Molecular Nutrition & Food Research (Mol Nutr Food Res )

Publisher: John Wiley and Sons

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

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 1613-4133
OCLC 56493322
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

John Wiley and Sons

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • See Wiley-Blackwell entry for articles after February 2007
    • On personal web site or secure external website at authors institution
    • Deposit in institutional repositories is not allowed
    • JASIST authors may deposit in an institutional repository
    • Non-commercial
    • Pre-print must be accompanied with set phrase (see individual journal copyright transfer agreements)
    • Published source must be acknowledged with set phrase (see individual journal copyright transfer agreements)
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • 'John Wiley and Sons' is an imprint of 'Wiley'
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Insulin-regulated glucose metabolism in cells is critical for proper metabolic functioning, and insulin resistance leads to type 2 diabetes. We performed a human study to assess the availability of structurally related dietary flavonols and tested their ability to affect cellular glucose uptake, metabolism and glucose transporter gene expression in a liver HepG2 cell model. Eight healthy volunteers consumed a meal containing galangin, kaempferol, quercetin and myricetin. In plasma, myricetin was absent, but the others were present, mostly as conjugates. In HepG2 cells, a combination of galangin, kaempferol and quercetin (5 μM each) for 12 h increased the acute uptake of [U-(14) C]-glucose and 2-[U-(14) C]-deoxyglucose by almost 100 and ∼10% respectively. All of the combinations increased glucose metabolism, but the effect on transport was less pronounced and mixed. A mixture of all flavonols significantly increased mRNA expression of the main glucose transporter Glut1 in HepG2 cells. These results for the first time show the presence of galangin conjugates in human plasma, and allow direct comparison between absorption of flavonols. A combination of flavonols has the potential to modulate sugar metabolism, both uptake into cells as evident from effects on deoxyglucose, and also further cellular glucose metabolism. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: In humans, urinary hydroxytyrosol (OHTyr) concentrations have been associated to alcohol and wine consumption. To explore the role of wine components on promoting an endogenous OHTyr generation we performed a crossover, double-blind, randomized controlled clinical trial (n = 28 healthy volunteers). Ethanol (wine and vodka), dealcoholized wine, and placebo were administered. Alcohol, dealcoholized wine, and particularly wine promoted a de novo OHTyr generation in vivo in humans. Potential OHTyr precursors (tyrosine, tyrosol, tyramine) were investigated in rats. Tyrosol was metabolized to OHTyr. Collating both studies, it is postulated that an increased Tyr bioavailability, a shift to a reductive pathway in dopamine and tyramine oxidative metabolism, and the biotransformation of Tyr to OHTyr were mechanisms involved in the OHTyr endogenous generation. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: To obtain an up-to-date quantification of the association between dietary glycemic index (GI) and glycemic load (GL) and the risk of cancer. We conducted a systematic review and meta-analysis of observational studies updated January 2015. Summary relative risks (RR) were derived using random-effects models. Seventy-five reports were evaluated in the systematic review (147090 cases), and 72 were included in the meta-analyses. Considering hormone-related cancers, summary RRs comparing the highest versus the lowest GI and GL intake were, respectively, 1.05 and 1.07 for breast, 1.13 and 1.17 for endometrial, 1.11 and 1.19 for ovarian, and 1.06 and 1.04 for prostate cancers. Considering digestive-tract cancers, summary RRs for GI and GL were, respectively, 1.46 and 1.25 for esophageal (squamous cell carcinoma), 1.17 and 1.10 for stomach, 1.16 (significant) and 1.10 for colorectal, 1.11 and 1.14 for liver, and 1.10 and 1.01 for pancreatic cancers. In most of these meta-analyses, significant heterogeneity among studies was observed. In subgroup analyses, case-control studies and studies from Europe tended to estimate higher RRs. High GI and GL diets are related to moderately increased risk of cancer at several common sites. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: This study aimed to assess the impact of the "often neglected" intestinal brush border membranes (BBM) hydrolases on dietary peptides, exploring the possibility that the disintegration of proteins progressed in the small intestine up to a "core" of intrinsically stable oligopeptides, persisting independently on the up-stream breakdown. Samples of sodium caseinate, skim milk powder and whey protein isolate were submitted to in vitro simulated gastro-pancreatic digestion using two different procedures: i) a simplified model involving the main compartmental specific proteases; ii) a static digestion method based on a frameset of parameters inferred from in vivo. The gastro-duodenal digesta were further hydrolyzed with peptidases from porcine jejunal BBM. The peptidomes arising from the two digestion models, characterized by combined HPLC and MS techniques, differed to some extent. However, only specific protein domains survived digestion, among which potential bioactive or immunogenic (food allergy) peptides. The degree of hydrolysis after BBM digestion (70-77%) practically did not differ between the digestion models and significantly increased the degree of hydrolysis after duodenal steps. Any in vitro digestion model should be supplemented with a jejunal phase to realistically determine the bioaccessibility and bioavailability of dietary peptides. