Journal of Nutritional Science and Vitaminology
Online ISSN : 1881-7742
Print ISSN : 0301-4800
ISSN-L : 0301-4800
Volume 61, Issue 5
Displaying 1-11 of 11 articles from this issue
Regular Paper
  • Katsumi SHIBATA, Nobuya MORITA, Tomoyo KAWAMURA, Ai TsUJI, Tsutomu FUK ...
    2015 Volume 61 Issue 5 Pages 355-361
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    Fatty liver is caused when rats are given orotic acid of the pyrimidine base in large quantities. The lack of B-group vitamins suppresses the biosynthesis of fatty acids. We investigated how orotic acid-induced fatty liver affects the concentrations of liver, blood, and urine B-group vitamins in rats. The vitamin B6 and B12 concentrations of liver, blood, and urine were not affected by orotic acid-induced fatty liver. Vitamin B2 was measured only in the urine, but was unchanged. The liver, blood, and urine concentrations of niacin and its metabolites fell dramatically. Niacin and its metabolites in the liver, blood, and urine were affected as expected. Although the concentrations of vitamin B1, pantothenic acid, folate, and biotin in liver and blood were decreased by orotic acid-induced fatty liver, these urinary excretion amounts showed a specific pattern toward increase. Generally, as for the typical urinary excretion of B-group vitamins, these are excreted when the body is saturated. However, the ability to sustain vitamin B1, pantothenic acid, folate, and biotin decreased in fatty liver, which is hypothesized as a specific phenomenon. This metabolic response might occur to prevent an abnormally increased biosynthesis of fatty acids by orotic acid.
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  • Koji FUKUI, Keisuke NAKAMURA, Masashi SHIRAI, Anna HIRANO, Hirokatsu T ...
    2015 Volume 61 Issue 5 Pages 362-368
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    Vitamin E inhibits oxidative processes in living tissues. We produced vitamin E-deficient mice by feeding them a vitamin E-deficient diet to verify the influence of chronic vitamin E deficiency on cognitive function. We measured cognitive function over a 5-d period using the Morris water maze task, as well as antioxidant enzyme activity and lipid peroxidation in discrete brain regions, and total serum cholesterol content. Three- and six-mo-old vitamin E-deficient and age-matched control mice were used. In addition, 24-mo-old mice were used as an aged-model. In the 3-mo-old mice, cognitive function in the vitamin E-deficient (short-term vitamin E-deficient) group was significantly impaired compared to age-matched controls. Although the lipid peroxidation products in the cerebral cortex, cerebellum and hippocampus did not significantly differ in 3-mo-old mice, the levels in the 6-mo-old vitamin E-deficient (long-term vitamin E-deficient) mice were significantly increased compared to age-matched controls. Serum cholesterol content was also significantly increased in the short- and long-term vitamin E-deficient mice compared to their respective age-matched controls. These results indicate that chronic vitamin E deficiency may slowly accelerate brain oxidation. Thus, vitamin E concentrations may need to be monitored in order to prevent the risk of cognitive dysfunction, even under normal conditions.
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  • Maria HAYASHI, Kazuto NOSAKA
    2015 Volume 61 Issue 5 Pages 369-374
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    Thiamin pyrophosphate is an essential cofactor in all living systems. In its biosynthesis, the thiamin structure is initially formed as thiamin phosphate from a thiazole and a pyrimidine moiety, and then thiamin pyrophosphate is synthesized from thiamin phosphate. Many eubacterial cells directly synthesize thiamin pyrophosphate by the phosphorylation of thiamin phosphate by thiamin phosphate kinase (ThiL), whereas this final step occurs in two stages in eukaryotic cells and some eubacterial cells: hydrolysis of thiamin phosphate to free thiamin and its pyrophosphorylation by thiamin pyrophosphokinase. In addition, some eubacteria have thiamin kinase, a salvage enzyme that converts the incorporated thiamin from the environment to thiamin phosphate. This final step in thiamin biosynthesis has never been experimentally investigated in archaea, although the putative thiL genes are found in their genome database. In this study, we observed thiamin phosphate kinase activity in the soluble fraction of the hyperthermophilic archaeon Pyrobaculum calidifontis. On the other hand, neither thiamin pyrophosphokinase nor thiamin kinase activity was detected, suggesting that in this archaeon the phosphorylation of thiamin phosphate is only way to synthesize thiamin pyrophosphate and it cannot use exogenous thiamin for the salvage synthesis of thiamin pyrophosphate. We also investigated the kinetic properties of thiamin phosphate kinase activity using the recombinant ThiL protein from P. calidifontis. Furthermore, the results obtained by site-directed mutagenesis suggest that the Ser196 of ThiL protein plays a pivotal role in the catalytic process.
