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
    4.31
  • 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: 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;
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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;
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    ABSTRACT: Scope: We aimed to investigate whether a novel dietary intervention consisting of an every-other-week calorie restricted diet could prevent non-alcoholic fatty liver disease (NAFLD) development induced by a medium-fat diet.Methods and results: Nine week-old male C57BL/6J mice received either a 1) control (C), 2) 30E% calorie restricted (CR), 3) medium-fat (MF; 25E% fat) or 4) intermittent (INT) diet, a diet alternating weekly between 40E% CR and an ad libitum MF diet until sacrifice at the age of 12 months. The metabolic, morphological, and molecular features of NAFLD were examined. The INT diet resulted in healthy metabolic and morphological features as displayed by the continuous CR diet: glucose tolerant, low hepatic triglyceride content, low plasma alanine aminotransferase. In contrast, the C- and MF-exposed mice with high body weight developed signs of NAFLD. However, the gene expression profiles of INT-exposed mice differed to those of CR-exposed mice and showed to be more similar with those of C- and MF-exposed mice with a comparable body weight.Conclusions: Our study reveals that the INT diet maintains metabolic health and reverses the adverse effects of the MF diet, thus effectively prevent the development of NAFLD in 12-month-old male C57BL/6J mice.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 12/2014;
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    ABSTRACT: Scope: High multivitamin (HV, 10-fold AIN-93G) gestational diets fed to Wistar rats increase food intake, obesity and characteristics of metabolic syndrome in the offspring. We hypothesized that methyl vitamins, and specifically folate, in the HV gestational diet contribute to the obesogenic phenotypes consistent with their epigenetic effects on hypothalamic food intake regulatory mechanisms.Methods and Results: Male offspring of dams fed the AIN-93G diet with high methyl vitamins (HMethyl; 10-fold folate, vitamins B12 and B6) (Study 1) and HV with recommended folate (HVRF) (Study 2) were compared with those from HV and recommended vitamin (RV) fed dams. All offspring were weaned to a high fat diet for 8 weeks. HMethyl diet, similar to HV, and compared to RV, resulted in higher food intake, body weight and metabolic disturbances. Removing folate additions to the HV diet in HVRF offspring normalized the obesogenic phenotype. Methyl vitamins, and folate in HV diets, altered hypothalamic gene expression toward increased food intake concurrent with DNA methylation and leptin and insulin receptor signaling dysfunction.Conclusion: Methyl vitamins in HV gestational diets contribute to obesogenic phenotypes and epigenetic alterations in the hypothalamic feeding pathways in the offspring. Folate alone accounts for many of these effects.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 12/2014;
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    ABSTRACT: Scope: Several epidemiological studies have shown that tea consumption is associated with higher bone mineral density in women. Flavonoids in tea are recognized as potential estrogen mimics and may positively influence bone metabolism in estrogen deficient women. Luteolin and orientin, flavonoids from rooibos tea, are of particular interest as rooibos tea contains no caffeine that can be detrimental to bone health. This study analyzed changes in mineral content when luteolin or orientin was added to a human osteoblast cell line and the potential mechanisms involved. Measurements included alkaline phosphatase (ALP) activity, cell mitochondrial activity, toxicity, and changes in regulatory proteins involved in osteoblast metabolism.Methods and results: Mineral was significantly elevated in Saos2 cells treated with orientin (0.1-1.0 μM, 15–100 μM) or luteolin (5.0 μM) and was associated with increased ALP and mitochondrial activity, as determined by the production of p-nitrophenol and the reduction of 2-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, respectively. Greater mineral content was also associated with lower toxicity as determined by lactate dehydrogenase activity and lower expression of TNFα, IL6, sclerostin, osteopontin and osteoprotegerin.Conclusion: Orientin and luteolin, flavonoids in rooibos tea, enhance mineral content in Saos2 cells. These findings provide guidance for doses to be studied in well-established animal models.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 12/2014;
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    ABSTRACT: Background: The biological impact of folates from folate rice, a metabolically engineered (biofortified) rice line, rich in folates, was investigated. Its consumption may be helpful to fight folate deficiency. Our objective was to investigate the potential of folate rice to supply the organism with folates and evaluate its biological effectiveness using a rat model.Methods and results: Five groups of 12 Wistar rats were monitored during a 7/12-week depletion/repletion trial. Animals receiving folate-free diet (0 μg/rat/day) and those additionally receiving wild type rice (on average 0.11 μg/rat/day) suffered from decreased hematocrit and lower folate concentrations in both plasma and RBCs. This resulted in serious morbidity and even lethality during the trial. In contrast, all animals receiving a daily supplement of folate rice or folic acid fortified rice (on average 3.00 μg/rat/day and 3.12 μg/rat/day respectively) and those receiving a positive control diet (11.4 to 25.0 μg/rat/day), survived. In these groups, the hematocrit normalized, plasma and RBC folate concentrations increased and pronounced hyperhomocysteinemia was countered.Conclusion: Using an animal model, we demonstrated that biofortified folate rice is a valuable source of dietary folate, as evidenced by folate determination in plasma and RBCs, the alleviation of anemia and counteraction of pronounced hyperhomocysteinemia.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 12/2014;
