Molecular Nutrition & Food Research (Mol Nutr Food Res)

Publisher: Wiley-VCH Verlag

Journal description

Molecular Nutrition & Food Research is a primary research journal devoted to linking the information arising from the scientific disciplines involved in molecular nutrition and food research. Thus, the areas covered by the journal are: Bioactivity and Safety / Chemistry / Immunology / Microbiology / Nutrition / Technology. Besides the regular contributions, Molecular Nutrition & Food Research (MNF) publishes special issues devoted to current topics from one of the above-mentioned fields, plus annual review issues.

Current impact factor: 4.60

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 4.603
2013 Impact Factor 4.909
2012 Impact Factor 4.31
2011 Impact Factor 4.301
2010 Impact Factor 4.713
2009 Impact Factor 4.356
2008 Impact Factor 3.308
2007 Impact Factor 3.439
2006 Impact Factor 2.687
2005 Impact Factor 2.071

Impact factor over time

Impact factor

Additional details

5-year impact 4.77
Cited half-life 4.80
Immediacy index 0.85
Eigenfactor 0.02
Article influence 1.11
Website Molecular Nutrition & Food Research website
Other titles Molecular nutrition & food research (Online), Molecular nutrition and food research
ISSN 1613-4133
OCLC 56493322
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Wiley-VCH Verlag

