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

Publications in this journal

  • R Rühl · J F Landrier ·
    [Show abstract] [Hide abstract]
    ABSTRACT: Adiponectin is an adipokine mainly secreted by adipocytes that presents anti-diabetic, anti-inflammatory and anti-atherogenic functions. Therefore, modulation of adiponectin expression represents a promising target for prevention or treatment of several diseases including insulin resistance and type II diabetes. Pharmacological agents such as the nuclear hormone receptor synthetic agonists like the PPARγ agonists are of particular interest in therapeutic strategies due to their ability to increase the plasma adiponectin concentration. Nutritional approaches are also of particular interest, especially in primary prevention, since some active compounds of our diet (notably vitamins, carotenoids or other essential nutrients) are direct or indirect lipid-activators of nuclear hormone receptors and are modifiers of adiponectin expression and secretion. The aim of the present review is to summarize current knowledge about the nutritional regulation of adiponectin by derivatives of actives compounds naturally present in the diet acting as indirect or direct activators of nuclear hormone receptors. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500619
  • Stefanie Platz · Carla Kühn · Sonja Schiess · Monika Schreiner · Margrit Kemper · Olga Pivovarova · Andreas F.H. Pfeiffer · Sascha Rohn ·
    [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Benzyl isothiocyanate (BITC), which occurs in Brassicales, has demonstrated chemopreventive potency and cancer treatment properties in cell and animal studies. However, fate of BITC in human body is not comprehensively studied. Therefore, the present human intervention study investigates the metabolism of the glucosinolate (GSL) glucotropaeolin and its corresponding BITC metabolites. Analysing BITC metabolites in plasma and urine should reveal insights about resorption, metabolism, and excretion. Methods and results: 15 healthy men were randomly recruited for a crossover study and consumed 10 g freeze-dried Indian cress as a liquid preparation containing 1,000 μmol glucotropaeolin. Blood and urine samples were taken at several time points and investigated by LC-ESI-MS/MS after sample preparation using SPE. Plasma contained high levels of BITC-glutathione (BITC-GSH), BITC-cysteinylglycine (BITC-CysGly), and BITC-N-acetyl-L-cysteine (BITC-NAC) 1-5 h after ingestion, with BITC-CysGly appearing as the main metabolite. Compared to human plasma, the main urinary metabolites were BITC-NAC and BITC-Cys, determined 4-6 h after ingestion. Conclusion: This study confirms that consumption of Indian cress increases the concentration of BITC metabolites in human plasma and urine. The outcome of this human intervention study supports clinical research dealing with GSL-containing innovative food products or pharmaceutical preparations. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500633
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Substantial studies have shown that curcumin, a dietary compound from turmeric, has beneficial effects on many diseases. However, curcumin rapidly degrades at physiological pH, making it difficult to interpret whether the observed actions of curcumin are from curcumin itself or its degradation products. Therefore, it is important to better understand the mechanisms involved in curcumin degradation and the roles of degradation in its biological actions. Methods and results: Here we show that a series of redox active antioxidants with diverse chemical structures, including gallic acid, ascorbate (vitamin C), tert-butylhydroquinone (TBHQ), caffeic acid, rosmarinic acid, and Trolox (a water-soluble analog of vitamin E), dramatically increased curcumin stability in phosphate buffer at physiological pH. When treated in basal cell culture medium in MC38 colon cancer cells, curcumin rapidly degraded with a half-life of several minutes and showed a weak anti-proliferative effect; co-addition of antioxidants enhanced stability and anti-proliferative effect of curcumin. Finally, co-administration of antioxidant significantly increased plasma level of curcumin in animal models. Conclusions: Together, these studies strongly suggest that a redox-dependent mechanism plays a critical role in mediating curcumin degradation. In addition, curcumin itself, instead of its degradation products, is largely responsible for the observed biological actions of curcumin. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500681
