Molecular Nutrition & Food Research (Mol Nutr Food Res )

Publisher: John Wiley and Sons

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.

Impact factor 4.91

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    Impact factor
  • 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: Scope: The Na+/glucose cotransporter 1 (SGLT1) plays a crucial role in glucose uptake in intestinal epithelial cells (IECs), which has been shown essential in ameliorating intestinal inflammation. Ginseng has historically been used to treat inflammatory disorders. Understanding the regulatory mechanism of ginseng-mediated induction of SGLT1 gene expression in human intestinal cells is therefore important.Methods and results: We demonstrate that ginsenoside compound K (CK) enhances SGLT1-mediated glucose uptake in mice and human intestinal Caco-2 cells. Transient transfection analysis using SGLT1 promoter-luciferase reporters demonstrated that the presence of an essential cAMP response element (CRE) is required for CK-mediated induction of SGLT1 gene expression. The ChIP assays indicated that Increased CRE-binding protein (CREB) and CREB-binding protein (CBP) binding to the SGLT1 promoter in CK-treated cells is associated with an activated chromatin state. Our result showed that the increased CREB phosphorylation is directly correlated with SGLT1 expression in IECs. Further studies indicated that the epidermal growth factor receptor (EGFR) signaling pathway is involved in the CK-mediated effect.Conclusion: These findings provide a novel mechanism for the CK-mediated up-regulation of SGLT1 expression through EGFR-CREB signaling activation, which could contribute to reducing gut inflammation..This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: Benzoxazinoids (BXs) are a group of natural chemical compounds with putative pharmacological and health-protecting properties. BXs were formerly identified in and isolated from selected dicot medicinal plants and young cereal plants. Recently, BXs were found to be present in mature cereal grains and bakery products, such that knowledge about the pharmacological properties of BXs, which until now have unknowingly been consumed through the daily bread and breakfast cereals, have come into new focus. This review discusses published results from in vitro studies and a few human and animal model studies on the health effects and pharmacological responses of various BX compounds. Many of these studies have reported antimicrobial, anticancer, reproductive system stimulatory, central nervous system stimulatory, immunoregulatory, and appetite- and weight-reducing effects of BXs and/or BX derivatives. The health benefits of wholegrain intake may be associated with the solitary and/or overlapping biological effects of fibers, lignans, phenolic acids, alkylresorcinols, BXs, and other bioactive compounds. In the context of BXs as dietary ingredients, further comprehensive investigations are required to understand their biological functions, to elucidate the underlying mechanisms, to explore their potential contribution on the health effects associated with wholegrain consumption, and to examine their potential as functional food ingredients.
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: Oxidative stress plays a main role in the pathogenesis of type 2 diabetes mellitus (T2DM). Cocoa and (-)-epicatechin (EC), a main cocoa flavanol, have been suggested to exert beneficial effects in T2DM because of their protective effects against oxidative stress and insulin-like properties. In this study, the protective effect of EC and a cocoa phenolic extract (CPE) against oxidative stress induced by a high glucose challenge, which causes insulin resistance, was investigated on hepatic HepG2 cells. Oxidative status, phosphorylated mitogen-activated protein kinases (MAPKs), nuclear factor E2-related factor 2 (Nrf2) and p-(Ser)-IRS-1 expression, and glucose uptake were evaluated. EC and CPE regulated antioxidant enzymes and activated ERK and Nrf2. EC and CPE pre-treatment prevented high glucose-induced antioxidant defences and p-MAPKs, and maintained Nrf2 stimulation. The presence of selective MAPK inhibitors induced changes in redox status, glucose uptake, p-(Ser)- and total IRS-1 levels that were observed in CPE-mediated protection. EC and CPE recovered redox status of insulin-resistant HepG2 cells, suggesting that the functionality in EC- and CPE-treated cells was protected against high glucose-induced oxidative insult. CPE beneficial effects on redox balance and insulin resistance were mediated by targeting MAPKs. