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: Ellagitannin-rich food products and medicinal plant materials were shown to have beneficial effects towards intestinal inflammation. Due to the questionable bioavailability of ellagitannins their gut microbiota metabolites-urolithins have come to be regarded as potential factors responsible for biological activities observed in vivo. The aim of the study was to determine the influence of the three most abundant bioavailable ellagitannin gut microbiota metabolites-urolithins A, B and C on inflammatory responses in RAW 264.7 murine macrophages, which are involved in the pathogenesis of intestine inflammation. Urolithins A, B and C decreased NO production via inhibition of the iNOS protein and mRNA expression. They decreased the expression of IL-1β, TNF-α and IL-6 mRNA in LPS challenged RAW 264.7 murine macrophages. A clear inhibition of NF-κB p65 nuclear translocation and p50 DNA binding activity was associated with the observed anti-inflammatory activities of urolithins. Among the tested compounds urolithin A had the strongest anti-inflammatory activity. The anti-inflammatory effects of urolithins at concentrations that are physiologically relevant for gut tissues (≥40 μM), as revealed in this study, support the data from in vivo studies showing the beneficial effects of ellagitannin-rich products towards intestinal inflammation. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500264
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    ABSTRACT: Diet-induced obesity is associated with changes in the gut microbiota and low-grade inflammation. Oligofructose was reported to ameliorate high fat diet-induced metabolic disorders in mice by restoring the number of intestinal bifidobacteria. However, this has not been experimentally demonstrated. We fed conventional mice, germfree mice, mice associated with a simplified human gut microbiota composed of eight bacterial species including Bifidobacterium longum (SIHUMI), and mice associated with SIHUMI without B. longum a low fat diet (LFD), a high fat diet (HFD) or a HFD containing 10% oligofructose (HFD+OFS) for five weeks. We assessed body composition, bacterial cell numbers and metabolites, markers of inflammation and gut permeability. Conventional mice fed HFD or HFD+OFS did not differ in body weight gain and glucose tolerance. The gnotobiotic mouse groups fed LFD or HFD+OFS gained less body weight and body fat, and displayed an improved glucose tolerance compared with mice fed HFD. These differences were not affected by the presence of B. longum. Mice fed HFD showed no signs of inflammation or increased intestinal permeability. The ability of oligofructose to reduce obesity and to improve glucose tolerance in gnotobiotic mice fed HFD was independent of the presence of B. longum. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500249
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    ABSTRACT: Resistance of proteins to gastrointestinal digestion may play a role in determining immune-mediated adverse reactions to foods. However, digestion studies have largely been restricted to purified proteins and the impact of food processing and food matrices on protein digestibility is poorly understood. Digestibility of a total gliadin fraction (TGF), flour (cv Hereward) and bread was assessed using in vitro batch digestion with simulated oral, gastric and duodenal phases. Protein digestion was monitored by SDS-PAGE and immunoblotting using monoclonal antibodies specific for celiac-toxic sequences (QQSF, QPFP) and starch digestion by measuring undigested starch. Whereas the TGF was rapidly digested during the gastric phase the gluten proteins in bread were virtually undigested and digested rapidly during the duodenal phase only if amylase was included. Duodenal starch digestion was also slower in the absence of duodenal proteases. The baking process reduces the digestibility of wheat gluten proteins, including those containing sequences active in celiac disease. Starch digestion affects the extent of protein digestion, probably because of gluten-starch complex formation during baking. Digestion studies using purified protein fractions alone are therefore not predictive of digestion in complex food matrices. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500262
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    ABSTRACT: Atherosclerosis is believed to be an independent predictor of cardiovascular diseases. A growing body of evidence suggests that quercetin is a potent antioxidant and anti-inflammatory compound. The molecular mechanisms underlying its protective effects against oxidative stress in human endothelial cells remain unclear. This study was designed to confirm the hypothesis that quercetin inhibits oxidized low-density lipoprotein (oxLDL)-induced endothelial oxidative damage by activating SIRT1 and to explore the role of AMPK, which is a negative regulator of NADPH oxidase and free radicals. HUVECs were treated with oxLDL with or without quercetin pretreatment. We found that quercetin pretreatment increased SIRT1 mRNA expression. In fact, quercetin protected against oxLDL-impaired SIRT1 and AMPK activities and reduced oxLDL-activated NOX2 and NOX4. However, silencing SIRT1 and AMPK diminished the protective function of quercetin against oxidative injuries. The results also indicated that oxLDL suppressed Akt/eNOS, impaired mitochondrial dysfunction, and enhanced ROS formation, activating the NF-κB pathway. These results provide new insight regarding the possible molecular mechanisms of quercetin. Quercetin suppresses oxLDL-induced endothelial oxidative injuries by activating SIRT1 and by modulating the AMPK/NADPH oxidase/AKT/eNOS signaling pathway. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500144
