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: 4.91

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 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
2004 Impact Factor

Impact factor over time

Impact factor
Year

Additional details

5-year impact 4.89
Cited half-life 4.00
Immediacy index 0.53
Eigenfactor 0.02
Article influence 1.21
Website Molecular Nutrition & Food Research website
Other titles Molecular nutrition & food research (Online), Molecular nutrition and food research
ISSN 1613-4125
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: http://www.interscience.wiley.com/
    • Publisher's version/PDF cannot be used
    • Some journal exceptions-check individual homepages
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope Inflammatory response of macrophages is regulated by vitamin E forms. The long-chain metabolite α-13′-carboxychromanol (α-13’-COOH) is formed by hepatic α-tocopherol (α-TOH) catabolism and acts as a regulatory metabolite via pathways that are different from its metabolic precursor Methods and results Using semi-synthetically-derived α-13’-COOH we profiled its action on lipopolysaccharide (LPS)-induced expression of pro- and anti-inflammatory genes using RT-qPCR and of key proteins by Western blotting. Effects on inflammatory response were assessed by measuring production of nitric oxide and prostaglandin (PG) E2, PGD2 and PGF2α. α-13’-COOH inhibits pro-inflammatory pathways in LPS-stimulated RAW264.7 macrophages more efficiently than α-TOH. Profiling inflammation-related genes showed significant blocking of interleukin (Il)1β by the metabolite and its precursor as well, while upregulation of Il6 was not impaired. However, induction of Il10, cyclooxygenase 2 (Cox2) and inducible nitric oxide synthase (iNos) by LPS and consequently the formation of nitric oxide and PG was significantly reduced by α-13’-COOH. Interestingly, α-13’-COOH acted independently from translocation of NFκB subunit p65 Conclusion Our study sheds new light on the mode of action of α-TOH on the inflammatory response in macrophages, which may be mediated in vivo at least in part by its metabolite α-13’-COOH. Our data show that α-13’-COOH is a potent anti-inflammatory molecule
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201400737
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Oxidized LDL (oxLDL) induced vascular endothelial cell injury is a key event in the pathogenesis of atherosclerosis (AS). In our previous studies, we showed that delphinidin-3-glucoside (Dp), a natural anthocyanin, attenuated oxLDL-induced injury in human umbilical vein endothelial cells (HUVECs), indicating its potential role in preventing AS. However, the involved mechanism is not fully understood. Methods and results: Via methyl thiazolyl tetrazolium and flow cytometry assay, we found that Dp-attenuated oxLDL-induced cell viability decrease and apoptosis in HUVECs. Depending on confocal microscopy, transmission electron microscopy, and Western blot assay, we found that Dp-induced autophagy in HUVECs, whereas suppression of autophagy significantly abolished the protective role of Dp against oxLDL-induced endothelial cell injury. Furthermore, Dp upregulated sirtuin 1 (SIRT1) expression and SIRT1 knockdown notably suppressed Dp-induced autophagy in HUVECs. Dp also increased the expression of phosphorylated adenosine monophosphate-activated protein kinase, while adenosine monophosphate-activated protein kinase (AMPK) knockdown remarkably abolished Dp-induced SIRT1 expression and subsequent autophagy. Conclusion: Our data suggested that Dp protected HUVECs against oxLDL-induced injury by inducing autophagy via the adenosine monophosphate-activated protein kinase/SIRT1 signaling pathway. This new finding might shed light to the prevention and therapy of AS.
    Molecular Nutrition & Food Research 10/2014; 58(10). DOI:10.1002/mnfr.201400161