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  • Chunmei LI, Taekil EOM, Yoonhwa JEONG
    2015 Volume 61 Issue 5 Pages 375-381
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    Glycyrrhiza glabra has been used in medicine for thousands of years. Our previous study revealed that the methanolic extract of Glycyrrhiza glabra L. (EGGR) exhibits significant nitric oxide (NO) inhibitory effect on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages among 100 other extracts. Accordingly, the aim of the present study was to investigate the potential anti-inflammatory effect of EGGR. The anti-inflammatory effect of EGGR on LPS-stimulated RAW 264.7 macrophages was measured by MTT assay, NO content analysis, reactive oxygen species (ROS) level analysis, RT-PCR, Western blot analysis, and ELISA assay. Low doses of EGGR were non-toxic to macrophages and imparted protective effect against LPS induced cell death. Incubation of LPS-treated macrophages with 100 μg/mL EGGR led to an increase in cell viability from 66.6 to 99%. Moreover, EGGR led to down regulation of NO (NO2+NO3) and ROS productions in a dose-dependent manner. In particular, 100 μg/mL EGGR led to a reduction in NO2+NO3 level from 336.2 to 24.1 pM/mL, and ROS level from 483.5 to 128.4%. Consistent with the result related to NO production, EGGR suppressed the ability of LPS to induce mRNA and protein expressions of nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) cytokines, tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), and IL-6 productions which were analyzed by an ELISA assay. These results provide a comprehensive approach into the anti-inflammatory effect of EGGR on LPS-stimulated macrophages; however, efforts are underway on gaining detailed insight into anti-inflammatory signaling pathways.
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  • Takako SUZUKI, Yasutaka KAJITA, Shin-ichi KATSUMATA, Hiroshi MATSUZAKI ...
    2015 Volume 61 Issue 5 Pages 382-390
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    We hypothesized that a zinc-deficient diet alters the mineral (calcium, magnesium, and phosphorus) components of bones, as well as hormones related to bone remodeling, and negatively affects bone metabolism. Four-week-old male Wistar rats were randomly assigned to one of three groups for 4 wk: a zinc-adequate group (C, 30 ppm); a zinc-deficient group (ZD, 1 ppm); and a pair-fed group (PF, 30 ppm), which was pair-fed to the ZD group. Bone mineral density and bone mechanical properties were reduced in the ZD group compared to the C and PF groups. Compared with the C and PF groups, serum osteocalcin, a bone formation marker, was reduced in the ZD group. Conversely, urine deoxypyridinoline, a bone resorption marker, was increased in the ZD group compared to the C and PF groups. Calcium and phosphorus concentrations in bone were not different among all groups. The bone magnesium concentration was significantly higher in the ZD group than in the PF and C groups. Interestingly, compared with the C and PF groups, the ZD group showed a reduction in serum calcium concentration along with an increase in serum parathyroid hormone (PTH) concentration. Although serum 1,25-dihydroxycholecalciferol concentration was significantly higher in the ZD and PF groups than in the C group, the rate of apparent calcium absorption was significantly lower in the ZD group than in the C and PF groups. Therefore, zinc deficiency is suspected to cause an increase in serum PTH concentration owing to an inability to maintain calcium homeostasis, resulting in bone fragility.
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  • Umon AGATA, Jong-Hoon PARK, Satoshi HATTORI, Yuki AIKAWA, Yuya KAKUTAN ...
