In order to verify whether vitamin E improves the cognitive impairment induced through aging, aged rats fed a vitamin E-supplemented diet had their learning and memory functions assessed in comparison with the aged rats fed a normal diet using a Morris water maze test. Although normal aged rats showed very poor learning ability concerning the place of a platform in the water maze apparatus, the aged rats fed the vitamin E-supplemented diet learned the place with a marked speed in only 5 trials. After old animals showed the maximum learning ability, they were kept in a normal atmosphere for 48 h without a trial followed by an assessment of their memory function using the same apparatus. The vitamin E-supplementation to aged rats resulted in marked retention of their maximum memory function, although normal aged rats showed a significant memory loss of about 60%. Pyrroloquinoline quinone (PQQ), which increases in the production of nerve growth factor, and protects neurons, had a similar effect on cognitive function to that of vitamin E in the aged rats. These results suggest that vitamin E may improve cognitive deficit caused through aging by not only its neuro-protecting effect but an antioxidant efficacy.
Types of dietary lipid affect the life span of rats. In this study, we investigated the influence of the life-long dietary n-6/n-3 ratio on life span and serum lipid and glucose levels. A semi-purified diet adjusted to a constant saturated : monounsaturated : polyunsaturated fatty acid ratio and an n-6/n-3 ratio of 1 (R1), 4 (R4) or 16 (R16) was fed to rats (n=33) from 4 wk of age until death. There were no significant differences in the food intake or body weight, nor were there survival curve or mean life span variations among the 3 groups. The serum cholesterol levels after feeding the test diet for 6 and 12 mo were significantly lower in the R1 group than in the other groups, and the serum triacylglycerol levels were significantly lower than those in the R16 group. However, no significant differences were noted in the serum cholesterol or triacylglycerol level after feeding for 18 mo among the 3 groups. A significantly higher serum glucose level was noted in the R1 group only at 18 mo of test diet ingestion, compared to that in the R4 group. The results suggest that the influence of the dietary n-6/n-3 ratio on the serum lipid and glucose levels varies, depending on the duration and life stage of feeding. Our findings further suggest that the life span of Wistar rats is not affected even if the ratio of dietary n-6/n-3 changes from 1 to 16.
To examine predictive factors for abdominal obesity or metabolic syndrome, we investigated the association of plasma fatty acid composition, estimated desaturase activity, and nutrient intakes, with abdominal obesity or metabolic syndrome in Japanese males. Clinical characteristics, the fatty acid composition of plasma cholesteryl esters, and energy and nutrient intakes were analyzed in 3 groups: metabolic syndrome (MS, n=24), abdominal obesity (OB, n=43), and control (n=27). The estimated desaturase activities were calculated by the ratio of 16:1n-7/16:0, 18:3n-6/18:2n-6, and 20:4n-6/20:3n-6 in plasma cholesteryl esters as surrogates of the measure of the delta 9, delta 6, delta 5 desaturase (D9-16D, D6D and D5D) activities, respectively. Plasma fatty acid composition did not differ significantly between the OB group and the control group. The MS group had higher levels of palmitoleic, oleic, and γ-linolenic acids, but a lower level of linoleic acid than the control. Stronger D6D activity and weaker D5D activity were observed in the OB group. A higher level of D9-16D activity as well as a higher level of D6D activity and a lower level of D5D activity was observed in the MS group. A logistic regression analysis showed that the low D5D activity and high D9-16D activity were predictive of the development of abdominal obesity from controls (odds ratio=0.39, p<0.05) and metabolic syndrome from abdominal obesity (odds ratio=2.44, p<0.05), respectively. In the multiple linear regression analysis, D5D activity positively correlated with the intake of eicosapentaenoic acid (EPA). In conclusion, the estimated D5D activity was a predictive factor for abdominal obesity and the estimated D9-16D activity was a predictive factor for developing metabolic syndrome from abdominal obesity in Japanese male subjects. Dietary intake of EPA would play an important role in preventing abdominal obesity and the development of metabolic syndrome.
Microelements have an important role in many vital enzymatic functions. Their optimal intake and serum concentration are not properly defined. For nursing home residents, this issue is further complicated by the high prevalence of oropharyngeal dysphagia. The purpose of this study was to measure microelement concentrations in 3 groups of elderly subjects that differ in their feeding methods and functional state. Forty-six frail elderly patients, in stable clinical condition, 15 on naso-gastric tube (NGT) feeding, 15 orally fed (OF), from skilled nursing departments were recruited to this study. As controls, we studied a group of 16 elderly independent ambulatory patients. A battery of 16 microelements was examined using the Inductively Coupled Plasma Atomic Emission Spectrometry (ICP-AES) and Inductively Coupled Plasma Mass Spectrometry (ICP-MS). The OF frail elderly patients had significantly lower levels of chromium as compared to the NGT fed and the control group. Both frail elderly groups had lower levels of zinc and copper as compared to the controls. In contrast, in the nursing groups, we found higher levels of aluminum, boron, barium, bromine and nickel. Elderly, in particular frail and disabled subjects, are vulnerable to insufficiency or overload of microelements. There is a need to evaluate the actual requirements for each microelement for this population.
