Both infection with Helicobacter pylori and alcohol abuse have been associated with low vitamin B12 serum levels. The interaction between both risk factors is unknown. The aim of this study was to determine whether Helicobacter pylori infection is associated with low vitamin B12 levels in alcohol dependent patients. Blood samples were obtained from adult alcohol dependent patients undergoing detoxification and analyzed for serum vitamin B12 levels. Helicobacter pylori infection was serologically measured. Patient characteristics, medication use and alcohol consumption at admission were assessed by interview. A total of 6 out of 8 9 patients included presented low vitamin B12 levels, all were sub clinical deficient (<250 pmol/L) and none were clinical deficient (<150 pmol/L). Infection with Helicobacter pylori was present in 29% of the patients. The average vitamin B12 levels in Helicobacter pylori seropositive and seronegative patients were 1, 033 pmol/L (SD 741) and 9 71 pmol/L (SD 717), respectively. The relation between Helicobacter pylori infection and vitamin B12 deficiency was not of significance (OR=0.48; 95% CI [0.05-4.32]). In conclusion, Helicobacter pylori infection is not a risk factor for low vitamin B12 levels in alcohol dependent patients.
We used a Simple Food Frequency Questionnaire (SFFQ) in combination with other dietary approaches to estimate the selenium intake from different food groups based on the average long-term diet, in two rural communities in Japan, one in a mountain area and the other in a coastal area. The intake frequencies of rice and wheat products were sig-nificantly different in the two districts. The intake frequencies of fish, meat, and eggs, which are rich in selenium, were not significantly different. The mean dietary selenium intake, estimated from the SFFQ and the 24-h recall method, was 82.7μg/d (n=234) (range 19.2-180.1μg/d) in the mountain community. The mean dietary selenium intake estimated from the SFFQ and average value of the normal portion size was 118.0μgld (n=123) (range 22.6-255.3μg/d) in the coastal community. These estimated mean values exceeded the Japanese RDA, although the range of daily selenium intake was large. In the mountain community, fish made the largest contribution to dietary selenium intake (48.2% of daily total), followed by eggs (24.3%), and meat (17.0%). In the coastal community, fish accounted for 5 7.7% of daily total selenium intake, followed by meat (17.5 %), and eggs (16.1 %). In both districts, the total contribution of rice and wheat products was around 10%. It was found that the contribution of fish to dietary selenium intake was high and the contribution of cereals was low among Japanese.
Chicken extract has been consumed in oriental countries for centuries for improving body conditions such as recovery from fatigue. It is a rich source of antioxidant dipeptides. The in vivo antioxidative abilities were evaluated. Diets mixed with 4 different amounts of chicken extract were investigated for in vivo antioxidation ability using healthy male Sprague-Dawley (SD) rats. Total antioxidant status (TAS), thiobarbituric reactive substances (TBARS), iron content, superoxide dismutase (SOD) activity, glutathion peroxidase (GPx) activity and uric acid content were determined. In healthy rats, most of the indexes were not affected by intake of chicken extract significantly. However, plasma TBARS in the chicken extract-fed groups increased at the end of the experiment, which could be due to some pro-oxidative minerals in the extract. In conclusion, we found no significant or minor changes on the activities of antioxidative enzymes, antioxidant conditions, or lipid oxidation in healthy rats from consuming chicken extract, which may be the result of a balanced body condition. However, because of its high content of dipeptides, we suggest that it should have liver protecting effects if oxidative stresses are introduced.
Chicken extract contains carnosine and anserine, both of which possess some antioxidant abilities. The objective of this study was to investigate the protective effects of chicken extract in male Sprague-Dawley (SD) rats under induced oxidative stress. Carbon tetrachloride was used as the oxidative stress inducer. Glutamic-oxalacetatic transaminase (GOT), glutamic-pyruvic transaminase (GPT), total antioxidant status (TAS), thiobarbituricreactive substances (TBARS), iron content, and the activities of antioxidant enzymes were determined. We concluded that under oxidative stress, the intake of chicken extract was helpful in promoting the activities of antioxidant enzymes and in protecting the liver from oxidative damage.
Lactobacillus rhamnosus KY-3 is a fermentative bacterium that is used for the industrial production of L-lactic acid. We have examined the effect of L. rhamnosus KY-3 and cellobiose as synbiotics on lipid metabolism in rats. Rats were fed on a 20% casein diet (C) supplemented with either 1.7% L, rhamnosus KY-3 (KY-3), 10% cellobiose (CEB), or 1.7% L. rhamnosus KY-3 and 10% cellobiose (KY-3+CEB) for 13 d. The concentrations of serum total lipids, triacylglycerol, total cholesterol, and phospholipids were significantly reduced in rats fed a KY-3+CEB diet in comparison to those on the C, KY-3 and CEB diets. There was an increase in the weight of cecal contents and a significant increase in the amount of cecal short-chain fatty acids (SCFA). The dry weight of excretion increased additively upon the simultaneous administration of L. rhamnosus KY-3 and cellobiose (KY-3 +CEB). The amount of excreted fecal bile acids did not differ among the groups in this study. These findings support the hypothesis that the promotion of cecal fermentation can lower the level of serum lipids. These results suggest that simultaneous administration of L, rhamnosus KY-3 and cellobiose as synbiotics has a beneficial effect on lipid metabolism.