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Aflatoxin exposure coincides with micronutrient deficiencies in developing countries. Animal feeding studies have postulated that aflatoxin exposure may be exacerbating micronutrient deficiencies. Evidence available in human subjects is limited and inconsistent. The aim of the study was to investigate the relationship between aflatoxin exposure and micronutrient status among young Guinean children. Method and results: A total of 305 children (28.8 ± 8.4 months) were recruited at groundnut harvest (rainy season), of which 288 were followed up 6 months later post-harvest (dry season). Blood samples were collected at each visit. Aflatoxin-albumin adduct levels were measured by ELISA. Vitamin A, vitamin E and β-carotene concentrations were measured using HPLC methods. Zinc was measured by atomic absorption spectroscopy. Aflatoxin exposure and micronutrient deficiencies were prevalent in this population and were influenced by season, with levels increasing between harvest and post-harvest. At harvest, children in the highest aflatoxin exposure group, compared to the lowest, were 1.98 (95%CI: 1.00, 3.92) and 3.56 (95%CI: 1.13, 11.15) times more likely to be zinc and vitamin A deficient. Conclusion: Although children with high aflatoxin exposure levels were more likely to be zinc and vitamin A deficient, further research is necessary to determine a cause and effect relationship. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500382
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Oleuropein possesses numerous health beneficial effects. We investigated the renoprotective effects of oleuropein against cisplatin (CP)-induced kidney injury. Methods and results: Male BALB/cN mice were orally gavaged with 5, 10 and 20 mg oleuropein/kg body weight for two days, 48 h after intraperitoneal injection of CP (13 mg/kg). Four days after CP administration, serum creatinine and blood urea nitrogen (BUN) levels were significantly elevated, with histopathological changes in renal tissue. In addition, renal oxidative stress was evidenced by increased expression of 3-nitrotyrosine (3-NT), 4-hydroxynonenal (4-HNE), cytochrome P450 E1 (CYP2E1) and heme oxygenase-1 (HO-1). The expression of nuclear factor-kappaB (NF-κB) p65, phospho-p65, tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 (COX-2) in the kidneys increased upon CP treatment, suggesting renal inflammation. CP intoxication increased the expression of p53, Bax and caspase-3 and induced apoptosis in the kidneys. CP administration also resulted in enhanced phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2). All these effects were dose-dependently diminished by oleuropein. Oral administration of PD0325901, an MEK inhibitor, coincided with the oleuropein-mediated suppression of apoptotic, inflammatory and antioxidant markers. Conclusion: The results of the current study suggest that oleuropein attenuated CP-induced acute renal injury, which was mediated through the inhibition of ERK signaling. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500409
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Dietary calcium has been inversely associated with body fat and energy balance. The main scope of this study has been to assess the potential contribution of gut microbiota on energy regulation mediated by calcium. Methods and results: Gut microbiota in C57BL/6J mice receiving calcium supplementation under a high-fat (HF) diet were analysed by PCR and their relationships with host metabolic parameters were determined. Calcium conferred a prebiotic-like effect on gut microbiota, and animals presented lower plasmatic endotoxin levels, increased expression of angiopoietin-like 4 in intestine and lower hepatic lipid content, although increased expression of stress markers in adipose tissue and of inflammation in liver was also found. To determine whether slimming effects could be transferred to obese mice, a faecal microbial transplant (FMT) was carried out, showing that host bacteria grown under a HF diet could not be superseded by those from calcium-fed animals. Therefore, FMT was not able to transfer the beneficial effects of calcium. Conclusion: In conclusion, calcium modulated gut microbiota in a prebiotic manner, establishing a host cross-talk and promoting a healthier metabolic profile. However, lack of effectiveness of FMT suggests the need of further appropriate dietary factors in addition to the bacteria per se. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500480
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: The consumption of tea polyphenols (TP) and stachyose contributes to preventive effects on hepatic injury. This study examined the effects of stachyose on absorption and hepatoprotective effects of TP in mice. Methods and results: GC-MS measurement showed that stachyose significantly increased serum total phenolic, ECG and EGCG contents in mice. The mice fed with high fructose (HF)-diet for 56 days exhibited oxidative stress observed by an increase in hepatic MDA levels and decreases in GSH-Px and SOD activities. Serum TC, TG, LDL-C and CRP levels, and ALT and AST activities were increased, while HDL-C concentrations were decreased following HF diet. Co-supplementation of stachyose and TP more effectively improved all parameters mentioned above when compared to administration of stachyose or TP alone. Histological observations of hepatic tissues also confirmed the beneficial effects of co-administration of stachyose and TP. Conclusion: Our results suggest that stachyose enhances absorption and hepatoprotective effects of TP, and combined ingestion of stachyose and TP is a novel strategy for alleviating HF diet-induced hepatic injury. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500547