Although several studies have shown that the type and degree of unsaturation of fatty acids alter the production of proinflammatory mediators, there have been few studies in which the effects of trans isomers on allergic responses were evaluated. NC/Nga (NC) mice raised in conventional conditions develop spontaneous atopic dermatitis-like lesions with IgE hyperproduction. We used this model to evaluate the effect of dietary trans fatty acids (TFAs) on the development of spontaneous dermatitis. NC mice were fed a 4 g TFAs/kg diet (4 g TFA), a 8 g TFAs/kg diet (8 g TFA) or a control diet with no TFA content for 10 wk. The dermatitis condition improved with the increasing intake of TFAs, and there was a significant difference from week 5 of the experimental period between the dermatitis conditions in 8 g TFA-fed mice and control mice. Production of total IgE was also suppressed in mice fed TFAs compared with that in control mice, correlating with the skin lesions. IFN-γ, but not IL-4, production was significantly greater in TFA-fed mice that in control mice. Our results suggest that intake of TFAs suppresses the development of atopic dermatitis-like lesions in NC mice. Even though we observed a decreased production of IgE levels, mechanisms involved in the development of dermatitis-like lesions seem to be IL-4-independent.
We have shown that urinary urea excretion decreased in rats fed a low gluten diet supplemented with dietary limiting amino acids. The purpose of present study was to determine whether the addition of dietary limiting amino acids to a low gluten diet affected the synthesis and degradation of N-acetylglutamate and regulated urea synthesis. Experiments were done on two groups of rats, given diets containing 10% gluten or 10% gluten+0.5% L-lysine, 0.2% L-threonine and 0.2% L-methionine for 10 d. The urinary excretion of urea, and the liver concentration of N-acetylglutamate, and the liver activity of N-acetylglutamate synthetase decreased with the addition of dietary L-lysine, L-threonine and L-methionine. N-Acetylglutamate concentration in the liver was closely correlated with the N-acetylglutamate synthetase activity in the liver and excretion of urea. The greater degradation of N-acetylglutamate was observed in the group fed the 10% gluten+L-lysine, L-threonine and L-methionine. The hepatic concentration of glutamate and plasma concentration of arginine were not related to the N-acetylglutamate concentration in the liver. These results suggest that the addition of limiting amino acids to the low gluten diet controls the synthesis and degradation of N-acetylglutamate in the liver and lowers urea synthesis.
Previous studies have demonstrated that fatty acid oxidation in the liver may affect food intake. This study examined the influence of preloading of medium-chain triacylglycerol (MCT) on food intake in comparison with long-chain triacylglycerol (LCT). Male rats were fasted for 18 h and then administered LCT or MCT emulsion orally. Each group of rats was allowed to rest for 30 min, and then food intake during 1 h was measured. Food intake in the MCT group was significantly lower than that in the LCT group. To examine the influence of hepatic oxidation, the MCT+MA group was injected intraperitoneally with mercaptoacetate (MA), an inhibitor of fatty acid oxidation, 2 h before ingestion of MCT emulsion. Then, 30 min after ingestion of LCT or MCT emulsion, food intake was measured for 1 h. Food intake in the MCT group was significantly lower than that in the LCT group, but there was no significant difference between the MCT+MA group and the LCT group. Food intake in the MCT+MA group was significantly higher than that in the MCT group. The hepatic ATP content after MCT ingestion was significantly higher than that after LCT ingestion, but there was no significant difference between the MCT+MA group and the LCT group. The hepatic ATP content after MCT+MA ingestion was significantly lower than that after MCT ingestion. These results suggest that ingestion of medium-chain fatty acid (MCFA) increases the liver ATP content in fasted rats, consequently decreasing food intake.
An immunostimulating glutamine-rich peptide was purified from a soybean protein fraction digested with Peptidase R produced by Rhizopus oryzae (Ro-digest) by a combination of SP-Sepharose column chromatography and reversed-phase high-performance liquid chromatography. The purified peptide was supposed to be located at or near the glutamine-rich region 202 to 222 of the glycinin G4 subunit. The peptide significantly increased the number of CD8+, CD11b+, and CD49b+ cells in C3H/HeN mouse spleen cell cultures, while 2 chemically synthesized glutamine-rich peptides corresponding to residues 202 to 213 (QQQQQQKSHGGR) and residues 214 to 225 (KQGQHQQEEEEE) of the glycinin G4 subunit increased the number of interleukin (IL)-12+CD11b+ cells. The peptide 202-213 also significantly increased the number of CD49b+, IL-2+CD4+, and interferon-γ+CD4+ cells and stimulated the cytotoxic activity of spleen cells toward the human erythroleukemia cell line K562. These results indicate that the glutamine-rich region of the soybean glycinin G4 subunit stimulates the cellular immune system in mouse spleen cell cultures.
