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

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

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: Dieckol is a major polyphenol of Ecklonia cava. This study demonstrates a mechanistic role for dieckol in the suppression of lipid accumulation using three models METHODS AND RESULTS: : Mice were split into four experimental groups (n = 10 per group): normal diet, high fat diet (HFD), and dieckol-supplemented diets. Dieckol-supplemented mice groups showed a significant decrease of body weight gain (38%) as well as fats of organs including epididymal (45%) compared with a HFD-fed group. LDL cholesterol level was reduced by 55% in dieckol-supplemented group. Adipogenic factors and lipid synthetic enzymes were analyzed via real-time polymerase chain reaction (PCR) or immunoblotting. Dieckol regulated mRNA expressions of early adipogenic genes in 3T3-L1 cells. These results were reflected in down-regulation of late adipogenic factors, resulting in a decrease in triacylglycerol content. These data were also verified in zebrafish and mouse models. Dieckol activated AMP-activated protein kinase α (AMPKα) signaling to inhibit lipid synthesis in 3T3-L1 and mouse model. Dieckol was also shown to inhibit mitotic clonal expansion (MCE) via cell cycle arrest CONCLUSION: : Our data demonstrate that dieckol inhibits lipid accumulation via activation of AMPKα signaling and cell cycle arrest This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201500021
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    ABSTRACT: Ursolic acid (UA) is a triterpenoid compound with multifold biological functions. Our previous studies have reported that UA protects against high-fat diet-induced obesity and improves insulin resistance (IR). However, the potential mechanisms are still undefined. Free fatty acid (FFA) metabolism in skeletal muscle plays a central role in obesity and IR. Therefore, in this study, we investigated the effect and the potential mechanisms of UA on skeletal muscle FFA metabolism METHODS AND RESULTS: : In diet-induced obese rats, 0.5% UA supplementation for 6 weeks markedly reduced body weight, increased energy expenditure, decreased FFA level in serum and skeletal muscle and triglyceride content in skeletal muscle. In vitro, the data provided directly evidence that UA significantly increased fluorescently-labeled FFA uptake and (3) H-labeled palmitic acid β-oxidation. UA-activated AMP-activated protein kinase (AMPK) and downstream targets were involved in the increase of FFA catabolism. Moreover, up-regulated uncoupling protein 3 (UCP3) by UA contributed to AMPK activation via elevating adenosine monophosphate/adenosine triphosphate ratio CONCLUSION: : UA increases FFA burning through enhancing skeletal muscle FFA uptake and β-oxidation via an UCP3/AMPK-dependent pathway, which provides a novel perspective on the biological function of UA against obesity and IR This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201400670
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    ABSTRACT: Scope: Main objectives of this study were 1) to demonstrate direct signaling of starch on human dendritic cells (DCs), 2) to study whether this is mediated by the pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and 3) to study whether intestinal epithelial cells (IECs) are involved in modulating the starch induced immune activation of DCs.Methods and results: Two different types of Resistant Starch, High-maize® 260 (RS2) and Novelose® 330 (RS3) were characterized for their starch content and particle size. Human DCs and reporter cells for TLRs were incubated with starches and analyzed for NF-kB/AP-1 activation. Complex co-culture systems were applied to study the cross talk. High-maize® 260 predominantly binds to TLR2 while Novelose® 330 binds to TLR2 and TLR5. The strong immune-stimulating effects of High-maize® 260 were attenuated by starch-exposed IECs illustrating the regulatory function of IECs. Despite these attenuating effects, DCs kept producing Th1 cytokines.Conclusion: Resistant starch possesses direct signaling capacity on human DCs in a starch type dependent manner. IECs regulate these responses. High-maize® 260 skews towards a more regulatory phenotype in coculture systems of DCs, IEC, and T-cells.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201500148
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    ABSTRACT: Capsaicin is an active component of chili peppers, having diverse effects. However, the effects of capsaicin on intestinal motility are still controversial. The present study aimed to investigate the effects of capsaicin on intestinal motility disorder and uncover related mechanisms. A rat model with intestinal motility disorder was established in vitro through adding different stimuli into tissue bath; in vivo using constipation and diarrhea model respectively. Capsaicin exerted dual effects on intestinal motility, i.e., the relaxation and contraction of jejunum induced by corresponding stimulus were respectively regulated to be normal contraction by capsaicin. The mechanisms underlined capsaicin induced dual effects were investigated using Western blotting, qRT-PCR, and whole cell patch clamp respectively. Results showed that cholinergic excitatory nerves, adrenergic nerves, and neurons containing nitric oxide synthase which are the main muscle motor neurons in enteric nervous system (ENS) are involved in capsaicin-induced dual effects. The competition for regulation of Ca(2+) influx by capsaicin induced the interaction with components of the ENS. Capsaicin significantly increased MLCK expression and myosin phosphorylation extent in jejunal segments of constipation-prominent rats and significantly decreased MLCK expression and myosin phosphorylation extent in jejunal segments of diarrhea-prominent rats. In summary, capsaicin alleviates abnormal intestinal motility through regulating enteric motor neurons and MLCK activity, which is beneficial for the treatment of gastrointestinal motility disorders. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201500039
