Journal of Nutritional Science and Vitaminology (J NUTR SCI VITAMINOL )

Publisher: Nihon Eiyō, Shokuryō Gakkai; Nihon Bitamin Gakkai

Description

Impact factor 0.87

  • Hide impact factor history
     
    Impact factor
  • 5-year impact
    1.37
  • Cited half-life
    8.60
  • Immediacy index
    0.09
  • Eigenfactor
    0.00
  • Article influence
    0.34
  • Other titles
    Journal of nutritional science and vitaminology
  • ISSN
    0301-4800
  • OCLC
    2105431
  • Material type
    Periodical
  • Document type
    Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Muscle atrophy is a complex process that occurs as a consequence of various stress events. Muscle atrophy-associated genes (atrogenes) such as atrogin-1/MAFbx and MuRF-1 are induced early in the atrophy process, and the increase in their expression precedes the loss of muscle weight. Although antioxidative nutrients suppress atrogene expression in skeletal muscle cells, the inhibitory effects of flavonoids on inflammation-induced atrogin-1/MAFbx expression have not been clarified. Here, we investigated the inhibitory effects of flavonoids on lipopolysaccharide (LPS)-induced atrogin-1/MAFbx expression. We examined whether nine flavonoids belonging to six flavonoid categories inhibited atrogin-1/MAFbx expression in mouse C2C12 myotubes. Two major flavones, apigenin and luteolin, displayed potent inhibitory effects on atrogin-1/MAFbx expression. The pretreatment with apigenin and luteolin significantly prevented C2C12 myotube diameter caused by LPS stimulation. Importantly, the pretreatment of LPS-stimulated myoblasts with these flavones significantly inhibited LPS-induced JNK phosphorylation in C2C12 myotubes, resulting in the significant suppression of atrogin-1/MAFbx promoter activity. These results suggest that apigenin and luteolin, prevent LPS-mediated atrogin-1/MAFbx expression through the inhibition of the JNK signaling pathway in C2C12 myotubes. Thus, these flavones, apigenin and luteolin, may be promising agents to prevent LPS-induced muscle atrophy.
    Journal of Nutritional Science and Vitaminology 01/2015;
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    ABSTRACT: In animal models, Fe overload is associated with organ oxidative stress and tissue injury. In this context, luminal Fe may affect the mucosal barrier and function or generate a pathological milieu in the intestine that triggers epithelial cell stress. Here, we hypothesized that increased liver Fe levels resulting from dietary Fe overload may be associated with architectural changes in the cecal mucosa. Weanling male Wistar rats (n=7-10/group) were fed diets (modified from AIN-93G) containing adequate or supplemental Fe (approximately 10 times the recommended levels) for 4 and 12 weeks. At euthanasia, the blood Hb was determined, and Fe analyses were performed in stool and liver samples using atomic absorption spectrophotometry. Cecal tissue was collected for histological and morphometric analysis. No significant differences were observed in the blood Hb and Hb Fe pool between groups in both periods. Iron overload led to a higher fecal Fe excretion, whereas the liver Fe was increased only after 12 weeks when compared with controls. After 4 weeks, the consumption of Fe-overloaded diets resulted in changes in the mucosal architecture of the cecum, which were intensified after 12 weeks. At this time, these changes were significantly correlated with the hepatic Fe content. These findings suggest that changes in the cecal mucosa may have occurred as a result of oxidative stress caused by excessive amounts of Fe in the intestinal lumen. The consequences of these effects on the intestinal absorption and its implications on liver Fe homeostasis should be considered in future studies.
    Journal of Nutritional Science and Vitaminology 08/2014; In press.
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    ABSTRACT: Poor growth in utero has been suggested to be associated with adverse levels of serum cholesterol concentrations in later life. In Asia, there have only been a limited number of studies examining the relationship between fetal status and serum lipids, especially in adolescents. The objective of this study was to examine the relationships between birth weight and serum high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol levels; adjusting for current physical status including percent body fat, physical activity and nutrient intake in healthy Japanese late adolescents. The data of 573 late adolescents with an average age of 17.6 (287 boys and 286 girls) who underwent physical examinations which included blood sampling and who had all the required data, were analyzed. Birth weight was obtained from their maternal and child health handbook. Multiple regression analysis showed that birth weight was positively associated with serum HDL in girls, independently of percent body fat or fat intake, when adjusted for current body height and weight. There were no associations between birth weight and serum HDL in boys, or serum LDL in either sex.
    Journal of Nutritional Science and Vitaminology 01/2014; 60(2):108-13.