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: Gut peptides regulate appetite and adipogenesis. Early weaning (EW) leads to later development of obesity, which can be prevented by calcium supplementation. We evaluated gut peptides that may have a role in the establishment of this dysfunction. At birth, lactating Wistar rats were separated in: EW, lactating rats involved with a bandage interrupting the lactation during the last 4 days of standard lactation, and C (control), dams whose pups had free access to milk during throughout lactation. At 120 days-old, half of EW group received calcium supplementation (EWCa); EW and C received standard diet. At 21 days-old, EW presented higher GLP-1 in plasma and GLP1-R in adipose tissue and hypothalamus, but lower GLP-1 and GLP1-R in the gut. At 180 days-old, GLP-1 response to food intake was blunted in EW and restored by calcium. GLP-1 in the gut was lower in EW and its receptor was lower in adipose tissue, and GLP1-R was higher in the gut of EWCa. Thus, EW had short and long-term effects upon GLP-1 profile, which may have contributed to obesity development, hyperphagia and insulin resistance, due to its adipogenic and appetite control roles. Calcium supplementation was able to prevent most of the changes in GLP-1 caused by EW. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: Scope: Epigallocatechin-3-gallate (EGCG), the most aboundent catechin of green tea, has beneficial effects on physiological functions of endothelial cells (ECs), yet the detailed mechanisms are not fully understood. In this study, we investigated the role of transient receptor potential vanilloid type 1 (TRPV1), a ligand-gated non-selective calcium channel, in EGCG–mediated endothelial nitric oxide synthase (eNOS) activation and angiogenesis.Methods and results: In endothelial cells (ECs), treatment with EGCG time-dependently increased the intracellular level of Ca2+. Removal of extracellular calcium (Ca2+) by EGTA or EDTA or inhibition of TRPV1 by capsazepine (CPZ) or SB366791 abrogated EGCG-increased intracellular Ca2+ level in ECs or TRPV1-transfected HEK293 cells. Additionally, EGCG increased the phsophorylation of eNOS at Ser635 and Ser1179, Akt at Ser473, calmodulin protein kinase II (CaMKII) at Thr286 and AMP-activated protein kinase (AMPK) at Thr172, all abolished by the TRPV1 antagonist CPZ. EGCG-induced NO production was diminished by pretreatment with LY294002 (an Akt inhibitor), KN62 (a CaMKII inhibitor) and compound C (an AMPK inhibitor). Moreover, blocking TRPV1 activation prevented EGCG-induced EC proliferation, migration and tube formation, as well as angiogenesis in Matrigel plugs in mice.Conclusion: EGCG may trigger activation of TRPV1–Ca2+ signaling, which leads to phosphorylation of Akt, AMPK and CaMKII, eNOS activation, NO production and, ultimately, angiogenesis in ECs.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: We have recently shown that cocoa flavanols may have anti-diabetic potential by promoting survival and function of pancreatic beta-cells in vitro. In this work, we investigated if a cocoa-rich diet is able to preserve beta-cell mass and function in an animal model of type 2 diabetes and the mechanisms involved. Our results showed that cocoa feeding during the pre-diabetic state attenuates hyperglycaemia, reduces insulin resistant and increases beta cell mass and function in obese Zucker diabetic (ZDF) rats. At the molecular level, cocoa-rich diet prevented beta-cell apoptosis by increasing the levels of Bcl-xL and decreasing Bax levels and caspase-3 activity. Cocoa diet enhanced the activity of endogenous antioxidant defenses, mainly glutathione peroxidase, preventing thus oxidative injury induced by the pre-diabetic condition and leading to apoptosis prevention. These findings provide the first in vivo evidence that a cocoa-rich diet may delay the loss of functional beta-cell mass and delay the progression of diabetes by preventing oxidative stress and beta-cell apoptosis. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: Scope: Breakdown products of certain glucosinolates induce detoxifying enzymes and demonstrate preventive activities against chemically induced tumourigenesis in animal models. However, other breakdown products are genotoxic. 