  • [Show abstract] [Hide abstract]
    ABSTRACT: Tea, a popular beverage made from leaves of the plant Camellia sinensis, has been shown to reduce body weight, alleviate metabolic syndrome, and prevent diabetes and cardiovascular diseases in animal models and humans. Such beneficial effects have generally been observed in most human studies when the level of tea consumption was 3 to 4 cups (600-900 mg tea catechins) or more per day. Green tea is more effective than black tea. In spite of numerous studies, the fundamental mechanisms for these actions still remain unclear. From a review of the literature, we propose that the two major mechanisms are: 1) decreasing absorption of lipids and proteins by tea constituents in the intestine, thus reducing calorie intake; and 2) activating AMPK by tea polyphenols that are bioavailable in the liver, skeletal muscle, and adipose tissues. The relative importance of these two mechanisms depends on the types of tea and diet consumed by individuals. The activated AMPK would decrease gluconeogenesis and fatty acid synthesis and increase catabolism, leading to body weight reduction and MetS alleviation. Other mechanisms and the health relevance of these beneficial effects of tea consumption remain to be further investigated. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500428
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: We studied the effects and mechanism of 2-(3,4-dihydroxyphenil)ethanol (or hydroxytyrosol, HT), a polyphenol from extra-virgin olive oil, investigating the regulation of epidermal growth factor receptor (EGFR) expression in colon tumour cells. Methods and results: We demonstrate that HT significantly down-regulates EGFR expression in human colorectal adenocarcinoma cells HT-29, CaCo2 and WiDr, and in HT-29 xenografts. HT accelerates EGFR degradation by reducing its half-life. Specifically, HT induces EGFR ubiquitination which is mediated by phosphorylation at pY1045, the docking site for Cbl, thereby enabling receptor ubiquitination and degradation. Pre-treatment with either the lysosomal inhibitor chloroquine, or the proteasomal inhibitor MG132 blocks HT-induced EGFR down-regulation. In colon cancer cells, EGFR down-regulation by HT is associated with reduced cell proliferation. Tumour growth and EGFR expression levels are also decreased by HT treatment in HT-29 xenograft. Discussion: We conclude that HT down-regulates EGFR expression via lysosomal and proteasomal degradation, activated by HT-induced EGFR phosphorylation at pY1045 and increased Cbl activity. Cbl activation induces, in turn, EGFR ubiquitination. Our results reveal a new mechanism for HT's anti-tumour effects that may be important for colon tumour prevention and treatment. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500498
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Iron overload contributes to the pathogenesis of atherosclerosis and iron chelators are beneficial through their antioxidant properties. Hepatic iron loading increases cholesterol synthesis. Whether iron depletion could affect hepatic cholesterol metabolism is unknown. Methods and results: We examined the effect of the iron chelator deferoxamine (DFO) on mRNA expression of genes involved in cholesterol metabolism and/or cholesterol uptake. Our results revealed that DFO increases LDLR-mRNA levels in human hepatocyte-derived cell lines HepG2 and Huh7 cells, and in K562 cells. In HepG2 cells, we observed that DFO increases: (a) LDLR-mRNA levels in a time- and dose-dependent manner; (b) LDLR-protein levels; (c) cell surface LDLR; and (d) LDL uptake. In contrast, the mRNA levels of 3-hydroxy-3-methylglutaryl-coenzyme-A-reductase, sterol-regulatory- element-binding proteins, and the mRNA/protein levels of PCSK9 were not modulated by DFO suggesting that the LDLR regulation by DFO is not at the transcriptional or post-translational levels. Since LDLR-mRNA was stabilized by DFO, a post-transcriptional mechanism is suggested for the DFO-mediated upregulation of LDLR. Conclusion: DFO induced an increase in LDLR expression by a post-transcriptional mechanism resulting in an enhancement of LDL uptake in HepG2 cells, suggesting increased LDLR activity as one of the underlying causes of the hypocholesterolemic effect of iron reduction. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500467
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Inflammation is intimately associated with many cardiovascular events and docosahexaenoic acid (DHA) has been shown to protect against CVD. Egr-1 has emerged as a key regulator in the development of atherosclerosis. Free fatty acid receptor 4 (FFA4) is an n-3 FA membrane receptor. Tumor necrosis factor alpha (TNFα) is an inflammatory mediator and transforming growth factor-β-activated kinase 1 (TAK1) is essential in the TNFα-mediated activation of NF-κB. We examined the mechanisms underlying DHA inhibition of inflammation in human EA.hy926 cells. Methods and results: TNFα markedly induced the interaction between TAK1 binding protein (TAB) 2 and TAK1/TAB1, the phosphorylation of ERK, p38 MAPK, and Akt, the expression of Egr-1 and ICAM-1, and HL-60 (monocyte-like) cell adhesion. Pretreatment with DHA attenuated TNFα-induced phosphorylation of ERK, expression of Egr-1 and ICAM-1, and HL-60 cell adhesion. Transfection with siFFA4 reversed the DHA-mediated inhibition of TNFα-induced Egr-1 and ICAM-1 expression, HL-60 cell adhesion, and NF-κB and DNA binding activity. Conclusion: Our results suggest that the anti-inflammatory effect of DHA on the endothelium is at least partially linked to FFA4, disruption of TAB2 interaction with TAK1/TAB1, and down-regulation of ERK-dependent Egr-1 and ICAM-1 expression, which leads to less HL-60 cell adhesion to TNFα-stimulated EA.hy926 cells. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500178