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    ABSTRACT: Gastrectomy (GX) induces osteopenia in rats. The present study examined the skeletal effects of vitamin K2 in GX rats. Thirty male Sprague-Dawley rats (12 wk old) were randomized by the stratified weight method into the following three groups of 10 animals each: sham operation (control) group; GX group; and GX+oral vitamin K2 (menatetrenone, 30 mg/kg, 5 d/wk) group. Treatment was initiated at 1 wk after surgery. After 6 wk of treatment, the bone mineral content (BMC), bone mineral density (BMD), and mechanical strength of the femoral diaphysis and distal metaphysis were determined by peripheral quantitative computed tomography and mechanical strength tests, respectively. GX induced decreases in the BMC, BMD, and ultimate force of the femoral diaphysis and distal metaphysis. Vitamin K2 did not significantly influence the BMC or BMD of the femoral diaphysis or distal metaphysis in GX rats, but attenuated the decrease in the ultimate force and increased the stiffness of the femoral diaphysis. The present study showed that administration of vitamin K2 to GX rats improved the bone strength of the femoral diaphysis without altering the BMC or BMD, suggesting effects of vitamin K2 on the cortical bone quality.
    Journal of Nutritional Science and Vitaminology 01/2014; 60(2):71-7.
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    ABSTRACT: Resveratrol (3,4',5-trihydroxy-trans-stilbene) is known to enhance the cytotoxicity of the anticancer drug doxorubicin. On the other hand, breast cancer MCF-7 cells acquire resistance to doxorubicin under hypoxic conditions. In this study, we investigated the effect of resveratrol on hypoxia-induced resistance to doxorubicin in MCF-7 cells. Resveratrol and its derivative 3,5-dihydroxy-4'-methoxy-trans-stilbene, but not 3,5-dimethoxy-4'-hydroxy-trans-stilbene, cancelled hypoxia-induced resistance to doxorubicin at a concentration of 10 μM. Carbonyl reductase 1 (CBR1) catalyzes the conversion of doxorubicin to its metabolite doxorubicinol, which is much less effective than doxorubicin. Hypoxia increased the expression of CBR1 at both mRNA and protein levels, and knockdown of CBR1 inhibited hypoxia-induced resistance to doxorubicin in MCF-7 cells. Knockdown of hypoxia-inducible factor (HIF)-1α repressed the hypoxia-induced expression of CBR1. Resveratrol repressed the expression of HIF-1α protein, but not HIF-1α mRNA, and decreased hypoxia-activated HIF-1 activity. Resveratrol repressed the hypoxia-induced expression of CBR1 at both mRNA and protein levels. Likewise, 3,5-dihydroxy-4'-methoxy-trans-stilbene decreased the hypoxia-induced expression of CBR1 protein, but not 3,5-dimethoxy-4'-hydroxy-trans-stilbene. Furthermore, resveratrol decreased the expression of HIF-1α protein even in the presence of the proteasome inhibitor MG132 in hypoxia. Theses results indicate that in MCF-7 cells, HIF-1α-increased CBR1 expression plays an important role in hypoxia-induced resistance to doxorubicin and that resveratrol and 3,5-dihydroxy-4'-methoxy-trans-stilbene decrease CBR1 expression by decreasing HIF-1α protein expression, perhaps through a proteasome-independent pathway, and consequently repress hypoxia-induced resistance to doxorubicin.
    Journal of Nutritional Science and Vitaminology 01/2014; 60(2):122-8.
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    ABSTRACT: Oral phosphorus supplementation stimulates fibroblast growth factor 23 (FGF23) secretion; however, the underlying mechanism remains unclear. The aim of this study was to investigate the involvement of parathyroid hormone (PTH) in increased plasma FGF23 levels after oral phosphorus supplementation in rats. Rats received single dose of phosphate with concomitant subcutaneous injection of saline or human PTH (1-34) after treatment with cinacalcet or its vehicle. Cinacalcet is a drug that acts as an allosteric activator of the calcium-sensing receptor and reduces PTH secretion. Plasma phosphorus and PTH levels significantly increased 1 h after oral phosphorus administration and returned to basal levels within 3 h, while plasma FGF23 levels did not change up to 2 h post-treatment, but rather significantly increased at 3 h after administration and maintained higher levels for at least 6 h compared with the 0 time point. Plasma PTH and FGF23 levels were significantly lower in the cinacalcet-treated rats than in the vehicle-treated rats. Plasma phosphorus levels were significantly higher in the cinacalcet-treated rats than in the vehicle-treated rats at 2, 3, 4, and 6 h after oral phosphorus administration. Furthermore, rats treated with cinacalcet+human PTH (1-34) showed transiently but significantly higher plasma FGF23 levels at 3 h after oral phosphorus administration compared with cinacalcet-treated rats. These results suggest that oral phosphorus supplementation secondarily increases circulating FGF23 levels at least partially by stimulation of PTH secretion.
    Journal of Nutritional Science and Vitaminology 01/2014; 60(2):140-4.
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    ABSTRACT: Energy metabolism and substrate oxidation during sleep correlate with sleep stage, suggesting that energy metabolism affects sleep architecture or vice versa. The aim of the present study was to examine whether changes in energy metabolism during sleep, induced by a high-carbohydrate or high-fat meal for dinner, affect sleep architecture. Ten healthy males participated in this study, sleeping 3 nonconsecutive nights in a whole-room calorimeter. The first night was scheduled as an adaptation to the experimental environment. The other 2 nights were experimental calorimetry in a balanced cross-over design with intrasubject comparisons. In each session, subjects comsumed a high carbohydrate (HCD: PFC=10 : 10 : 80) or high fat (HFD: PFC=10 : 78 : 12) meal at 2000 h and slept with a polysomnographic recording in a metabolic chamber for indirect calorimetry (0000 h to 0800 h). Slow wave sleep was decreased during the first sleep cycle and not changed during the second or third sleep cycle under HCD conditions compared with those of HFD. Energy expenditure was not affected by dietary condition but substrate oxidation reflected differences in dietary composition of the dinner during the first and second sleep cycle. The present study suggested the possibility that substrate availability during sleep affects substrate oxidation during sleep, and affects sleep architecture during the first sleep cycle.