1-Methoxy-3-indolylmethyl alcohol (1-MIM-OH) is mutagenic in bacterial and mammalian cells upon activation by sulphotransferases and forms DNA adducts in mouse tissues. This effect is enhanced in mice transgenic for human sulphotransferases 1A1/2 (FVB/N-hSULT1A1/2). Therefore, we explored gene expression changes induced by 1-MIM-OH in mouse liver.Methods and results: FVB/N-hSULT1A1/2 mice were orally treated with 1-MIM-OH for 21 or 90 days, leading to high levels of hepatic 1-MIM-DNA adducts. Genome-wide expression analyses demonstrated no influence on detoxifying enzymes, but up-regulation of many mediators of the tumour suppressor p53 and down-regulation of Fhit and other long genes. While this p53 response might indicate protection, it was unable to prevent the accumulation of DNA adducts. However, various epidemiological studies reported inverse associations between the intake of cruciferous vegetables and cancer. This association may be due to the presence of other glucosinolates with tumour-preventing influences possibly outweighing adverse effects of some metabolites.Conclusion: 1-MIM-OH is a genotoxic substance inducing a gene expression profile similar to the expression signature caused by known genotoxic hepatocarcinogens.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: Dairy products contain milkfat, proteins, minerals, vitamin D and other bioactive nutrients that have the potential to contribute to the association observed between increased dairy intake and a decreased risk of inflammation. The objective of this paper is to review the role of dairy bioactive molecules including: dairy fat, proteins, micronutrients and vitamins on inflammation markers in adipose, macrophage and vascular tissues, which play a key role in the regulation of inflammation. A review was conducted to identify current scientific literature on dairy nutrients and inflammation in cell studies published until November 2014. The majority of saturated fatty acids (FAs) activate pro-inflammatory markers. Therefore, other dairy FAs or components may offset these harmful effects. Protein and amino acid composition of dairy products may have anti-inflammatory action. Magnesium may have beneficial effects on inflammatory profile; on the contrary, studies on vitamin D demonstrate conflicting results. In conclusion, numerous studies assessed the effects of individual or mixtures of FAs on inflammatory markers; yet, there is far less research on the effects of other dairy bioactive nutrients. The exact bioactive molecule or combination of these molecules in dairy products which underlies the inverse association between dairy intake and inflammation remains to be elucidated.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 01/2015;
  • Molecular Nutrition & Food Research 01/2015; 59(1).
  • Molecular Nutrition & Food Research 01/2015; 59(1).
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    ABSTRACT: A substantial proportion of obese individuals does not present cardiometabolic complications such as diabetes, hypertension, or dyslipidemia. Some, but not all, prospective studies observe similar risk of cardiovascular events and all-cause mortality among individuals with this so-called "metabolically healthy obese" (MHO) phenotype, compared to the metabolically healthy normal weight or metabolically healthy non-obese phenotypes. Compared to the metabolically unhealthy obese (MUO) phenotype, MHO is often characterized by a more favourable inflammatory profile, less visceral fat, less infiltration of macrophages into adipose tissue, and smaller adipocyte cell size. Tipping the inflammation balance in adipose tissue might be particularly important for metabolic health in the obese. While the potential role of genetic predisposition or lifestyle factors such as diet in the MHO phenotype is yet to be clarified, it is well known that diet affects inflammation profile and contributes to the functionality of adipose tissue. This review will discuss genetic predisposition and the molecular mechanisms underlying the potential effect of food on the development of the metabolic phenotype characteristic of obesity. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 01/2015;
  • Carrie Waterman, Patricio Rojas‐Silva, Tugba Boyunegmez Tumer, Peter Kuhn, Allison J. Richard, Shawna Wicks, Jacqueline M. Stephens, Zhong Wang, Randy Mynatt, William Cefalu, Ilya Raskin