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    ABSTRACT: The objective of this study was to evaluate the effect of fenugreek furostanolic saponin (Fenfuro(TM) ) either alone, or in combination with chlorogenic acid (GCB-70(TM) ) on insulin resistance in mice. Male C57BL/6J mice were subjected to a normal or HFD and were randomly assigned to receive Fenfuro(TM) , GCB-70(TM) or combination for 24 weeks. Metabolic parameters, glucose tolerance, serum triglycerides (TG), cardiac function and hepatic insulin signaling were evaluated using indirect open-circuit calorimetry, intraperitoneal glucose tolerance test (IPGTT), oil-red O-staining, echocardiography and Western Blotting respectively. IPGTT revealed glucose intolerance in the mice receiving HFD, which was attenuated by Fenfuro(TM) . Serum TG which was elevated following a HFD was reconciled by both Fenfuro(TM) and the combination. HFD compromised myocardial contractile function which was unaffected by the treatment. Insulin-stimulated phosphorylation of Akt in the liver was attenuated in mice receiving HFD which was partially rescued by GCB-70(TM) . Neither treatment altered metabolic parameters or energy expenditure. Collectively, our data suggest that fenugreek and green coffee-bean extract may have potential benefits in treating insulin resistance and related conditions. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500197
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    ABSTRACT: There are two types of adipose tissue with distinct functions - white adipose tissue (WAT) stores chemical energy as triglycerides, whereas brown adipose tissue (BAT) consumes energy and releases heat (thermogenesis) in response to sympathetic nerve activity. In humans, treatments that promote greater BAT deposition and/or activity would be highly beneficial in regimes aimed at reducing obesity. Adult humans have restricted populations of prototypical brown adipocytes in the neck and chest areas, but recent advances have established that adipocytes with similar properties, termed "brite" adipocytes, can be recruited in subcutaneous depots thought to be primarily WAT. These brite adipocytes express the protein machinery required for thermogenesis, but to assess brite adipocytes as viable therapeutic targets, we need to understand how to promote conversion of white adipocytes to brite adipocytes and ways to increase optimal energy consumption and thermogenesis in these brite adipocytes. This can be accomplished by pharmacological and nutritional therapies to differing degrees, as reviewed in detail here. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500251
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    ABSTRACT: This study investigates whether pectin supplementation in adult rats can ameliorate age-associated disturbances in peripheral insulin and leptin actions. 7-month-old male Wistar rats were divided into three groups: control (rats fed ad libitum a standard-diet), pectin (rats fed ad libitum a standard-diet supplemented with 10% pectin), and pair-fed (rats pair-fed to the pectin group). They were sacrificed after one month. Pectin and pair-fed rats showed lower body-weight gain and food intake than controls and underwent a decrease in leptin levels and an increase in adiponectin levels. Pectin-treated animals, but not pair-fed ones, showed lower body-fat content and HOMA-IR index after dietary intervention. Compared to controls, pectin-treated rats showed a decline in the expression of genes related to energy uptake (WAT) and lipogenesis (WAT and liver), and increased expression levels of lipolysis- and fatty-acid oxidation-related genes (liver). Some of the changes were not evidenced in the pair-fed group. These effects appear to be associated with improved leptin signaling. 10% pectin supplementation for one month in adult rats decreases body-fat content and ameliorates age-related insulin and leptin resistance more intensely than what could be attributed to the decrease in energy intake, overall contributing to better metabolic health. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500292
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    ABSTRACT: Maternal diabetes can program metabolic and cardiovascular diseases in the offspring. The aim of this work was to address whether an olive oil-supplemented diet during pregnancy can prevent lipid metabolic alterations in the heart of the offspring of mild diabetic rats. Control and diabetic Wistar rats were fed during pregnancy with either a standard diet or a 6% olive oil-supplemented diet. The heart of adult offspring from diabetic rats showed increases in lipid concentrations (triglycerides in males and phospholipids, cholesterol and free fatty acids in females), which were prevented with the maternal diets enriched in olive oil. Maternal olive oil supplementation increased the content of unsaturated fatty acids in the heart of both female and male offspring from diabetic rats (possibly due to a reduction in lipoperoxidation), increased the expression of Δ6 desaturase in the heart of male offspring from diabetic rats, and increased the expression of PPARα in the heart of both female and male offspring from diabetic rats. Relevant alterations in cardiac lipid metabolism were evident in the adult offspring of a mild diabetic rat model, and regulated by maternal diets enriched in olive oil. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500334