This study evaluated the effects of supplementation of carnitine and antioxidants on lipids, carnitine concentrations, and exercise endurance time in both trained and untrained rats as compared to non-supplemented rats. Thirty-two male SD rats, age 7 wk were divided into four groups according to exercise training and modified AIN-76 diets: NTNS (non-trained non-supplemented), NTS (non-trained supplemented), LTNS (longtrained non-supplemented) and LTS (long-trained supplemented). The trained rats were run on a treadmill for 60min per day (100 incline, 20m/min for 8 wk). Carnitine (0.5%/diet) and vitamin E (0.5mg/g b.w.) were supplemented in rat diets and vitamin C (0.5mg/g b.w.) and melatonin (1μg/g b.w.) were administered into the stomachs of the rats. LTNS and LTS rats had significantly lower serum total lipid, triglyceride, total cholesterol and liver triglycerides, but had higher serum HDL-cholesterol. There were no changes in exercise endurance time by supplementation in untrained animals, however endurance times were longer in LTS animals than in LTNS. The supplementation and training tended to increase carnitine palmitoyltransferase (CPT I) activities, although the differences were not statistically significant. Likewise, CPT-I mRNA levels were higher in both supplemented and exercise trained rats. These results suggest that supplementation of carnitine and antioxidants may improve lipid profiles and exercise ability in exercise-trained rats.
Objectives: To obtain information regarding the actual methods used for nutri-tional assessment at institutions and schools in order to establish a nutritional assessment method for individuals with disabilities. Methods: Questionnaires were sent to 1, 080 selected institutions and schools for individuals with intellectual disabilities (ID) and/or motor disabilities (MD). The response rate was 76.5%. Results: The implementation rates for height and weight measurements were generally very high at both institutions and schools for individuals with ID and/or MD (85.5-100%), but those for other items were very low and varied among different disability types. The implementation rate for BMI was 17.9-71.9%, demonstrating that BMI was not widely used among institutions and schools for individuals with ID and/or MD. As for the methods for calculating percent body fat, a high percentage of institutions and schools for individuals with ID and/or MD indicated the use of bioelectrical impedance analysis for most disability types (60-77.9%). Conclusions: The percentages of institutions for individuals with ID and/or MD and of schools for individuals with ID and/or MD that implement nutritional assessment are very low, with variations among different disability types.
We compared the effects of capsinoid, a non-pungent component, on serum and liver lipids, with that of synthetic capsaicin in hyperlipidemic rats. Male Wistar rats of 9 wk old were divided into 4 groups: a control group receiving a high-fat diet containing 1% cholesterol, and capsaicin, capsinoid-I and capsinoid-II groups supplemented with 0.1 mmol of N pelargonylvanillylamide (synthetic capsaicin), and 0.1 mmol and 1.0 mmol of capsinoid (capsiate: dihydrocapsiate=63:37) per kg of control diet, respectively. All groups were pair-fed for 4 wk. Compared with the control group, serum lipid levels in both capsinoid groups and liver lipid contents in the capsinoid-II group showed the same reduction as that of the capsaicin group. In the capsaicin and capsinoid-I groups, fatty acid synthase (FAS) activities were lower and hepatic triacylglycerol lipase (HTGL) [EC 3, 1.1.3] activities tended to be higher than those of control group. Lipoprotein lipase (LPL) [EC 18.104.22.168] activity in adipose tissue was higher in the capsaicin and capsinoid-II groups than in the control group. These results showed that capsinoid can improve serum and liver lipid metabolism comparable to synthetic capsaicin.
The purpose of present study was to determine whether the regulation of urea synthesis is mediated through changes in supply of amino acids by protein synthesis and whether the concentration of ammonia, or activities of amino acid catabolizing enzymes, regulate urea synthesis when the dietary protein quality is manipulated. Experiments were done on three groups of rats given diets containing 10g gluten, 10g casein or 10g whole egg protein/100g for 10d. The urinary excretion of urea, and the liver concentrations of glutamate, serine and alanine increased with a decrease in quality of dietary protein. The fractional and absolute rates of protein synthesis in tissues declined with the decrease in quality of dietary protein quality. The ammonia concentration in plasma and liver, and activities of hepatic amino acid catabolizing enzymes was not related to urea excretion under these conditions. These results suggest that the lower protein synthesis seen in tissues of rats given the lower quality of protein is likely to be one of the factors to increasing the supply of amino acids and stimulating urea synthesis.