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • Upon funder agreement with publisher
  • Conditions
    • Pre-print may be deposited on personal intranet or institutional intranet repository, but not on a public repository
    • Pre-print must not updates with future versions
    • Published source must be acknowledged with set phrases (See policy)
    • Must link to publisher's site:
    • Publisher's version/PDF cannot be used
    • Some journal exceptions-check individual homepages
  • Classification
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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: The pharmacokinetics, bioavailability and regional brain distribution of polyphenols from apple-grape seed extract (AGSE) mixture and bilberry extract was studied after three weeks of dosing in weanling pigs. Materials and methods: Weanling piglets were treated for 3 weeks with extracts of (AGSE) or bilberry extracts, using a physiological (27.5 mg/kg) or supplement (82.5mg/kg) dose. A 24 hour pharmacokinetic study was conducted and brain tissue was harvested. Major flavan-3-ol and flavonol metabolites including catechin-O-β-glucuronide, epicatechin-O-β-glucuronide, 3'O-methyl-catechin-O-β-glucuronide, 3'methyl-epicatechin-O-β-glucuronide, quercetin-O-β-glucuronide and O-methyl-quercetin-O-β-glucuronide were analyzed in plasma, urine and regional brain extracts from AGSE groups. Anthocyanidin-O-galactosides and O-glucosides of delphinidin (Del), cyanidin (Cyn), petunidin (Pet), peonidin (Peo) and malvidin (Mal) were analyzed in plasma, urine and brain extracts from bilberry groups CONCLUSION: : Significant plasma dose-dependence was observed in flavan-3-ol metabolites and methyl-quercetin-β-glucuronide of the AGSE group and in Del and Cyn galactosides and Pet, Peo, and Cyn glucosides of the bilberry groups. In the brain, a significant dose-dependence was found in the cerebellum and frontal cortex in all major flavan-3-ol metabolites. All anthocyanidin glycosides except for delphinidin, showed a dose-dependent increase in the cerebellum. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500224
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    ABSTRACT: Scope: To identify the most discriminant dietary biomarkers of nuts exposure in subjects with metabolic syndrome (MetS), and investigate the potential association between exposure and the severity of the MetS diagnostic traits. Methods and results: We applied the untargeted LC-ESI-qToF-MS-driven metabolomic workflow to explore the changes occurring in the plasma metabolome of MetS subjects following 12-week intake of mixed nuts (30 g/d) (nuts versus control groups). Urolithin A glucuronide was the most discriminative biomarker of nut exposure, showing the highest predictive capacity [ROC AUC = 89.6% (80.8-98.4)] despite the inter-individual variation expected for a host-microbial cometabolite. Furthermore, the detection of urolithin A glucuronide in plasma showed significant inverse correlation with basal abdominal adiposity (waist circumference: r = -0.550, p<0.01; waist-hip ratio: r = -0.409, p<0.05) and impaired glycemic control (fasting insuli & HOMA-IR: r = -0.417, p<0.05). Significant changes in medium-chain dicarboxylic acids, recognized as alternative energy substrates that are particularly relevant in the case of glycemic control impairment, were also associated with nut consumption. Conclusion: Higher levels of urolithin are reported in subjects with less severe MetS traits, especially in females. We believe that this inverse correlation may be related with profile of gut microbial dysbiosis, recently associated to subjects with MetS. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500549
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    ABSTRACT: Scope: Blackcurrants (Ribes nigrum L., Grossulariaceae) contain high amounts of anthocyanin polyphenols, which have antioxidant and anti-carcinogenic health benefits. This study analyzed the potential phytoestrogenic effects of blackcurrant extract (BCE) in breast cancer (MCF-7) and human endometrial cancer (Ishikawa) cell lines that over-express estrogen receptor alpha (ERα), as well as in immature female rats. Methods and results: Microarray analysis and Ingenuity® Pathway Analysis showed that BCE activated the ERα pathway, whereas quantitative-PCR confirmed that BCE and four types of anthocyanins up-regulated genes downstream of ERα. BCE (0.1-1.0 μg/mL) and anthocyanins (0.1-10 μM) induced MCF-7 cell proliferation; however, this effect was blocked by ER antagonist fulvestrant. Flow cytometry showed that anthocyanins reduced and increased the number of MCF-7 cells in the G0/G1 and G2/M phases, respectively. Anthocyanins stimulated ERα transcriptional activity in human ERα reporter assays and induced alkaline phosphatase activity in Ishikawa cells. Competition assays and in silico analysis indicated that anthocyanins bind to ERα. Finally, BCE focally induced stratification of columnar epithelial cells in the rat uterus and increased cytoplasmic mucin levels in these cells. Conclusion: These results suggest that blackcurrant anthocyanins act as phytoestrogens in vitro and in vivo. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500479
