significantly correlated with lactate levels (r=0.691, P<0.01), but not with propionate or n-butyrate levels (r=0.449 and 0.493, respectively, P>0.05). The current study, to the best of our knowledge, is the first to indicate that FOS intake significantly increases the level of intestinal ethanol. Therefore, dietary FOS may affect the intestinal health status of animals by elevating their ethanol levels, without direct ethanol consumption.

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.

Consumption of an acid protease derived from Aspergillus oryzae causes bifidogenic effect in rats.

A marked elevation in the abundance of Bifidobacterium was found in the cecum of rats that were fed a high-fat diet supplemented with an Amano protease preparation (derived from Aspergillus oryzae). The protease preparation contains several digestive enzymes, including acid protease (AcP), alkaline protease, and amylase. We hypothesized that the elevation in the abundance of Bifidobacterium by Amano protease preparation is associated with the digestive enzymes involved in the protease preparation. To test this hypothesis, this study was conducted to investigate if such bifidogenic effect is because of the AcP. Rats were fed a high-fat diet containing purified AcP obtained from the Amano protease preparation for 2 weeks. The numbers of Bifidobacterium in the cecum and feces of rats were markedly elevated by the dietary supplementation of 1 g/kg Amano protease. Bifidobacterium numbers were unaffected by supplementation with purified AcP (0.096 g/kg) at the level equivalent to the AcP amount found in the 1-g/kg Amano protease diet. Bifidobacterium numbers in the cecum and feces, and lactate levels in the cecum were significantly (P<.05) elevated when rats were fed a diet containing 0.384 g/kg AcP (4-fold higher amount of AcP than that used in the 1-g/kg Amano protease diet). Thus, the bifidogenic effect of 1 g/kg Amano protease diet could not be explained by the AcP. However, intriguingly, supplemental AcP was found to cause a significant bifidogenic effect at the dose that is 4-fold higher than that used in the 1-g/kg Amano protease diet.

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.

Feeding of the water extract from Ganoderma lingzhi to rats modulates secondary bile acids, intestinal microflora, mucins, and propionate important to colon cancer.

Consumption of reishi mushroom has been reported to prevent colon carcinogenesis in rodents, although the underlying mechanisms remain unclear. To investigate this effect, rats were fed a high-fat diet supplemented with 5% water extract from either the reishi mushroom (Ganoderma lingzhi) (WGL) or the auto-digested reishi G. lingzhi (AWGL) for three weeks. Both extracts markedly reduced fecal secondary bile acids, such as lithocholic acid and deoxycholic acid (colon carcinogens). These extracts reduced the numbers of Clostridium coccoides and Clostridium leptum (secondary bile acids-producing bacteria) in a per g of cecal digesta. Fecal mucins and cecal propionate were significantly elevated by both extracts, and fecal IgA was significantly elevated by WGL, but not by AWGL. These results suggest that the reishi extracts have an impact on colon luminal health by modulating secondary bile acids, microflora, mucins, and propionate that related to colon cancer.

Protective Effect of Dietary Lily Bulb on Dextran Sulfate Sodium-Induced Colitis in Rats Fed a High-Fat Diet.

Lily bulb is traditionally consumed in East Asia and contains high amounts of glucomannan. This study investigated the effect of dietary lily bulb on dextran sulfate sodium (DSS)-induced colitis in rats fed a high-fat (HF) diet. Male Sprague-Dawley rats were fed a diet containing 30% beef tallow with or without 7% steamed lily bulb powder for 17 d. Experimental colitis was induced by replacing drinking water with DSS during the last 7 d. The disease activity index (DAI) was significantly lower in the lily bulb+DSS group than in the DSS group on day 17. The fecal abundance of Bifidobacterium was significantly reduced in the DSS group compared with that in the control group, but it was recovered by lily bulb intake. Cecal butyrate, fecal mucins, and alkaline phosphatase (ALP) activity were significantly higher in the DSS group than in the control group. Dietary lily bulb potentiated the increase in cecal butyrate, fecal mucins, and the ALP activity caused by DSS treatment. These results indicate that lily bulb attenuates DSS-induced colitis by modulating colonic microflora, organic acids, mucins, and ALP activity in HF diet-fed rats.

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.

Consumption of lily bulb modulates fecal ratios of firmicutes and bacteroidetes phyla in rats fed a high-fat diet.