    2015 Volume 61 Issue 5 Pages 391-399
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    Reduced estrogen secretion and low calcium (Ca) intake are risk factors for bone loss and arterial calcification in female rodents. To evaluate the effects of Ca intake at different amounts on bone mass changes and arterial calcification, 8-wk-old female Wistar rats were randomly placed in ovariectomized (OVX) control and OVX with vitamin D3 plus nicotine (VDN) treatment groups. The OVX with VDN rats were then divided into six groups to receive different amounts of Ca in their diets: 0.01%, 0.1%, 0.3%, 0.6%, 1.2%, or 2.4% Ca. After 8 wk of administration, low Ca intake groups with 0.01% and 0.1% Ca diets had significantly reduced bone mineral density (BMD) and bone mechanical properties as compared with those of the other groups, whereas high Ca intake groups with 1.2% and 2.4% Ca diets showed no differences as compared with the 0.6% Ca intake group. For both the 0.01% and 2.4% Ca intake groups, Ca levels in their thoracic arteries were significantly higher as compared with those of the 0.6% Ca diet group, and that was highly correlated with serum PTH levels. An increase in relative BMP-2 mRNA expression in the arterial tissues of the 0.01% and 2.4% Ca diet groups was also observed. These results suggested that extremely low Ca intake during periods of estrogen deficiency may be a possible risk for the complications of reduced BMD and arterial calcification and that extremely high Ca intake may promote arterial calcification with no changes in BMD.
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  • Akihiro MAETA, Mayuko KAJI, Minami NAGAISHI, Aoi HIRAKAWA, Kyoko TAKAH ...
    2015 Volume 61 Issue 5 Pages 400-405
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    Oral immunotherapy (OIT) is a promising therapeutic approach for treating food allergy. Past studies have shown that OIT reduces allergic response only in severe allergy model mice. We worked to establish mild allergy model mice, and investigated whether ‘rush’ OIT for 10 d improved the allergic response and biomarkers in these mice. Balb/c mice were sensitized to ovomucoid (OM) in alum. The rush OIT was done for 10 d. Oral OM challenge was used to determine the impact of OIT on the allergic response. We measured allergic biomarkers, such as vascular permeability in the skin, plasma levels of total IgE, OM-specific IgE, IgG1 and IgG2a and cytokines in splenocyte culture supernatant. OIT for 10 d did not improve allergy symptoms and increased vascular permeability. Total IgE in the plasma of OIT-treated mice was significantly higher than in that of non-treated mice. OM-specific IgG1 and IgG2a plasma levels were not significantly different between OIT-treated and non-treated mice. Among the cytokine secretion of splenocyte from OIT-treated mice, IFN-γ and IL-10 were significantly lower than in non-treated mice, and IL-4 and IL-5 were significantly higher. Total TGF-β in the OIT-treated group was not detected. The IFN-γ/IL-4 ratio of the OIT-treated group was about 1/8 that of the non-treated group. OIT for 10 d was not effective and some biomarkers showed negative responses in the mild allergy model mice. We suggest OIT should be used very carefully as this treatment carries a risk of worsening allergy symptoms for mice with mild allergy.
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  • Noriyuki MORI, Saki NAKANISHI, Seiko SHIOMI, Shoko KIYOKAWA, Sachie KA ...
    2015 Volume 61 Issue 5 Pages 406-416
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    Licorice flavonoid oil (LFO) is a new functional food ingredient consisting of hydrophobic licorice polyphenols in medium-chain triglycerides. Recent studies reported that LFO prevented and ameliorated diet-induced obesity via the regulation of lipid metabolism-related gene expression in the livers of mice and rats, while it reduced body weight in overweight human subjects by reducing total body fat. However, the direct effects of LFO on energy metabolism have not been studied in human subjects. Therefore, we investigated the effects of ingestion of LFO on energy metabolism, including fat oxidation, by measuring body surface temperature under resting conditions and respiratory gas analysis under exercise conditions in healthy humans. We showed that ingestion of a single 600 mg dose of LFO elevated body trunk skin temperature when measured in a slightly cooled air-conditioned room, and increased oxygen consumption and decreased the respiratory exchange ratio as measured by respiratory gas analysis during 40% Vo2max exercise with a cycle ergometer. Furthermore, repeated ingestion of 300 mg of LFO for 8 d decreased respiratory exchange during the recovery period following 40 min of 30% Vo2max exercise on a treadmill. These results suggest that LFO enhances fat oxidation in humans during light exercise.