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: The aim of our study was to investigate dose-dependent effects of isoflavone (ISO) exposure during adolescence on the androgen sensitivity of various physiological endpoints in male Wistar rats. Methods and results: During embryogenesis and adolescence rats were exposed to an ISO-depleted diet (IDD) or one of two diets enriched with different concentrations of a soy based ISO extract causing plasma concentrations observed averagely (IRDlow) and maximally (IRDhigh) in Asian men. Most of the rats were orchiectomized at postnatal day (PND) 81 and were treated with testosterone propionate or vehicle from PND 89 to 99. In intact rats (PND99) body weight, food intake and fat mass were not influenced by ISO, but serum triglycerides and hepatic FAS expression were decreased. Trabecular bone mineral density (BMD) was reduced in IRDlow, but not in IRDhigh rats. Orchiectomy induced loss of BMD, which was antagonized by IRDhigh. ISO increased androgen sensitivity of seminal vesicle and levator ani. Besides, ISO plasma levels were reduced by orchiectomy compared to intact and testosterone propionate treated rats. Conclusion: In summary, the results of this study indicate that exposure to ISO during adolescence affects bone homeostasis, lipid metabolism and modulates androgen sensitivity in young adult male rats. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500559
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Estrogen deficiency has been associated with central obesity, muscle loss, and metabolic syndrome in postmenopausal women. This study assessed naringenin accumulation in tissues and investigated the hypothesis that naringenin reverses diet-induced metabolic disturbances in obese ovariectomized mice. Methods and results: In study 1, we measured naringenin concentrations in plasma, liver, perigonadal and subcutaneous adipose tissues, and muscle of ovariectomized C57BL/6J female mice after 11 weeks of naringenin supplementation. Naringenin accumulated 5-12 times more in mice fed a 3% naringenin diet than in mice fed a 1% naringenin diet. In study 2, ovariectomized mice were fed a high-fat diet (60 kcal% fat) for 11 weeks and half of the mice were then supplemented with 3% naringenin for another 11 weeks. Dietary naringenin suppressed weight gain, lowered hyperglycemia, and decreased intra-abdominal adiposity evaluated by magnetic resonance imaging. Naringenin-fed mice exhibited elevated locomotor activity monitored by infrared beam breaks, maintained muscle mass, and reduced muscle diacylglycerol content. Real-time PCR analysis in muscle revealed decreased mRNA level for genes involved in de novo lipogenesis, lipolysis, and triglyceride synthesis/storage. Conclusions: Long-term 3% naringenin supplementation resulted in significant naringenin accumulation in plasma and tissues, associated with attenuated metabolic dysregulation and muscle loss in obese ovariectomized mice. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500379
  • [Show abstract] [Hide abstract]
    ABSTRACT: Scope: Enhanced adiposity and metabolic inflammation are major features of obesity that could be impacted by dietary emulsifiers. We investigated in high-fat fed mice the effects using a new polar lipid emulsifier from milk (MPL) instead of soybean lecithin (SPL) on adipose tissue and intestinal mucosa function. Methods and results: Four groups of C57BL6 mice received for 8 weeks a low-fat diet (LF) or a high-fat diet devoid of polar lipids (HF) or a high-fat diet including MPL (HF-MPL) or SPL (HF-SPL). Compared with HF diet, HF-SPL diet increased white adipose tissue (WAT) mass (P<0.05), with larger adipocytes (P<0.05) and increased expression of MCP-1, LBP and leptin (P<0.05). This was not observed with HF-MPL diet despite similar dietary intakes and increased expression of FATP4 and MTTP, involved in lipid absorption, in upper intestine (P<0.05). HFP-MPL mice had a lower expression in WAT of CD68, marker of macrophage infiltration, vs HF and HFP-SPL mice (P<0.05), and more goblet cells in the colon (P<0.05). Conclusions: Unlike SPL, MPL in a high fat diet did not induce WAT hypertrophy and inflammation but increased colonic goblet cells. This supports further clinical exploration of different sources of dietary emulsifiers in the frame of obesity outbreak. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2015; DOI:10.1002/mnfr.201500703