It has been recently suggested a high ratio of fecal Firmicutes and reduction in the Bacteroidetes in obese animals. This study investigated the effect of dietary lily bulb (LB) on fecal Firmicutes and Bacteroidetes in rats fed a high-fat (HF) diet. In experiment 1, rats were fed an HF diet with or without 7% raw (R) or steamed (S) LB. In experiment 2, rats were fed the HF diet with or without 7% RLB, 0.9% ethanol extract of LB, or 6.1% ethanol extract residue of LB. In experiment 1, fecal Firmicutes was reduced and Bacteroidetes was increased in both the RLB and SLB groups. In experiment 2, the fecal Firmicutes/Bacteroidetes ratio was not affected by the ethanol extract or ethanol extract residue of LB. These results suggest that LB in its entirety modulates colonic microflora, regardless of heat treatment.

Supplemental fermented plant product ('Manda Koso') reduces succinate and deoxycholate, as well as elevates IgA and mucin levels, in rats fed a high-fat diet.

'Manda Koso' is a commercial fermented plant product (FPP) made from 53 types of fruits and vegetables that have been fermented for >3 years and 3 months. We hypothesized that FPP intake improves the luminal environment of rats fed a high-fat diet. Thus, the present study examined the effects of consumption of 5% FPP diet for 3 weeks on colonic luminal parameters in rats fed a 30% beef tallow diet. Food intake and body weight gain were unaffected. Consumption of the FPP diet did not influence the proportions of Bifidobacterium, Lactobacillus, Bacteroides, Prevotella or Clostridium in cecal contents. However, the FPP diet caused a significant reduction (-88%) in the level of cecal succinate, a putative inflammatory signal (P<0.01), but did not affect the levels of n-butyrate, propionate, acetate and lactate. The fecal levels of deoxycholate and hyodeoxycholate, which are toxic bile acids, were also significantly reduced by the FPP diet (P<0.05). The FPP diet significantly increased fecal immunoglobulin A and mucins responsible for intestinal immune and barrier functions (P<0.05). The results suggest that the consumption of FPP is beneficial for the colonic luminal environment in rats fed a high-fat diet.

Anthocyanin-rich Phytochemicals from Aronia Fruits Inhibit Visceral Fat Accumulation and Hyperglycemia in High-fat Diet-induced Dietary Obese Rats.

Aronia fruits (chokeberry: Aronia melanocarpa E.) containing phenolic phytochemicals, such as cyanidin 3-glycosides and chlorogenic acid, have attracted considerable attention because of their potential human health benefits in humans including antioxidant activities and ability to improved vision. In the present study, the effects of anthocyanin-rich phytochemicals from aronia fruits (aronia phytochemicals) on visceral fat accumulation and fasting hyperglycemia were examined in rats fed a high-fat diet (Experiment 1). Total visceral fat mass was significantly lower in rats fed aronia phytochemicals than that in both the control group and bilberry phytochemicals-supplemented rats (p < 0.05). Moreover, perirenal and epididymal adipose tissue mass in rats fed aronia phytochemicals was significantly lower than that in both the control and bilberry phytochemicals group. Additionally, the mesenteric adipose tissue mass in aronia phytochemicals-fed rats was significantly low (p < 0.05). Furthermore, the fasting blood glucose levels significantly decreased in rats fed aronia phytochemicals for 4 weeks compared to that in the control rats (p < 0.05). Therefore, we investigated the effects of phytochemicals on postprandial hyperlipidemia after corn oil loading in rats, pancreatic lipase activity in vitro, and the plasma glycemic response after sucrose loading in order to elucidate the preventive factor of aronia phytochemical on visceral fat accumulation. In the oral corn oil tolerance tests (Experiment 2), aronia phytochemicals significantly inhibited the increases in plasma triglyceride levels, with a half-maximal inhibitory concentration (IC(50)) of 1.50 mg/mL. However, the inhibitory activity was similar to that of bilberry and tea catechins. In the sucrose tolerance tests (Experiment 3), aronia phytochemicals also significantly inhibited the increases in blood glucose levels that were observed in the control animals (p < 0.05). These results suggest that anthocyanin-rich phytochemicals in aronia fruits suppress visceral fat accumulation and hyperglycemia by inhibiting pancreatic lipase activity and/or intestinal lipid absorption.

Dietary polyphenols increase fecal mucin and immunoglobulin A and ameliorate the disturbance in gut microbiota caused by a high fat diet.