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    ABSTRACT: The gut microbiota is linked with human health, and by manipulating its composition, health conditions might be improved. The aim of this study was to investigate whether two barley products, whole-grain barley and barley malt, caused differentiation of the caecal microbiota in rats fed high-fat diets and whether there were correlations with the short-chain fatty acids formed. Male Wistar rats were given barley or malt (7 dietary fibre/) for 4 weeks. Cellulose was used as a control, and the caecal microbiota was analysed with next-generation sequencing of 16S rDNA. The barley group had higher abundances of Verrucomicrobia and Actinobacteria and lower abundances of Firmicutes and Deferribacteres than the control group; the alpha diversity was also lower. At the genus level, the barley group had higher abundances of Akkermansia, Ruminococcus, Blautia and Bilophila. Turicibacter and Roseburia were more abundant in the malt group, and Parabacteroides, Dorea and rc4-4 were enriched in the control group. Most genera correlated with acetic and propionic acids, but Roseburia and Turicibacter instead correlated with butyric acid. Succinic acid correlated with Clostridium and Akkermansia. Bioprocessing is a potential method to modulate the gut microbiota for enhanced effects on human health. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500187
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    ABSTRACT: Obesity is a major public health crisis, with 1.6 billion adults worldwide being classified as overweight or obese in 2014. Therefore, it is not surprising that the number of women who are overweight or obese at the time of conception is increasing. Obesity during pregnancy is associated with the development of gestational diabetes and preeclampsia. The developmental origins of health and disease hypothesis proposes that perturbations during critical stages of development can result in adverse fetal changes, which leads to an increased risk of developing diseases in adulthood. Of particular concern, children born to obese mothers are at a greater risk of developing cardiometabolic disease. One subset of the population who are predisposed to developing obesity are children born small for gestational age, which occurs in 10% of pregnancies worldwide. Epidemiological studies report that these growth restricted children have an increased susceptibility to type 2 diabetes, obesity and hypertension. Importantly during pregnancy, growth restricted females have a higher risk of developing cardiometabolic disease, indicating that they may have an exacerbated phenotype if they are also overweight or obese. Thus the development of early pregnancy interventions targeted to obese mothers may prevent their children from developing cardiometabolic disease in adulthood. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500289
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    ABSTRACT: Although ingestion of coffee and its constituent chlorogenic acid (CGA) protects the retina from oxidative stress, the bioaccessibility and bioavailability of coffee metabolites are not well understood. The aim of this study was to determine which coffee metabolites reach the retina and protect against retinal degeneration. UPLC-MS/MS was used to detect CGA and coffee metabolites in the rat eye. The methyl thiazolyl tetrazolium assay and double staining with Hoechst and propidium iodide showed that CGA, caffeic acid (CA), and dihydrocaffeic acid (DHCA) protect retinal ganglion cells from hypoxia-induced damage. Western blots showed that treatment with coffee metabolites up-regulated anti-apoptotic proteins such as Bcl-2 and Bcl-XL and down-regulated pro-apoptotic proteins such as Bad, PARP, and cleaved caspase 3. Adult ICR mice were subjected to optic nerve crush-induced retinal ganglion cell death with intravitreal pre-treatment with coffee metabolites 1 day before and 1 hour after the procedure. Retrograde Fluorogold(TM) labeling showed severe retinal ganglion cell loss after optic nerve crushing, and coffee metabolites significantly reduced damage to retinal ganglion cells. CGA and coffee metabolites, especially, CA, and DHCA, reach the eye, where they can significantly reduce apoptosis induced by hypoxia and optic nerve crush stress, and thus prevent retinal degeneration. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201400897