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    ABSTRACT: Scope: Selenium (Se)-conjugated compounds have been established as anti-carcinogenic compounds. The use of chemicals as cancer chemotherapeutic agents to induce programmed cell death (PCD) involves genetic and epigenetic modifications. In this study, we investigated the underlying molecular mechanisms of Se-allylselenocysteine (ASC)-induced PCD and protocadherin 17 (PCDH17) expression in HT-29 cells. Methods and results: Cell viability analysis indicated that the ability of ASC to induce cancer cell death was greater than that of Se-methylselenocysteine in colorectal cancer cells. ASC also decreased global DNA methylation levels via downregulation of DNA methyltransferase 1 expression. The autophagic cell death is the cause in ASC-induced cytotoxicity that was inhibited by pretreatment with autophagy inhibitor. At the molecular level, ASC induced PCDH17 expression through decreased PCDH17 promoter hypermethylation. PCDH17 is also an important role in ASC-induced autophagy by HT-29 transfected with PCDH17 shRNA or expression plasmid. Our western blot analysis showed that ASC significantly induced autophagy via the AMPK/mTOR pathway that was also regulated PCDH17 expression. Additionally, we used the HT-29 tumor xenograft models to confirm the ability of ASC inhibited tumor growth. Conclusion: These results reveal that ASC is an effective inducer of autophagy through regulating the AMPK/mTOR and PCDH17 expression via epigenetic modification. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500373
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    ABSTRACT: Scope: Fructose consumption can induce insulin resistance and metabolic syndrome, which are associated with glomerular podocyte dysfunction and proteinuria. This study investigated whether fructose caused insulin signaling impairment in podocyte dysfunction and injury, and whether curcumin reduced these disturbances. Methods and results: Rats were exposed to 10% fructose for 6 weeks and then orally co-treated with curcumin for next 6 weeks. Metabolic syndrome, podocyte injury, microRNA (miRNA) expression and insulin signaling were evaluated. Curcumin significantly alleviated fructose-induced podocyte injury and proteinuria, miR-206 low-expression, protein tyrosine phosphatase-1B (PTP1B) overexpression, as well as down-regulation of insulin receptor, insulin receptor substrate-1, caveolin-1, protein kinase B, and extracellular signal-regulated kinases 1 and 2 phosphorylation in kidney cortex or glomeruli of fructose-fed rats. These effects were further confirmed in cultured differentiated podocytes exposed to 5 mM fructose in the presence or absence of curcumin, PTP1B siRNA, lentivirus-mediated PTP1B recombinant overexpression, miR-206 mimic or miR-206 inhibitor transfection, showing that miR-206 up-regulation may contribute to improve insulin signaling through regulating PTP1B expression. Conclusion: Curcumin may activate miR-206 expression to down-regulate PTP1B, and then improve insulin signaling, protect against fructose-induced glomerular podocyte injury and proteinuria, which may provide new evidence regarding curcumin's effects on fructose-associated podocyte injury. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500370
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    ABSTRACT: Scope: Very few studies have evaluated serum hepcidin in patients with type 2 diabetes and they have reported conflicting results. In addition, the effect of antidiabetic drugs on circulating hepcidin has not been explored so far. The aims of the study were to evaluate hepcidin concentrations and hepcidin/ferritin ratio in type 2 diabetes subjects and healthy non-diabetic controls and to evaluate the effect of metformin on hepcidin concentrations. Methods and results: Study 1) Cross-sectional multivariate study of 239 non-diabetic individuals and 65 people with type 2 diabetes. The multivariate analysis included covariates of chronic inflammation, BMI, pharmacological treatment, menopausal status and insulin resistance. Study 2) Randomized, double-blinded, placebo-controlled 4-month trial metformin compared to placebo among 36 type 2 diabetic patients. In both groups diet was controlled by maintaining a hypocaloric intake across the trial. Hepcidin levels were significantly lower in patients with type 2 diabetes than in non-diabetic individuals either in crude or adjusted regression models (P<0.05). Hepcidin decreased in both arms of the trial (Placebo, p = 0.004; metformin, p = 0.022). Conclusion: Circulating hepcidin was significantly and independently lower in type 2 diabetes. Metformin treatment is not associated with reductions in hepcidin but hypocaloric diet could be involved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500310
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    ABSTRACT: Scope: This study aimed to examine the effects of Val-Pro-Pro (VPP), a food-derived peptide with an angiotensin-converting enzyme (ACE) inhibitory property, on obesity-linked insulin resistance and adipose inflammation in vivo and in vitro. Methods and results: C57BL/6J mice were fed high-fat high-sucrose diet and VPP (0.1% in water) for 4 months. For in vitro analysis, co-culture of 3T3-L1 adipocytes over-expressing either ACE (3T3-ACE) or GFP (3T3-GFP) and RAW264 macrophages was conducted with VPP. In diet-induced obese mice, VPP improved insulin sensitivity, concomitant with a significant decrease in tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) expression in adipose tissue, with a tendency (p = 0.06) towards decreased CC chemokine ligand 5 (CCL-5) expression. Additionally, VPP administration inhibited macrophage accumulation and activation in fat tissues. In vitro, VPP attenuated TNF-α mRNA induced by ACE-overexpression in 3T3-L1 adipocytes. TNF-α and IL-1β expression decreased following VPP treatment of RAW264 macrophage and 3T3-ACE adipocyte co-cultures, but not in RAW264-3T3-GFP adipocyte co-cultures. Conclusion: Our data suggest that VPP inhibits adipose inflammation in the interaction between adipocytes and macrophages, acting as an ACE inhibitor, thereby improving obesity-related insulin resistance. Thus, ingestion of VPP may be a viable protective and therapeutic strategy for insulin resistance and obesity-associated adipose inflammation. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500324
  • Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500605
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    ABSTRACT: Scope: Hydroxytyrosol acetate (HTy-Ac), an extra virgin olive oil (EVOO) polyphenol, has recently been reported to exhibit antioxidant and anti-inflammatory effects on LPS-stimulated macrophages and ulcerative colitis. This study was designed to evaluate dietary HTy-Ac supplementation effects on collagen-induced arthritis (CIA) in mice. Methods and results: DBA-1/J mice were fed from weaning with 0.05% HTy-Ac. After 6 weeks, arthritis was induced by type II collagen. Mice were sacrificed 42 days after first immunization. Blood was recollected and paws were histological and biochemically processed. HTy-Ac diet significantly prevented arthritis development and decreased serum IgG1 and IgG2a, cartilage olimeric matrix protein (COMP) and metalloproteinase-3 (MMP-3) levels, as well as, pro-inflammatory cytokines levels (TNF-α, IFN-γ, IL-1β, IL-6 and IL-17A). The activation of Janus kinase-signal transducer and activator of transcription (JAK/STAT), mitogen-activated protein kinases (MAPKs) and nuclear transcription factor-kappa B (NF-κB) pathways were drastically ameliorated whereas nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) protein expressions were significantly up-regulated in those mice fed with HTy-Ac. Conclusion: HTy-Ac improved the oxidative events and returned pro-inflammatory proteins expression to basal levels probably through JAK/STAT, MAPKs and NF-κB pathways. HTy-Ac supplement might provide a basis for developing a new dietary strategy for the prevention of rheumatoid arthritis. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500304
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    ABSTRACT: ScopeNobiletin (NBT) is a major citrus flavonoid with various health benefits. Herein, we investigated the colon cancer chemopreventive effects of NBT and its colonic metabolites in a colitis-associated colon carcinogenesis mouse model as well as in human colon cancer cell models.Methods and resultsIn azoxymethane (AOM)/dextran sulfate sodium (DSS)-treated mice, oral administration of NBT effectively decreased both incidence and multiplicity of colonic tumors. NBT showed significant anti-proliferative, pro-apoptotic and anti-inflammatory effects in the mouse colon. HPLC analysis revealed that oral administration of NBT resulted in high levels of metabolites, i.e. 3'-demethylnobiletin (M1), 4'-demethylnobiletin (M2), and 3', 4'-didemethylnobiletin (M3) in the colonic mucosa. In contrast, the colonic level of NBT was about 20-fold lower than the total colonic level of three metabolites. Cell culture studies demonstrated that the colonic metabolites of NBT significantly inhibited the growth of human colon cancer cells, caused cell cycle arrest, induced apoptosis, and profoundly modulated signaling proteins related with cell proliferation and cell death. All of these effects were much stronger than those produced by NBT alone.Conclusions Our results demonstrated that oral administration of NBT significantly inhibited colitis-associated colon carcinogenesis in mice, and this chemopreventive effect was strongly associated with its colonic metabolites.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 09/2015; DOI:10.1002/mnfr.201500378
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    ABSTRACT: Catechol moieties are commonly present in dietary natural products that exert cancer chemopreventive activity. While the oxidative conversion of catechols into their corresponding o-quinones is generally considered to contribute to their cancer chemopreventive effects, the mechanism of the intracellular conversion has not been fully elucidated. Among resveratrol and its hydroxylated analogs examined, only 3,4-dihydroxy-trans-stilbene exerted cytoprotective effects against t-butylhydroperoxide-induced death of HepG2 cells. This resveratrol analog activated the Nrf2 pathway through stimulating phosphorylation of Akt and inducing keap1 modification, thereby resulting in its nuclear translocation and subsequent transcriptional induction of phase II detoxifying enzymes. Its cytoprotective effect through Nrf2 activation was largely abrogated by pretreatment of cells with DTT, a sulfhydryl-containing nucleophile, and neocuproine, a specific chelating agent for copper ions. We identified 3,4-dihydroxy-trans-stilbene as a novel Nrf2 activator which is converted intracellulary into its corresponding o-quinone electrophile by Cu2+ ions. The copper-mediated oxidation was required for the Nrf2 activation, subsequent transcriptional induction of phase II detoxifying enzymes and ultimately for cytoprotection. The findings demonstrate a previously under-recognized role for intracellular copper ions in the cancer chemopreventive effects of catechol-containing dietary natural products. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 08/2015; DOI:10.1002/mnfr.201500297