The effects of dietary polyphenols on human health have mainly been discussed in the context of preventing degenerative diseases, particularly cardiovascular diseases and cancer. The antioxidant properties of polyphenols have been widely studied, but it has become clear that the mechanism of action of polyphenols extends beyond the modulation of oxidative stress, as they are poorly absorbed from the digestive tract. The purpose of this study was to clarify the effects of polyphenols on the colonic environment, intestinal barrier function, and gut microbiota. We demonstrated that dietary polyphenols derived from aronia, haskap, and bilberry, markedly elevated the amount of fecal mucin and immunoglobulin A (IgA) as an intestinal barrier function and ameliorated the disturbance in gut microbiota caused by a high fat diet in rats. These results suggest that dietary polyphenols play a significant role in the prevention of degenerative diseases through improvement of the colonic environment without any absorption from the digestive tract.

Beneficial effects of protease preparations derived from Aspergillus on the colonic luminal environment in rats consuming a high-fat diet.

The present study investigated the effects of the dietary addition of the protease preparations derived from Aspergillus on the colonic luminal environment. Rats were fed a 30% beef tallow diet with or without the protease preparations, including Amano protease (protease A 'Amano SD', neutral proteases from Aspergillus spp.) or orientase (orientase AY, acid proteases from Aspergillus niger) at the dose of 0.2% for 3 weeks. Cecal Bifidobacterium was significantly elevated in the dietary Amano protease group (194-fold, P<0.05), but not in the orientase group. Lactobacillus was elevated in the two groups (P<0.05). Cecal n-butyrate, propionate and lactate were higher in the Amano protease and orientase groups compared with the controls (P<0.05). Fecal immunoglobulin A and mucins were elevated in the Amano protease group (P<0.05). These results suggest the potential effect of the consumption of Aspergillus-derived protease preparations that are favorable for the colonic luminal environment in rats fed a high-fat diet.

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.

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.

Dietary anthocyanin-rich Haskap phytochemicals inhibit postprandial hyperlipidemia and hyperglycemia in rats.

Haskap (Lonicera caerulea L.) fruit contains some bioactive phenolic phytochemicals, mainly cyanidin-3-glucoside (cy3-glc) and chlorogenic acid. The purpose of this study was to investigate the effects of anthocyanin-rich phenolic phytochemical (containing 13.2% anthocyanin) purified from a Haskap fruit (named Haskap phytochemical) on postprandial serum triglyceride and blood glucose levels. The Haskap phytochemical (containing cy 3-glc at 300 mg/kg of body weight) was administered orally to rats fasted for 24 h and 30 min later, a corn oil emulsion was administered to these rats. After the administration, serum triglyceride concentration was measured. An increase in serum triglyceride concentration and the AUC significantly lowered in the Haskap phytochemical-administered group than in the saline-administered group. To evaluate the effect of serum glucose levels, the Haskap phytochemical was orally administered to rats fasted for 24 h and sucrose solution (2 g/kg of body weight) was administered to these rats after 30 min. After the administration, blood glucose level was measured. The Haskap phytochemical significantly reduced the increase in blood glucose levels and AUC in the Haskap phytochemical-administered group than in the saline-administered group. Furthermore, to investigate the long-term effects of Haskap phytochemical intake, high-fat diet (HF diet) with 1.5% or 3.0% Haskap phytochemical was administered to rats for four weeks. The investigation of chronological changes in the serum components of the rats fed HF diets in addition to the administration of Haskap phytochemical showed that the increase in serum triglyceride concentrations, total cholesterol concentrations and blood glucose were significantly suppressed compared to the HF diet-fed control (HF-control). These results suggest that the decrease in postprandial blood lipids and blood glucose by short or long-term Haskap phytochemical ingestion is due to anthocyanin and other polyphenols contained in the Haskap phytochemical.

Beneficial effect of a low dose of ethanol on liver function and serum urate in rats fed a high-fat diet.

This study investigated the effects of the consumption of 1% or 2% (v/v) ethanol in drinking water for 12 wk on rats fed a high-fat diet. Body weight gain, food intake, and fluid intake were unaffected by ethanol intake. Adipose tissue weight, and serum glucose and lipids were unaffected. Compared to the control (no ethanol), 1% ethanol intake significantly reduced serum levels of alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and ammonia (p<0.05), whereas 2% ethanol intake did so to a lesser extent. Serum urate was significantly lower in both the 1% and 2% ethanol groups than that in the control group (p<0.05). The results suggest a low dose of ethanol has beneficial effects on liver function and serum urate in rats fed a high-fat diet.