    Journal of Nutritional Science and Vitaminology 01/2014; 60(2):114-21.
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    ABSTRACT: Two compounds are known as the vitamin niacIn: nicotinic acid (NiA) and nicotinamide (Nam). The physiological functions and metabolic fates of NiA and Nam are identical, but differ when pharmacological doses are administered. Our study aimed to investigate the metabolic interactions between NiA and Nam when their pharmacological doses were administered together. We measured seven major niacin catabolites, including NiA, Nam, N(1)-methylnicotinamide (MNA), N(1)-methyl-2-pyridone-5-carboxamide (2-Py), N(1)-methyl-4-pyridone-3-carboxamide (4-Py), Nam N-oxide, and nicotinuric acid (NuA). Under physiological conditions, niacin is chiefly catabolized to 4-Py via MNA. However, this was not the primary pathway when rats were fed a diet containing excess niacin. When rats were fed a diet containing excess NiA, NuA was the major catabolite, and on being fed a diet containing excess Nam, MNA was the major catabolite. When rats were fed a diet containing an excess of both NiA and Nam, MNA and NuA were the major catabolites. The metabolic fates of excess NiA and Nam did not mutually interfere. Therefore, the administration of NiA and Nam together may be better than the administration of NiA or Nam alone because different pharmacological effects are expected.
    Journal of Nutritional Science and Vitaminology 01/2014; 60(2):86-93.
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    ABSTRACT: Intake of the antioxidant lycopene has been reported to decrease oxidative stress and have beneficial effects on bone health. However, few in vivo studies have addressed these beneficial effects in growing female rodents or young women. The aim of this study was to investigate the effect of lycopene intake on bone metabolism through circulating oxidative stress in growing female rats. Six-week-old Sprague-Dawley female rats were randomly divided into 3 groups according to the lycopene content in their diet: 0, 50, and 100 ppm. The bone mineral density (BMD) of the lumbar spine and the tibial proximal metaphysis increased with lycopene content in a dose-dependent manner; the BMD in 100 ppm group was significantly higher than in the 0 ppm group. The urine deoxypyridinoline concentrations were significantly lower in the 50 and 100 ppm groups than in the 0 ppm group, and the serum bone-type alkaline phosphatase activity was significantly higher in 100 ppm group than in the 0 ppm group. No difference in systemic oxidative stress level was observed; however, the oxidative stress level inversely correlated with the tibial BMD. Our findings suggested that lycopene intake facilitates bone formation and inhibits bone resorption, leading to an increase of BMD in growing female rats.
    Journal of Nutritional Science and Vitaminology 01/2014; 60(2):101-7.
  • Journal of Nutritional Science and Vitaminology 01/2012; 59(Supplement):S36-S43.
  • Journal of Nutritional Science and Vitaminology 01/2012; 59(Supplement):S1-S1.
  • Journal of Nutritional Science and Vitaminology 01/2012; 58(1):20-28.
  • Journal of Nutritional Science and Vitaminology 01/2012; 59(Supplement):S2-S2.
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    ABSTRACT: Porphyran (POR) from the red alga Porphyra yezoensis is a water soluble dietary fiber. In this study, we investigated the effect of dietary POR on glucose metabolism in KK-Ay mice (a model for type 2 diabetes). Mice were divided into 4 groups and fed a diet containing 5% cellulose (control), POR, POR Arg or POR K. After 3 wk of feeding, plasma insulin levels and the calculated homeostasis model assessment-insulin resistance (HOMA-IR) index were significantly lower in the POR group than in the control group. Compared with the control group, plasma adiponectin levels were significantly increased in the POR, POR Arg and POR K groups. These results suggest that dietary POR should improve glucose metabolism in diabetes via up-regulation of adiponectin levels. In addition, the amount of propionic acid in the cecum of the POR group was significantly higher than in the control group and the profile of bacterial flora was changed by dietary POR. In the cecum of the POR, POR Arg and POR K groups, Bacteroides was significantly increased and Clostridium coccoides was significantly decreased compared with in the control group. The effects of dietary POR on the hindgut environment might contribute to the improvement of glucose metabolism.
    Journal of Nutritional Science and Vitaminology 01/2012; 2012;58(1):14-9.(58(1)):14-19.
  • Journal of Nutritional Science and Vitaminology 01/2012; 58(1):59-62.
  • Journal of Nutritional Science and Vitaminology 01/2012; 59(Supplement):S83-S90.
  • Journal of Nutritional Science and Vitaminology 01/2010; 56(1):77-81.