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    ABSTRACT: Scope: Moringa oleifera (moringa) is tropical plant traditionally used as an antidiabetic food. It produces structurally unique and chemically stable moringa isothiocyanates (MICs) that were evaluated for their therapeutic use in vivo.Methods and results: C57BL/6L mice fed very high fat diet (VHFD) supplemented with 5% moringa concentrate (MC, delivering 66 mg/kg/d of MICs) accumulated fat mass, had improved glucose tolerance and insulin signaling, and did not develop fatty liver disease compared to VHFD-fed mice. MC-fed group also had reduced plasma insulin, leptin, resistin, cholesterol, IL-1β, TNFα, and lower hepatic glucose-6-phosphatase (G6P) expression. In hepatoma cells, MC and MICs at low micromolar concentrations inhibited gluconeogenesis and G6P expression. MICs and MC effects on lipolysis in vitro and on thermogenic and lipolytic genes in adipose tissue in vivo argued these are not likely primary targets for the anti-obesity and anti-diabetic effects observed.Conclusion: Data suggest that MICs are the main anti-obesity and anti-diabetic bioactives of MC, and that they exert their effects by inhibiting rate-limiting steps in liver gluconeogenesis resulting in direct or indirect increase in insulin signaling and sensitivity. These conclusions suggest that MC may be an effective dietary food for the prevention and treatment of obesity and type 2 diabetes.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: Scope: This study evaluated the capacity of dietary catechin (C), quercetin (Q) and the combination of both (CQ), to attenuate adipose inflammation triggered by high fructose (HFr) consumption in rats and by tumor necrosis factor alpha (TNFα) in 3T3-L1 adipocytes.Methods and results: In rats, HFr consumption for 6 wk caused dyslipidemia, insulin resistance, reduced plasma adiponectin, adiposity, and adipose tissue inflammation. Dietary supplementation with 20 mg/kg/d of C, Q and CQ improved all these parameters. In 3T3-L1 adipocytes, C and Q attenuated TNFα-induced elevated protein carbonyls, increased pro-inflammatory cytokine expression (MCP-1, resistin), and decreased adiponectin. The protective effects of C and Q on adipose inflammation are in part associated with their capacity to: i) decrease the activation of the mitogen activated kinases (MAPKs) JNK and p38; and ii) prevent the downregulation of PPARƔ. In summary, C and Q, and to a larger extent the combination of both, attenuated adipose pro-inflammatory signaling cascades and regulated the balance of molecules that improve (adiponectin) or impair (TNFα, MCP-1, resistin) insulin sensitivityConclusion: Together, these findings suggest that dietary Q and C may have potential benefits in mitigating MetS associated adipose inflammation, oxidative stress, and insulin resistance.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: Scope: Aim of the study was to identify and monitor metabolite markers of dry bean consumption in parallel human and mouse studies that each had shown chemopreventive effects of dry bean consumption on colorectal neoplasia risk.Methods and Results: Using liquid chromatography/mass spectroscopy +/- electrospray ionization and gas chromatography/mass spectroscopy, serum metabolites of dry beans were measured in 46 men before and after a four-week dry bean-enriched diet (250 g/d) and 12 mice that received a standardized diet containing either 0 or 10% navy bean ethanol extract for 6 weeks; we also investigated fecal metabolites in the mice. The serum metabolites identified in these controlled feeding studies were then investigated in 212 polyp-free participants from the Polyp Prevention Trial who self-reported either increased (≥+31 g/d from baseline), high dry bean intake of ≥42 g/d in year 3 or low, unchanged dry bean consumption of <8 g/d; serum was analyzed from baseline and year 3. Serum pipecolic acid and S-methyl-cysteine were elevated after dry bean consumption in human and mouse studies and reflected dry bean consumption in the Polyp Prevention TrialConclusions: Serum levels of pipecolic acid and S-methyl-cysteine are useful biomarkers of dry bean consumption.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: Scope: In the present study the direct interaction of commonly consumed fibers with epithelial or dendritic cells (DC) was studied.Methods & Results: The fibers were characterized for their sugar composition and chain length profile. When in direct contact, fibers activate DCs only mildly. This was different when DCs and fibers were co-cultured together with supernatants from human epithelial cells (Caco-SM). Caco-SM enhanced the production of IL-12, IL-1Ra, IL-6, IL-8, TNF-α, MCP-1, and MIP-1α but this was strongly attenuated by the dietary fibers. This attenuating effect on proinflammatory cytokines was dependent on the interaction of the fibers with Toll-like receptors as it was reduced by Pepinh-myd88. The interaction of GOS, chicory inulin, wheat arabinoxylan, barley β-glucan with epithelial cells and DCs led to changes in the production of the Th1 cytokines in autologous T-cells, while chicory inulin, and barley β-glucan reduced the Th2 cytokines IL-6. The Treg promoting cytokine IL-10 was induced by GOS whereas chicory inulin decreased the IL-10 production.Conclusions: Our results suggest that dietary fibers can modulate the host immune system not only by the recognized mechanism of effects on microbiota but also by direct interaction with the consumer's mucosa. This modulation is dietary fiber type dependent.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 01/2015;
