Journal of Nutritional Science and Vitaminology Impact Factor & Information

Publisher: Nihon Eiyō, Shokuryō Gakkai; Nihon Bitamin Gakkai

Journal description

Current impact factor: 0.87

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 0.868
2012 Impact Factor 0.992
2011 Impact Factor 1.199
2010 Impact Factor 1.228
2009 Impact Factor 0.929
2008 Impact Factor 0.797
2007 Impact Factor 0.784
2006 Impact Factor 0.758
2005 Impact Factor 0.787
2004 Impact Factor 0.741
2003 Impact Factor 0.701
2002 Impact Factor 0.72
2001 Impact Factor 0.727
2000 Impact Factor 0.653
1999 Impact Factor 0.617
1998 Impact Factor 0.452
1997 Impact Factor 0.68
1996 Impact Factor 0.613
1995 Impact Factor 0.515
1994 Impact Factor 0.585
1993 Impact Factor 0.387
1992 Impact Factor 0.383

Impact factor over time

Impact factor
Year

Additional details

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: 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. DOI:10.3177/jnsv.60.101
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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. DOI:10.3177/jnsv.60.140
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    ABSTRACT: To determine the rates of cellular NAD+ synthesis and breakdown, incorporation of stable isotope-labeled precursors into NAD+ should be quantified. Although with 2H (D)-labeled precursors [2,4,5,6-D4]nicotinamide ([D4]Nam) and [2,4,5,6-D4]nicotinic acid ([D4]NA), [D3]NAD+ is formed in human cells, why only three of four D atoms from [D4]Nam and [D4]NA are present in NAD+ remains unknown. Using a liquid chromatography-tandem mass spectrometry, we tested the involvement of D/1H (H) exchange at the redox site of NAD+/NADH (C-4 carbon of the pyridine ring) by oxidoreductases exhibiting opposite stereospecificity for the coenzymes in the 1-Da mass decrease in the cellular NAD+ formation. In all cells examined, [Nam-D3]NAD+, but not [Nam-D4]NAD+, was obtained after the incubation with the D4-labeled precursors, whereas [Nam-D4]NAD+, but not [Nam-D3]NAD+, was synthesized from the same precursors with purified recombinant NAD+ biosynthetic enzymes. [D4]Nam group of [Nam-D4]NAD+ was converted to [D3]Nam group via [D4]NADH by in vitro sequential reduction and oxidation with oxidoreductases exhibiting opposite stereospecificity for the coenzymes. Furthermore, using [2,5,6-D3]Nam, which has H instead of D at the C-4 carbon, as a precursor of NAD+ in the cells, the 1-Da mass decrease in the nucleotide was not observed. Based on these observations, we conclude that following the synthesis of [Nam-2,4,5,6-D4]NAD+, cellular redox reactions of NAD+/NADH convert [Nam-2,4,5,6-D4]NAD+ to [Nam-2,5,6-D3]NAD+. Quantification of [Nam-2,5,6-D3]NAD+ and [2,5,6-D3]Nam would successfully determine the rate of the NAD+ turnover and provide clues to understand regulatory mechanisms of cellular NAD+ concentrations.
    Journal of Nutritional Science and Vitaminology 01/2014; 60(1):17-21. DOI:10.3177/jnsv.60.17
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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. DOI:10.3177/jnsv.60.71
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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. DOI:10.3177/jnsv.60.122
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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. DOI:10.3177/jnsv.60.108
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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. DOI:10.3177/jnsv.60.114
  • Journal of Nutritional Science and Vitaminology 01/2014; 60(6):455-456. DOI:10.3177/jnsv.60.455
  • Journal of Nutritional Science and Vitaminology 01/2013; 59(4):264-271. DOI:10.3177/jnsv.59.264
  • Journal of Nutritional Science and Vitaminology 01/2012; 59(Supplement):S36-S43. DOI:10.3177/jnsv.59.S36
  • Journal of Nutritional Science and Vitaminology 01/2012; 58(1):59-62. DOI:10.3177/jnsv.58.59
  • Journal of Nutritional Science and Vitaminology 01/2012; 59(Supplement):S83-S90. DOI:10.3177/jnsv.59.S83
  • Journal of Nutritional Science and Vitaminology 01/2012; 59(Supplement):S26-S35. DOI:10.3177/jnsv.59.S26
  • Journal of Nutritional Science and Vitaminology 01/2012; 58(1):45-49. DOI:10.3177/jnsv.58.45