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: Resveratrol reportedly improves fatty liver. This study purposed to elucidate the effect of resveratrol on fatty liver in mice fed a high-fat (HF) diet, and to investigate the role of liver macrophages (Kupffer cells). C57BL/6 mice were divided into three groups, receiving either a control diet, HF diet (50% fat), or HF supplemented with 0.2% resveratrol (HF+res) diet, for 8 weeks. Compared with the HF group, the HF+res group exhibited markedly attenuated fatty liver, and reduced lipid droplets (LDs) in hepatocytes. Proteomic analysis demonstrated that the most down-regulated protein in the livers of the HF+res group was adipose differentiation-related protein (ADFP), which is a major constituent of LDs and reflects lipid accumulation in cells. The HF+res group exhibited greatly increased numbers of CD68(+) Kupffer cells with phagocytic activity. Immunohistochemistry showed that several CD68(+) Kupffer cells were co-localized with ADFP immunoreaction in the HF + res group. Additionally, the HF + res group demonstrated markedly decreased TNF-alpha production, which confirmed by both liver mononuclear cells stimulated by lipopolysaccharide (LPS) in vitro and in situ hybridization analysis, compared with the HF group. Resveratrol ameliorated fatty liver and increased CD68-positive Kupffer cells with down-regulating ADFP expression. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: Poor oral bioavailability of curcuminoids limited their various applications, and one of the main reasons is their rapid metabolism in vivo. Sulfonation via sulfotransferases (SULTs) is an important metabolic pathway for such compounds. The objective of this study is to determine the SULT-isoform-specific metabolic fingerprint, tissue-specific rate, and reaction kinetic profiles to describe the characterization and contribution of curcuminoids sulfonation. Sulfonation of curcuminoids was investigated by using nine expressed SULT isoforms and four pooled human tissue S9 fractions. The results showed that human small intestine is the predominant tissue responsible for sulfonation of curcuminoids. SULT1A3 is a major isoform catalyzing sulfonation of curcumin and demethoxycurcumin, but not for bisdemethoxycurcumin. SULT1B1 is only responsible for sulfonation of curcumin. Although SULT1C4 and 1E1 could highly catalyze the sulfate conjugations toward all the three compounds, the correlativities with human small intestine S9 fractions were much weaker (R(2) = 0.100-0.482). Almost all the kinetic profiles of the SULT isoforms for curcuminoids exhibited substrate inhibition kinetics. This investigation contributed to elucidate the SULT-mediated metabolism and detoxication of curcuminoids at molecular levels and in different organs. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: The causal relationship between diet-induced obesity and metabolic disorders is not clear yet. One hypothesis is whether the obese state or high-fat diet per se affects intestinal barrier function provoking metabolic co-morbidities. In three independent experiments with AKR/J, SWR/J or BL/6J mice, we addressed the impact of genetic background, excess body fat storage, duration of high-fat feeding and quality/quantity of dietary fat on glucose tolerance and gut barrier integrity in vivo and ex vivo. Impaired glucose tolerance in diet-induced obese BL/6J and AKR/J mice was not accompanied by an altered intestinal barrier function. Enforced dietary challenge by prolonged feeding and increasing fat quantity in BL/6J mice still failed to aggravate metabolic and intestinal deterioration. Despite a low-grade inflammatory status in adipose tissue, barrier function of BL/6J mice fed lard high-fat diet revealed no evidence for a diet-induced loss in barrier integrity. None of our results provided any evidence that gut barrier function is a subject to dietary regulation and obesity per se seems not to cause gut barrier impairment. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: Scope: Aging process makes older adults especially vulnerable to neurodegeneration and mental disorders. Overconsumption-related neurotoxic effects of certain dietary nutrients by older population could represent a contribution factor for the development of neuropsychiatric conditions by this sub-population. Thus, we here investigated whether chronic supplementation with retinyl palmitate, at doses commonly found in vitamin supplements (300, 600 and 3,000 mcg of RAE/kg/day), could have an impact on emotional behaviour of middle-aged Wistar rats. Methods and Results: We report that supplementation with retinyl palmitate for 28 days induces an altered emotional state of middle-aged Wistar rats and oxidative stress in cerebellum, cerebral cortex, hippocampus, and striatum, associated with imbalance of enzymatic antioxidant defences, decrease in non-enzymatic antioxidant defences, and increase in protein and lipid damages. Conclusion: Our data show evidence for i) changes in emotional reactivity, similar to anxiety, in middle-aged rats chronically supplemented with retinyl palmitate; and ii) suggest a possible interrelation between pro-oxidant events in the brain and these differences in the behavioural profile that cannot be attributed to hepatotoxicity. Our results invite for additional studies to further investigate such interrelation.