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    ABSTRACT: Arsenic-containing hydrocarbons (AsHCs) and arsenic-containing fatty acids (AsFAs) represent two classes of arsenolipids occurring naturally in marine food. Toxicological data are yet scarce and an assessment regarding the risk to human health has not been possible. Here we investigated the transfer and presystemic metabolism of five arsenolipids in an intestinal barrier model. Three AsHCs and two AsFAs were applied to the Caco-2 intestinal barrier model. Thereby, the short-chain AsHCs reached up to 50% permeability. Transport is likely to occur via passive diffusion. The AsFAs showed lower intestinal bioavailability, but respective permeabilities were still 2- to 5-times higher as compared to arsenobetaine or arsenosugars. Interestingly, AsFAs were effectively biotransformed while passing the in vitro intestinal barrier, whereas AsHCs were transported to the blood-facing compartment essentially unchanged. AsFAs can be presystemically metabolised and the amount of transferred arsenic is lower than that for AsHCs. In contrast, AsHCs are likely to be highly intestinally bioavailable to humans. Since AsHCs exert strong toxicity in vitro and in vivo, toxicity studies with experimental animals as well as a human exposure assessment are needed to assess the risk to human health related to the presence of AsHCs in seafood. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500286
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    ABSTRACT: Laminaria japonica is an important marine vegetable with great health-benefits for preventing atherosclerosis. Since the foam cell formation is an important hallmark for the initiation of atherosclerosis, we examined the effect and underlying mechanism of a purified L. japonica polysaccharide (LJP) on the suppression of macrophage foam cell formation in this study. The chemical structure was further characterized. Using oxidized low-density lipoprotein (ox-LDL)-induced foam cell model, we found that the cellular lipid accumulation was significantly attenuated by 25 μg/mL LJP. Meanwhile, LJP caused a remarkable decrease in mRNA expression of peroxisome proliferator-activated receptor γ which was accompanied by the reduction of CD36 and Acyl coenzyme A:cholesterol acyltransferase-1 mRNA levels, and the enhancement of ATP-binding cassette transporters A1 and scavenger receptor B1 mRNA levels. Beside these, the ox-LDL-induced cellular inflammation was also restricted by LJP treatment via mammalian target of rapamycin-mediated toll-like receptor 2/4-mitogen-activated protein kinases/nuclear factor kappa-B pathways. The structure of LJP was characterized as a repeating unit consisting of →3,6)-α-D-Manp-(1→, →4)-α-D-Manp-(1→, →4)-2-O-acetyl-β-D-Glcp-(1→, →4)-β-D-Glcp-(1→, →6)-4-O-SO3 -β-D-Galp-(1→, →6)-β-D-Galp-(1→, →3)-β-D-Galp-(1→ and a terminal residue of α-D-Glcp-(1→. Our findings suggest that LJP inhibits the conversion of macrophage into foam cell via regulating cellular lipid metabolism and suppressing cellular inflammation. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500113
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    ABSTRACT: The "dietary xenomiR hypothesis" proposes that microRNAs (miRNAs) in foodstuffs survive transit through the mammalian gastrointestinal tract and pass into cells intact to affect gene regulation. However, debate continues as to whether dietary intake poses a feasible route for such exogenous gene regulators. Understanding on miRNA levels during pre-treatments of human diet is essential to test their bioavailability during digestion. This study makes the novel first use of an in vitro method to eliminate the inherent complexities and variability of in vivo approaches used to test this hypothesis. Plant miRNA levels in soybean and rice were measured during storage, processing, cooking, and early digestion using real-time PCR. We have demonstrated for the first time that storage, processing, and cooking does not abolish the plant miRNAs present in the foodstuffs. In addition, utilizing a simulated human digestion system revealed significant plant miRNA bioavailability after early stage digestion for 75 min. Attenuation of plant messenger RNA and synthetic miRNA was observed under these conditions. Even after an extensive pretreatment, plant-derived miRNA, delivered by typical dietary ingestion, has a robustness that could make them bioavailable for uptake during early digestion. The potential benefit of these regulatory molecules in pharma-nutrition could be explored further. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 07/2015; DOI:10.1002/mnfr.201500137
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    ABSTRACT: Scope: The present study aimed to compare the effects of diets containing high-fat, high-cholesterol and saturated fatty acids (HFHC-SFA) and HFHC-polyunsaturated fatty acids-containing (HFHC-PUFA) diets on two major antiatherogenic functions of HDL, the HDL antioxidant function and the macrophage-to-feces reverse cholesterol transport. Methods and Results: Experiments were carried out in mice fed a low-fat, low-cholesterol (LFLC) diet, an HFHC-SFA diet or an HFHC-PUFA diet in which SFAs were partly replaced with an alternative high-linoleic and α-linolenic fat source. The HFHC-SFA caused a significant increase in serum HDL cholesterol and phospholipids as well as elevated levels of oxidized HDL and oxidized LDL. Replacing SFA with PUFA significantly reduced the levels of these oxidized lipoproteins and enhanced the ability of HDL to protect LDL from oxidation. The SFA-mediated impairment of HDL antioxidant potential was not associated with the cholesterol content of the diet, obesity or insulin resistance. In contrast, the effect of the HFHC diets on fecal macrophage-derived cholesterol excretion was independent of the fatty acid source. Conclusion: SFA intake impairs the antioxidant potential of HDL and increases serum levels of oxidized lipoprotein species whereas the antioxidant potential of HDL is enhanced after PUFA consumption. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 06/2015; DOI:10.1002/mnfr.201500336