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    ABSTRACT: Scope: To provide updated quantitative estimates of the associations between allium vegetables intake and risk of colorectal cancer and colorectal adenomatous polyps. Methods and results: We combined all published data on the issue, using a meta-analytic approach. Pooled relative risks (RRs) were calculated using random-effects models. Sixteen studies (13 333 cases) were included in the meta-analyses of colorectal cancer. Seven studies provided information on garlic, six on onion, and four on total allium vegetables. The pooled RRs of colorectal cancer for the highest versus the lowest category of intake were 0.85 (95% confidence interval; CI, 0.72-1.00) for garlic (0.76 for case-control, 0.99 for cohort studies), 0.85 (95% CI, 0.70-1.04) for onion (0.74 for case-control, 1.04 for cohort studies), and 0.78 (95% CI, 0.56-1.08) for total allium vegetables. Significant heterogeneity was found for the three meta-analyses. The pooled RR of colorectal adenomatous polyps for the highest versus the lowest category of total allium vegetables intake was 0.88 (95% CI, 0.80-0.98, three studies), with no heterogeneity. Conclusion: High garlic intake may reduce the risk of colorectal cancer. However, evidence of such protection derived mainly from case-control studies. High intake of total allium vegetables may be associated with a risk reduction of colorectal adenomatous polyps.
    Molecular Nutrition & Food Research 09/2014; 58(9). DOI:10.1002/mnfr.201400169
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    ABSTRACT: Trigonelline (1-methylpyridinium-3-carboxylate), an alkaloid present in coffee and fenugreek seed, has been reported to exhibit phytoestrogenic activity. The aim of the present study was to investigate the effects of trigonelline on bone mechanical properties of rats with normal estrogen level and estrogen deficiency (developing osteoporosis).
    Molecular Nutrition & Food Research 07/2014; 58(7). DOI:10.1002/mnfr.201300936
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    ABSTRACT: Scope: This study investigated the effects of supplementing different ratios of omega-6 and omega-3 fatty acids (O6H = 10:1, O3O6 = 4:1, and O3H = 1:4) to western-style diets on cow �-lactoglobulin (BLG) induced allergic reactions in Balb/c mice. Methods and results: Three-week-old mice were randomly assigned to three diet groups (n = 20/group). At 9 wk of age, half of the mice from each dietary treatment (n = 10) were intraperitoneally (i.p.) sensitized with three weekly doses of BLG and alum while the remaining half from each group was sham sensitized (controls). One week after the final sensitization, all mice were orally challenged with BLG. Elevated BLG-specific serum Igs were observed in all sensitized and challenged mice. IFN-�,MCP-1, and IL-12p40 concentrations from lymphocytes of mesenteric lymph nodes were highest in O3H mice, compared to O3O6 and O6H mice. O6H mice had the highest IL-4 concentrations from splenic lymphocytes and a significantly lower rectal temperature after the challenge in comparison to O3O6 and O3H mice. Conclusions: Our results suggest that the �-3 PUFA rich diets alleviated the severity of allergic reactions, and may modulate immune response toward T helper cell (Th)1-favoured immune response while the �-6 PUFA rich diet exhibited no allergy alleviation with a stronger Th2 polarized immune response.
    Molecular Nutrition & Food Research 06/2013;
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    ABSTRACT: Type 2 diabetes is a chronic condition in which cells have reduced insulin signalling, leading to hyperglycemia and long-term complications, including heart, kidney and liver disease. Macrophages activated by dying or stressed cells, induce the transcription factor nuclear factor kappa-B leading to the production of pro-inflammatory cytokines including TNF and IL-6. These inflammatory macrophages in liver and adipose tissue promote insulin resistance, and medications which reduce inflammation and enhance insulin signalling improve glucose control. Curcumin is an anti-oxidant and nuclear factor kappa-B inhibitor derived from turmeric. A number of studies have shown that dietary curcumin reduces inflammation and delays or prevents obesity-induced insulin resistance and associated complications, including atherosclerosis and immune mediate liver disease. Unfortunately dietary curcumin is poorly absorbed by the digestive system and undergoes glucuronidation and excretion rather than being released into the serum and systemically distributed. This confounds understanding of how dietary curcumin exerts its beneficial effects in type 2 diabetes and associated diseases. New improved methods of delivering curcumin are being developed including nanoparticles and lipid/liposome formulations that increase absorption and bioavailability of curcumin. Development and refinement of these technologies will enable cell-directed targeting of curcumin and improved therapeutic outcome.
    Molecular Nutrition & Food Research 03/2013;
  • Molecular Nutrition & Food Research 01/2012; 56 (2):345-351.
  • Molecular Nutrition & Food Research 01/2010; 54:1546-1555.