The saline and dimethylsulfoniopropionate (DMSP) solutions at 5, 10 and 20 mM were preliminarily injected intraperitoneally every other day into two control and three DMSP groups of mice (n=8) for 2 wk and thereafter Ehrlich ascites-carcinoma (EAC) cells were peritoneally injected to one control and three DMSP groups of mice, leaving one control group without the EAC injection. Then, the body weight and survival time of all mice were examined over a long rearing time up to 300 d. All EAC-bearing mice, especially the carcinoma control and 5 mM DMSP-carcinoma group mice, rapidly increased their body weights early and then died by day 50 and day 90, respectively. In contrast, the administration of 10 and 20 mM DMSP solutions prolonged the lives of EAC-bearing mice at the survival rate of 50 and 63% respectively up to 300 d without any side effects. Furthermore, the administration of 10 mM DMSP solution proved to activate the delayed-type hypersensitivity of EAC bearing-mice, and the DMSP solutions over the concentrations of 5 to 30 mM to slightly reduce the dead cells in EAC cells on the synthetic medium. Accordingly, the preliminary supplementation of 10 and 20 mM DMSP solutions to EAC-bearing mice was proven to maintain their lives at high survival rates without direct damage to EAC cells for a long time, probably due to the activation of the immune system without any side effects.
The aim of this study was to evaluate the relationship between folate and homocysteine levels in alcoholics taking into consideration the liver enzyme activity as sensitive markers of hepatocellular injury. Folate and homocysteine concentrations did not differ between alcoholics classified according to the liver enzyme activity. The association between folate and homocysteine levels exists in the alcoholics with normal liver enzyme activity and in the controls. Therefore, we concluded that before the liver hepatocellular injury due to alcohol abuse, the correlation between folate and homocysteine concentrations in alcoholics exists as in the healthy controls. In the presence of hepatocellular injury, the association disappears.
This study demonstrates the effect of soybean components on the tumor necrosis factor-α (TNF-α)-induced production of interleukin-8 (IL-8), one of the major inflammatory chemokines, in intestinal epithelial-like Caco-2 cells. Among the soybean components, an isoflavone fraction (IFF) suppressed the TNF-α-induced IL-8 secretion by Caco-2 cells in a dose-dependent manner, whereas a soyasaponin fraction and soypeptide fraction had no significant effect on TNF-α-induced IL-8 secretion. The IL-8 secretion induced by hydrogen peroxide and by IL-1β was not suppressed by IFF, suggesting that the inhibitory effect of isoflavone was specific for the TNF-α-induced regulation of IL-8. The increased expression of IL-8 mRNA by TNF-α was almost completely suppressed by IFF. Furthermore, the transcriptional activity of the human IL-8 promoter was increased by the TNF-α treatment, and IFF significantly suppressed the IL-8 promoter activity. These results indicate that IFF suppressed TNF-α-induced IL-8 production at the transcriptional level in human intestinal Caco-2 cells, suggesting IFF of soybean as a promising food component for preventing intestinal inflammation such as inflammatory bowel disease.
Much attention has been paid to the beneficial health effect of tea catechins as one of the effective strategies to prevent obesity. The current study was carried out to investigate the role of tea catechins on the utilization of dietary energy sources in rats. The addition of 1% (w/w) tea catechins, mostly in gallate forms, to the diet brought about significant reductions in body weight gains and abdominal adipose tissue weights after 4-wk feeding periods compared to the control. A 2-d output of feces collected at the third week of feeding was significantly increased by a tea catechin diet (average dry weight±SD of 7.2±1.5 g) over that with a control diet (3.8±0.4 g). Only 0.1% of ingested starch appeared in the feces of rats fed the control diet, whereas 4.8% was excreted in the feces of the tea catechin group. Moreover, both apparent digestibility values for lipid and protein in the rats fed tea catechins were also lower than those of the control, suggesting that tea catechins increased the fecal excretion of these energy nutrients. Of the gross energy that the rats consumed from their respective diets during the fecal collection period, 1.6% (for control diet) and 5.8% (for tea catechin diet) were estimated to be excreted in feces. The energy loss originating from carbohydrate should contribute to the overall amount of energy in the feces, followed by protein. Intake of tea catechins suppressed the intestinal absorption of energy nutrients via the inhibition of digestive enzymes, which may at least partially influence the body fat reduction by tea catechins.