The author prepared low-salt miso by koji fermentation using soy-oncom and okara-oncom (9:1), at which time soybeans and okara were fermented with Neurospora intermedia (oncom miso, i.e. O-miso). Its usefulness as a seasoning, as well as high antioxi-dative activity in vitro and antimutagenicity have already been presented. In this study, the antioxidative activity of O-miso in vivo, as well as serum cholesterol-lowering action, were investigated concerning contribution to health. In rats fed O-miso, the serum a-tocopherol level and isoflavone-aglycone-intake were higher than in rats fed low-salt soybean miso (S-miso). The activities of serum GSH-Px and hepatic catalase were also higher in rats fed O-miso than in rats fed S-miso, while the TBARS values were lower in both the serum and livers of rats fed O-miso. Furthermore, O-miso intake suppressed a rise in serum cholesterol level and increased fecal bile acid excretion. Such a cholesterol-lowering action of O-miso may be attributable to the micelle-breaking or evacuant effects of indigestible proteinous residues and the antioxidative activity of isoflavone-aglycones. O-miso seems to be more beneficial to health than S-miso in view of these aspects.
Wheat gliadin is known mainly as the causative substance for enteropathy accompanied by diarrhea (celiac disease) and food-dependent exercise-induced anaphylaxis. However, little is known in regards to the allergenicity of gliadin in atopic dermatitis. In this study, the allergenicity of gliadin was demonstrated using sera of wheat-allergic patients with atopic dermatitis. Since there are many repeated sequences in gliadin, peptides containing each motif were synthesized to evaluate their IgE-binding abilities. As a result, OOPFP and POOPF were found to be epitopes (minimum structures for the IgE-binding). Gliadin might crosslink patient's IgE-antibodies via these epitopes and trigger subsequent allergic reactions.
We examined whether gastric mucosal ascorbic acid status changes with the formation, progression, and recovery of acute gastric mucosal lesions in rats treated with compound 48/80, a mast cell degranulator. Fasted Wistar rats received a single intraperito-neal injection of compound 48/80 (0.75mg/kg). Apparent gastric mucosal lesions occurred 0.5h after compound 48/80 treatment, progressed gastric mucosal lesions were observed at 3h, and a partial recovery of the progressed lesions was found at 6h. The gas-tric mucosal concentrations of total and reduced ascorbic acids in compound 48/80-treated rats decreased to approximately 60% of the levels of untreated rats at 3h after the treatment but the decreased concentrations of total and reduced ascorbic acids were almost completely returned to the levels of untreated rats at 6h. The gastric mucosal concentration of oxidized ascorbic acid in compound 48/80-treated rats showed little change. The serum concentra-tions of total and reduced ascorbic acids in compound 48/80-treated rats increased at 0.5h after the treatment and further increased at 3h but the increased concentrations of total and reduced ascorbic acids were almost completely returned to the levels of untreated rats at 6h. The serum concentration of oxidized ascorbic acid in compound 48/80-treated rats increased transiently at 0.5h after the treatment. The hepatic concentrations of total, reduced, and oxidized ascorbic acids in compound 48/80-treated rats increased 3h after the treatment, but these increases were not observed at 6h. These results indicate that gastric mucosal ascorbic acid status is disrupted with the progression of acute gastric mucosal lesions in rats treated with compound 48/80.
The effects of riboflavin on the formation of 6, 7-dimethyl-8-ribityllumazine (DMRL) were examined using the growing cells of a riboflavin, adenine deficient-mutant, Bacillus subtilis. The administration of low concentrations (50-500ng/mL) of riboflavin to the basal medium significantly inhibited the formation of DMRL without any change in growth. Especially, the supplementation of more than 250ng/mL riboflavin completely restricted the formation of DMRL under the experimental conditions. The results clearly indicate that a rigid negative feedback inhibition is operative for the biosynthetic pathway of riboflavin in B. subtilis.
We examined the hepatoprotective effect of water-extract from adzuki bean (Vigna angularis) hulls on acetaminophen (AAP)-induced damage in rat liver. F344/DuCrj rats of 8 weeks of age were fed diets without and with 0.5% AAP or besides it 5% adzuki extract (lyophilized) on a daily basis over a period of 4 wk. At that time, serum aspartate aminotransferase activity in only AAP-treated group was higher than in both control and AAP plus adzuki extract (AAPA)-treated groups, while hepatic glutathione content and hepatic glutathione reductase and catalase activities in the AAP-treated group were lower than in the control group in contrast to the reverse in the AAPA-treated group. Hepatic phosphatidylcholine hydroperoxide and phosphatidylethanolamine hydroperoxide concentrations were higher in the AAP-treated group than in the control group, and were lower in the AAPA-treated group than in the AAP-treated group. Hepatic glutathione peroxidase activity was higher in the AAP-treated group than in the control group, although there was no significant difference between both AAP- and AAPA-treated groups in this respect. These findings suggest that the adzuki extract will serve as a prophylactic against oxidative damage to the liver.