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    ABSTRACT: Resveratrol (RSV), a natural polyphenol, has been reported to attenuate non-alcoholic fatty liver disease (NAFLD); however, its underlying mechanism is unclear. Autophagy was recently identified as a critical protective mechanism during NAFLD development. Therefore, we investigated the role of autophagy in the beneficial effects of RSV on hepatic steatosis METHODS AND RESULTS: : Via Oil red O staining, triglyceride and β-hydroxybutyrate detection, we found that RSV decreased palmitate-induced lipid accumulation and stimulated fatty acid β-oxidation in hepatocytes. Based on western blot assay, confocal microscopy and transmission electron microscopy, we found that RSV induced autophagy in hepatocytes, whereas autophagy inhibition markedly abolished RSV-mediated hepatic steatosis improvement. Moreover, RSV increased cAMP levels and the levels of SIRT1 (sirtuin 1), pPRKA (phosphorylated protein kinase A) and pAMPK (phosphorylated AMP-activated protein kinase), as well as SIRT1 activity in HepG2 cells. Incubation with inhibitors of AC (adenylyl cyclase), PRKA, AMPK, SIRT1, or with AC, PRKA, AMPK, or SIRT1 siRNA abolished RSV-mediated autophagy. Similar results were obtained in mice with hepatic steatosis CONCLUSIONS: : RSV improved hepatic steatosis partially by inducing autophagy in vitro and in vivo, via the cAMP-PRKA-AMPK-SIRT1 signaling pathway, which provides new evidence regarding RSV's effects on NAFLD treatment This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201500016
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    ABSTRACT: Scope: The study was designed to identify the regulatory mechanisms underlying the effects of ethanol exposure on intestinal folate transport and to investigate the reversibility of such effects.Methods and results: Caco-2 cells were grown in control and ethanol containing medium for 96 hours. Thereafter, one subgroup of cells was shifted on ethanol free medium and grown for next 72hours. For in vivo studies, rats were given 1g ethanol/kg body weight/day either for 3 or 5 months and after 3 months of ethanol treatment, one group of rats received no ethanol for two months. A significant decrease in folic acid transport as well as expression of folate transporters was observed on ethanol treatment and the effects were reversible upon removal of ethanol. Ethanol exposure had no impact on CpG island methylation of the folate transporters however, an increase in their mRNA half life was observed which seems to be a homeostatic mechanism. ChIP assay revealed a decrease in binding of SP1 transcription factor to the promoter regions of folate transporters.Conclusion: Reduced binding of SP1 to the promoter region of folate transporters may be a part of the regulatory mechanism resulting in decreased expression of folate transporters on ethanol exposure.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201400874
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    ABSTRACT: Bioprocessing of whole grain cereals may affect the bioavailability of phytochemicals associated with grain fiber and ultimately lead to different health outcomes. Here, we studied the impact of long-term feeding with intact and bioprocessed rye bran on the urinary phytochemical profile of mice. Non-targeted HILIC-ESI-qTOF-MS metabolite profiling approach was applied on urine samples collected from 3 groups of diet-induced obese mice fed for 8 weeks with one of the three diets: high-fat (HF) control diet, HF diet enriched with intact rye bran, or HF diet enriched with bioprocessed rye bran. The most striking finding was the increased urinary excretion of several amino-acid derived betaines after both rye diets. These included proline betaine, alanine betaine, valine betaine, phenylalanine betaine, pipecolic acid betaine, and trigonelline, but not glycine betaine. Furthermore, bioprocessing may have improved the bioavailability of rye derived phytochemicals, as higher increase in e.g. ferulic acid and benzoxazinoid metabolites were observed in urine of mice fed with bioprocessed than intact rye bran. Urinary excretion of various betaines was greatly increased in mice fed rye brans. Furthermore, bioprocessing of rye bran appears to serve as a beneficial way to improve the bioavailability of various phytochemicals. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201500066
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    ABSTRACT: Insulin resistance represents an independent risk factor for metabolic and cardiovascular diseases. Researchers have been interested in identifying active harmless compounds, as many insulin-sensitizing drugs have shown unwanted side-effects. It has been demonstrated that anthocyanins and one of their representative metabolites, protocatechuic acid (PCA), ameliorate hyperglycemia and insulin sensitivity. This study investigated the mechanism of action of PCA responsible for the glucose uptake up-regulation METHODS AND RESULTS: : In human visceral adipocytes, PCA stimulated IRS-1 tyrosine phosphorylation (+40% with respect to untreated cells) and the downstream events, i.e. PI3K binding to IRS-1 and Akt phosphorylation (+100%,+180%, respectively, with respect to untreated cells). The insulin-like activity of PCA seemed to be mediated by insulin receptor since by inhibiting its autophosphorylation, the PCA effects were completely abolished. Furthermore, PCA was able to activate AMPK, a serine/threonine kinase whose activation elicits insulin-sensitizing effects CONCLUSION: : This study showed that PCA stimulates the insulin signaling pathway in human adipocytes increasing GLUT4 translocation and glucose uptake. Decreasing insulin resistance is a most desirable aim to be reached for an effective therapeutic/preventive action against metabolic syndrome and type 2 diabetes. Identifying specific food/food components able to improve glucose metabolism can offer an attractive, novel and economical strategy This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201400816