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Note
  • Shoko SUZUMURA, Kazuyo TUJIOKA, Takashi YAMADA, Hidehiko YOKOGOSHI, Sa ...
    2015 Volume 61 Issue 5 Pages 417-421
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    Brain protein synthesis and the plasma concentration of growth hormone (GH) are sensitive to dietary ornithine. The purpose of this study was to determine whether dietary arginine, the metabolite of ornithine, affects the brain protein synthesis, and to that end, the effects of arginine on brain protein synthesis were compared with that of ornithine treatment in young rats. Two experiments were done on five or three groups of young rats (5-wk-old) given 0%, 0.25%, 0.5%, 0.7% arginine or 0.7% ornithine-HCl added to a 20% casein diet for 1 d (only one 3 h period) (Experiment 1), or given a diet containing 0% or 0.7% ornithine-HCl or 0.7% arginine added to a 20% casein diet (Experiment 2). The concentrations of plasma growth hormone (GH) and fractional rates of protein synthesis in the brains increased significantly with the 20% casein+0.7% arginine diet and still more with the 20% casein+0.7% ornithine diet compared with the 20% casein diet alone. In the cerebral cortex and cerebellum, the RNA activity [g protein synthesized/(g RNA•d)] significantly correlated with the fractional rate of protein synthesis. The RNA concentration (mg RNA/g protein) was also related to the fractional rate of protein synthesis in these organs. The results suggest that the treatment with arginine is likely to increase the concentrations of GH and the rate of brain protein synthesis in rats, and that the effects of arginine on brain protein synthesis and GH concentration were lower than that of ornithine. The RNA activity is at least partly related to the fractional rate of brain protein synthesis.
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  • Hiroyuki TAKEUCHI, Yui NISHIMURA, Akira OHMORI, Eiichi TABUCHI
    2015 Volume 61 Issue 5 Pages 422-425
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    The excessive intake of trans fatty acids (TFAs) increases serum LDL-cholesterol and reduces HDL-cholesterol. Limited data exist regarding the low-level intake of TFAs, and the tolerable upper-limit level remains to be fully elucidated. A randomized, double-blind, parallel trial was conducted to assess the effects of a low level of TFA supplementation on serum cholesterol levels in healthy adult Japanese women. The volunteers who participated in this examination took in approximately 0.4% of energy (%E) TFAs from daily meals. Fifty-one volunteers consumed one cookie containing 0.6%E (TFA) or 0.04%E (control) of TFAs every day for 4 wk, and blood was harvested after overnight fasting. The mean TFA intakes of the control and TFA groups during the experimental period were 0.4%E and 1.1%E, respectively. There were no significant differences in serum total, LDL- or HDL-cholesterol levels between the control and TFA groups. The serum glucose and insulin levels were not influenced by TFA supplementation. These results confirm that dietary supplementation with 0.6%E TFAs (a total TFA intake of approximately 1%E) would have little effect on serum cholesterol levels in healthy adult Japanese women.
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  • Yuichi OSHIMA, Saikyo RIN, Hisaaki KITA, Yoshimune HIRAMOTO, Shinji MO ...
    2015 Volume 61 Issue 5 Pages 426-431
    Published: 2015
    Released on J-STAGE: December 04, 2015
    JOURNAL FREE ACCESS
    Visceral fat accumulation is regarded as one of the major phenotypes of metabolic syndrome. There have not been enough data on the relationship between the fish-eating habit and visceral adiposity. A total of 94 male participants received abdominal CT for the measurement of the visceral fat area (VFA), serum sampling for the fatty acid composition and questionnaires about their life-style. We divided the participants into two groups: whether they ate their fill (group F, n=70) or they ate in moderation (group M, n=24). Stepwise multiple linear regression analyses showed that usual alcohol consumption and lower daily physical activity in group F, and infrequent fish-eating and frequent fat-rich deserts in group M were the significant positive correlates with the VFA. The serum eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio showed significant correlation with the frequency of fish-eating in both groups. Interestingly, in group M, the serum EPA/AA ratio negatively correlated with the VFA, while it failed in group F. In conclusion, the present data suggest that the fish-eating habit might negatively associate with visceral fat accumulation only in those who are moderate in eating in the general population.
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