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    ABSTRACT: The average length of human life is increasing, but so does the incidence of age- and lifestyle-related diseases. Improving diet and lifestyle is a key strategy for lifelong health and underlying mechanisms may well include increasing resilience pathways. The purpose of this review is to highlight and evaluate novel mechanisms by which dietary pro-oxidants, including bioactive phytochemicals and fatty acids, increase ROS concentrations just enough to activate transcription factor activation of Nuclear factor erythroid 2-related factor 2 (Nrf-2) and heat shock factor (HSF), leading to an increase in levels of antioxidant enzymes and heat shock proteins that protect against the damaging effects of ROS. An increasing number of in vivo studies have now shown that dietary pro-oxidant compounds can increase the production of such resilience products. In most studies, dietary pro-oxidants normalized levels of antioxidant enzymes that were decreased by a range of different challenges, rather than raising levels of resilience products per se. Also, it is important to consider that the antioxidant response can be different for different organs. For future studies, however, the measurement of resilience markers may significantly improve our ability to prove the efficacy by which dietary bioactives with pro-oxidant capacities improve lifelong health. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 12/2014;
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    ABSTRACT: This study elucidates effects of long term nutritional preconditioning by resveratrol on I/R injury and its underlying mechanisms. Mice were treated with resveratrol at 2.0 mg/kg.day by gastric gavages for 6 weeks. Then hearts were isolated and subjected to I/R injury in a Langendorff apparatus. Resveratrol significantly improved LVP, ±dp/dtmax and CF, decreased the LDH and CPK activity, and reduced the infarction size. Additionally, long-term oral resveratrol intake prevented mPTP opening and subsequently inhibited mitochondria-mediated apoptosis, as demonstrated by decrease of cytochrome c release, inactivation of caspase-3 and reduction of TUNEL-positive cells. Furthermore, resveratrol inhibited the up-regulation of VDAC1 expression induced by I/R injury. Local left ventricle overexpression of VDAC1 by adenovirus diminished the protective effect of resveratrol against I/R injury, indicating that VDAC1 plays an important role in resveratrol-mediated cardioprotection. Our data revealed that long-term oral intake of resveratrol sets nutritional preconditioning in coping with myocardial I/R injury. Strikingly, we found that resveratrol down-regulates VDAC1, leading to prevention of mPTP opening and cardiomyocyte apoptosis. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 12/2014;
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    ABSTRACT: Inflammatory bowel disease (IBD) is an incurable disease which affects millions of people. Garlic (Allium sativum) preparations have been traditionally employed for the treatment of diseases affecting the digestive tract. Here, we have investigated the effect of diallyl sulfide (DAS) and diallyl disulfide (DADS), two garlic-derived sulfur compounds, on intestinal inflammation in vivo as well as in intestinal isolated cells. Colitis was induced in mice by intracolonic administration of dinitrobenzenesulfonic acid. Intestinal damage was assessed by evaluating colon weight/colon length ratio and by histology. Murine intestinal epithelial cells stimulated with interferon-γ (IFN-γ) were used to evaluate the possible in vitro DAS and DADS anti-inflammatory effects. DAS and DADS, given for two consecutive days after DNBS administration, reduced inflammation and damage. In IFN-γ-stimulated intestinal epithelial cells, DADS reduced IP-10 and IL-6 levels, while DAS inhibited nitric oxide production and STAT-1 expression CONCLUSION: : DAS and DADS exert therapeutic effects in the DNBS model of colitis. The actions of these compounds on the production of IP-10, IL-6, hydrogen sulfide or nitric oxide and on the expression of STAT-1 observed in intestinal cells stimulated with IFN-γ, might explain the protective action of DAS and DADS in experimental IBD. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 12/2014;