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    ABSTRACT: Scope: In this study human exposure to the mycotoxin ochratoxin A (OTA) and its thermal degradation product 2’R-ochratoxin A (2’R-OTA, previously named as 14R-Ochratoxin A [22]) through coffee consumption was assessed. LC-MS/MS and the dried blood spot (DBS) technique were used for the analysis of blood samples from coffee and non-coffee drinkers (n = 50), and food frequency questionnaires were used to document coffee consumption.Methods and results: For the detection of OTA and 2’R-OTA in blood, a new sensitive and efficient sample preparation method based on DBS was established and validated. Using this technique 2’R-OTA was for the first time detected in biological samples. Comparison between coffee drinkers and non-coffee drinkers showed for the first time that 2’R-OTA was only present in blood from the first group while OTA could be found in both groups in a mean concentration of 0.21 μg/L. 2’R-OTA mean concentration was 0.11 μg/L with a maximum concentration of 0.414 μg/L. Thus, in average 2’R-OTA was approx. half the concentration of OTA but in some cases even exceeded OTA levels. No correlation between the amounts of coffee consumption and OTA or 2’R-OTA levels was observed.Conclusion: The results of this study revealed for the first time a high exposure of coffee consumers to 2’R-OTA, a compound formed from OTA during coffee roasting. Since little information is available regarding toxicity and possible carcinogenicity of this compound, further OTA monitoring in blood including 2’R-OTA is advisable.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 05/2015; DOI:10.1002/mnfr.201500220
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    ABSTRACT: L-Cysteine is a nutritionally semi-essential amino acid and is present mainly in the form of L-cystine in the extracellular space. With the help of a transport system, extracellular L-cystine crosses the plasma membrane and is reduced to L-cysteine within cells by thioredoxin and reduced glutathione (GSH). Intracellular L-cysteine plays an important role in cellular homeostasis not only as a precursor for protein synthesis, but also for the production of GSH, H2 S, and taurine. L-Cysteine-dependent synthesis of GSH has been investigated in many pathological conditions, while the pathway for L-cysteine metabolism to form H2 S has received little attention with regard to prevention and treatment of disease in humans. The main objective of this review is to highlight the metabolic pathways of L-cysteine catabolism to GSH, H2 S, and taurine, with special emphasis on therapeutic and nutritional use of L-cysteine to improve the health and well-being of animals and humans This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 04/2015; DOI:10.1002/mnfr.201500031
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    ABSTRACT: Urinary tract infections (UTI) are one of the most frequent extra-intestinal infections caused by Escherichia coli (ExPEC). Cranberry juice has been used for decades to alleviate symptoms and prevent recurrent UTI. The putative compounds in cranberries are proanthocyanidins (PAC), specifically PAC with "A-type" bonds. Since PAC are not absorbed, their health benefits in UTI may occur through interactions at the mucosal surface in the gastrointestinal tract. Recent research showed that higher agglutination of ExPEC and reduced bacterial invasion are correlated with higher number of "A-type" bonds and higher degree of polymerization of PAC. An understanding of PAC structure-activity relationship is becoming feasible due to advancements, not only in obtaining purified PAC fractions that allow accurate estimation, but also in high-resolution mass spectrometry methodologies, specifically, matrix assisted laser/desorption ionization time-of-flight (MALDI-TOF MS). A recent MALDI-TOF MS deconvolution method allows quantification of the ratios of "A-type" to "B-type" bonds enabling characteristic fingerprints. Moreover, the generation of fluorescently labeled PAC allows visualization of the interaction between ExPEC and PAC with microscopy. These tools can be used to establish structure-activity relationships between PAC and UTI and give insight on the mechanism of action of these compounds in the gut without being absorbed This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 04/2015; DOI:10.1002/mnfr.201500108
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    ABSTRACT: This study examined the associations of serum transferrin and metabolic disorders among Chinese population. This study is based on nation-wide, population-based China Health and Nutrition survey including 8564 men and women aged 18 years or older. Anthropometric and fasting blood glucose, insulin, lipids, and transferrin data were collected. Elevated transferrin concentrations associated with higher body mass index, waist circumference, lipids, insulin, glucose (all p<0.0001). Serum transferrin concentrations increased gradually with increasing numbers of metabolic syndrome (MetS) components among men and women (p = 0.0003). Elevated concentrations of transferrin were significantly related with higher risk of MetS (p = 0.0006), obesity (p = 0.0089), overweight (p<0.0001). No associations between transferrin concentrations and risk of diabetes and high blood pressure were observed in both men and women. Elevated transferrin concentrations were positively associated with risk MetS and obesity, but not with risk of diabetes among Chinese. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 04/2015; DOI:10.1002/mnfr.201500038