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: Inflammatory bowel disease is a chronic inflammatory disorder of the gastrointestinal tract. Citrus nobiletin can exert robust anti-inflammatory effects in vivo and in vitro. We evaluated the impact of nobiletin on the excessive inflammatory response and impaired barrier function in a rodent colitis model. Colitis was established by infusion with 1 mL 2,4,6-trinitrobenzene sulfonic acid (TNBS) dissolved in ethanol (40% v/v) in rats at a 125 mg/kg dose. Caco-2 cell monolayer exposed to lipopolysaccharides (LPS) is used as a culture model for intestinal permeability measurements. Nobiletin decreased rat epithelial pro-inflammatory cytokines and mediators production. Nobiletin restored impaired barrier function in colitic rats and Caco-2 monolayer. Nobiletin decreased protein expressions of Akt, nuclear factor-kappa B (NF-κB), and myosin light chain kinase (MLCK) isolated from rat intestinal epithelial tissue and Caco-2 cell respectively. PI3K inhibitor or siRNA targeting of either Akt or NF-κB mitigated the impact of nobiletin on MLCK expression and barrier function in Caco-2 monolayer respectively. Nobiletin exerted anti-inflammatory effects in TNBS-induced colitis through the down-regulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expression. Nobiletin restored barrier function, which had been damaged after TNBS administration, through the inhibition of the Akt-NF-κB-MLCK pathway. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: Zinc deficiency results in immune dysfunction and promotes systemic inflammation. The objective of this study was to examine the effects of zinc deficiency on cellular immune activation and epigenetic mechanisms that promote inflammation. This work is potentially relevant to the aging population given that age-related immune defects, including chronic inflammation, coincide with declining zinc status. An in vitro cell culture system and the aged mouse model were used to characterize immune activation and DNA methylation profiles that may contribute to the enhanced proinflammatory response mediated by zinc deficiency. Zinc deficiency up-regulated cell activation markers ICAM1, MHC class II, and CD86 in THP1 cells, that coincided with increased IL1β and IL6 responses following LPS stimulation. A decreased zinc status in aged mice was similarly associated with increased ICAM1 and IL6 gene expression. Reduced IL6 promoter methylation was observed in zinc deficient THP1 cells, as well as in aged mice and human lymphoblastoid cell lines derived from aged individuals. Zinc deficiency induced inflammatory response in part by eliciting aberrant immune cell activation and altered promoter methylation. Our results suggested potential interactions between zinc status, epigenetics, and immune function, and how their dysregulation could contribute to chronic inflammation. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: Scope: Reports on the protective effect of certain foods on brain functions are numerous; however, the permeability of the brain barriers by food components is still hardly recognised. There have been in vitro studies aimed at demonstrating this possibility but not much is known about this phenomenon in in vivo systems. The objective of the study was to determine the metabolites of dietary quercetin (Q) in urine, blood plasma and cerebrospinal fluid (CSF) after intrarumen administration of Q rich onion dry skin in an animal model.Methods and results: Eleven sheep had permanently implanted cannulas in the third ventricle of the brain as the means for CSF collection. The animals were administered Q at the dose of 10mg/kg bwt. For 12h the concentration of Q metabolites was measured in urine, blood plasma and CSF. It was demonstrated that while in blood plasma Q and isorhamnetin (IR) mono -glucuronides or -sulphates were the main metabolites (80%), in CSF their aglycones were the dominating ones (88%).Conclusions: Q and IR aglycones are the main Q metabolites present in CSF after dietary Q intake. Their passive transport through blood-CSF barrier or a deconjugating mechanism within that barrier may be involved.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: There is a pressing need for countermeasures against diabetes, which has increased in incidence, becoming a global issue. Glucagon-like peptide-1 (GLP-1), a molecule secreted in enteroendocrine L cells in the lower small and large intestines, is thought to be one of the most important molecular targets for the prevention and treatment of diabetes. There has been increasing interest in the possible ability of dietary factors to treat diabetes via modulating GLP-1 secretion. There is thought to be a close relationship between incretin and diet, and the purported best approach for using dietary factors to increase GLP-1 activity is promotion of secretion of endogenous GLP-1. It have been reported that nutrients as well as various non-nutrient dietary factors can function as GLP-1 secretogogues. Here, we present our findings on the GLP-1 secretion-stimulating functions of two dietary factors, curcumin and extract of edible sweet potato leaves, which contain caffeoylquinic acid derivatives. However, it is necessary to reveal in greater detail the stimulation of GLP-1 secretion by dietary factors for preventing and treating diabetes. It is desirable to clarify the exact GLP-1 secretory pathway, the effect of metabolites derived from dietary factors in gut lumen, and the relationship between incretin and meal. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: Accumulating evidence suggests relationship of compositional changes of gut microbiota with onset of metabolic disorders and obesity. Kimchi, a traditional Korean side dish, is known for its beneficial impact on metabolic parameters and anti-obesity effects. The current study was designed to evaluate the association between gut microbiota and human genome after kimchi intervention in an effort to understand the molecular mechanism(s) underlying the anti-obesity impact of kimchi. Twenty four obese women were randomly assigned to either fresh or fermented kimchi group for eight weeks of kimchi intervention. Pyrosequencing of fecal microbiota and microarray analyses of blood samples revealed that fresh and fermented kimchi interventions exerted differential effects on the obesity-related clinical parameters. Correlations of these effects with changes in blood gene expression and gut microbial population were more evident in the fermented kimchi group than the fresh kimchi group. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: In this study we investigated the ability of a phenolic extract from extra virgin olive oil (OPE) to modulate the inflammatory response in intestinal epithelial cells. Undifferentiated and differentiated Caco-2 cells were challenged with LPS (50 μg/ml) or IL-1β (5 ng/ml) to mimic the early and intermediate phase of intestinal inflammation, respectively. The effects of OPE on NF-κB-driven transcription and IL-8 promoter activity were evaluated in transfection assays, coupled to p65 nuclear translocation. Modulation of IL-8 mRNA levels by OPE was measured by quantitative RT-PCR while effects on protein levels by ELISA. Specific MAPKs inhibitors were used to investigate mRNA stability and the involvement of related signalling pathways. OPE prevented IL-8 expression and secretion in LPS-treated Caco-2 cells. In the presence of IL-1β OPE exhibited opposing effects on IL-8 gene transcription and mRNA/protein levels. While in IL-1β-treated cells IL-8 promoter activity was inhibited by treatment with OPE, IL-8 mRNA stability was strongly enhanced, leading to increased protein expression. Inhibitors of p38 and ERKs partly prevented OPE effect on IL-8 mRNA levels. Intestinal epithelial cells represent a direct target of the action of olive oil phenols where they regulate IL-8 expression by transcriptional and post-transcriptional mechanisms. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: Flavonoids and related compounds seem to have favorable effects on non-alcoholic fatty liver disease (NAFLD) progression, although the exact mechanisms implicated are poorly understood. In this study, we aimed to investigate the effect of the flanovol quercetin on gene expression deregulation involved in the development of NAFLD, as well as the possible implication of phosphatidylinositol 3-kinase (PI3K)/AKT pathway modulation. We used an in vivo model based on methionine and choline deficient (MCD) diet-fed mice and an in vitro model consisting of Huh7 cells incubated with MCD medium. MCD-fed mice showed classical pathophysiological characteristics of non-alcoholic steatohepatitis (NASH), associated with altered transcriptional regulation of fatty acid uptake- and trafficking-related gene expression, with increased lipoperoxidation. PI3K/AKT pathway was activated by MCD and triggered gene deregulation causing either activation or inhibition of all studied genes as demonstrated through cell incubation with the PI3K inhibitor LY294002. Treatment with quercetin reduced AKT phosphorylation and oxidative/nitrosative stress, inflammation and lipid metabolism-related genes displayed a tendency to normalize in both in vivo and in vitro models. These results place quercetin as a potential therapeutic strategy for preventing NAFLD progression by attenuating gene expression deregulation, at least in part through PI3K/AKT pathway inactivation. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 02/2015;
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    ABSTRACT: Scope: Formula-derived Dietary Advanced Glycation End products (AGEs) may promote programming of inflammation and oxidative stress in the kidney of intrauterine growth retarded (IUGR) piglets.Methods and results: IUGR piglets received either a Low Temperature Heated Formula (LHF: n = 8) or a High Temperature Heated Formula (HHF: n = 8) or suckled naturally for 3 weeks postnatally. Then they were fed with normal ad libutum regular diet. Nɛ carboxymethyllysine (CML) was measured in plasma, feces and formula by HPLC/MS-MS. CML was detected by immunofluoresence in kidney cells. Target renin-angiotensin, apoptotic, proinflammatory genes, p62 NF-κB and sRAGE levels were quantified. Compared with that in controls, free CML and plasma urea increased significantly in the HHF fed group at PND36 (P<0.05). CML was detected in nuclei of renal tubular cells of fed formula piglets but not in suckled ones. This presence of CML was associated with the activation of the soluble sRAGE. AT1, AT2, caspase 3, caspase 8, NF-κB, p62 NF-κB and total protein oxidation in kidney were higher in HHF fed group as compared to LHF fed group (P<0.05).Conclusion: Food processes aimed at reducing the concentration of AGEs in infant formula are urgently needed and may be therapeutically relevant for premature and/or IUGR babies.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 01/2015;