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    ABSTRACT: Obesity is associated with hyperlipidemia, hepatic steatosis and low-grade inflammation. Studies have shown that MUFA as well as PUFA have beneficial effects on blood lipids and the inflammatory state. This study investigates a daily supplementation of either 50 g of rapeseed/canola (RA) or olive (OL) oil over four weeks on serum lipids, serum liver enzymes and inflammatory gene expression in subcutaneous (s. c.) adipose tissue in obese men. Consuming RA resulted in increased serum n-3 fatty acids and a reduction in total cholesterol, LDL cholesterol and serum aspartate aminotransferase compared to OL. In s. c. adipose tissue gene expression of the pro-inflammatory cytokine IL6 was reduced in RA compared to OL. However, after four hours after a test meal, containing the appropriate oil, white bread and 400 mL of liquid diet drink (835 kcal in total), gene expression of IL6, IL1B and EMR1 was increased in RA and of monocyte chemoattractant protein-1 (CCL2) in both, RA and OL. This demonstrates that consuming RA for four weeks improves serum lipids, liver enzymes and basal inflammation in s. c. adipose tissue, but mediates an acute pro-inflammatory response in adipose tissue upon consuming a meal. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Squalene is a polyunsaturated triterpene which has exhibited anti-cancer and anti-oxidant activities among others. We investigated dietary squalene supplementation effect on an acute colitis model induced by dextran sulfate sodium (DSS) in C57BL/6 mice.
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Coffee is rich in quinic acid esters of phenolic acids (chlorogenic acids) but also contains some free phenolic acids. A proportion of phenolic acids appear in the blood rapidly after coffee consumption due to absorption in the small intestine. We investigated in vitro whether this appearance could potentially be derived from free phenolic acids in instant coffee or from hydrolysis of chlorogenic acids by pancreatic or brush border enzymes.
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Our study aims to investigate molecular events associated to methyl donor deficiency (MDD) by analysing the transcriptome and the methylome of MDD rats in liver.
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Marine polysaccharides have been found as the principle component in cell wall structures of seaweeds or exoskeletons of crustaceans. Due to numerous pharmaceutical properties of marine polysaccharides such as antioxidant, anti-inflammatory, anti-allergic, anti-tumor, anti-obesity, anti-diabetes, anti-coagulant, anti-viral, immunomodulatory, cardioprotective, and anti-hepatopathy activities, they have been applied in many fields of biomaterials, food, cosmetic, and pharmacology. Recently, several marine polysaccharides such alginate, porphyran, fucoidan, and chitin and its derivatives have been evidenced as down-regulators of allergic responses due to enhancement of innate immune system, alteration of Th1/Th2 balance forward to Th1 cells, inhibition of IgE production, and suppression of mast cell degranulation. This contribution, therefore, focuses on anti-allergic properties of marine polysaccharides and emphasizes their potential application as bioactive food ingredients as well as nutraceuticals for prevention of allergic disorders. This article is protected by copyright. All rights reserved.
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Scope: Here we have tested the hypothesis that prebiotic galacto-oligosaccharides (GOS) may enhance mucosal barrier function through direct modulation of goblet cell function.Methods and results: Human adenocarcinoma-derived LS174T cells, which exhibit an intestinal goblet cell-like phenotype, were used to examine the non-prebiotic effects of GOS on goblet cell functions. LS174T cells were treated with GOS, and the expression of goblet cell secretory product genes mucin 2 (MUC2), trefoil factor 3 (TFF3), resistin-like molecule beta (RETNLB) and the Golgi-sulfotransferase genes, carbohydrate (N-acetylglucosamine-6-O) sulfotransferase 5 (CHST5) and galactose-3-O-sulfotransferase 2 (GAL3ST2), was determined by real-time quantitative RT-PCR. In addition, the abundance of CHST5, TFF3 and RETNLB was confirmed by Western blot analysis. Following treatment with GOS for 72 h, the expression of MUC2 was significantly upregulated 2-4-fold, CHST5 and RETNLB, 5-7-fold, and TFF3 2-4-fold. Western blot analysis demonstrated increased abundance of RETNLB, TFF3 and CHST5. Addition of the Th2 cytokine IL-13 along with GOS resulted in synergistic induction of RETNLB and CHST5. IL-8 secretion was not affected by GOS treatment, suggesting that the effects of GOS are not mediated through an inflammatory pathway.Conclusion: Collectively, the data indicate that GOS may enhance mucosal barrier function through direct stimulation of intestinal goblet cells.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Human norovirus is the leading cause of sporadic gastroenteritis, which is responsible for more than 90% of all non-bacterial gastroenteritis outbreaks. While norovirus infections typically cause mild and self-limiting symptoms lasting 24–48 h, chronic persistent infections can cause severe symptoms. Although recent advances have been made in understanding the molecular characteristics of norovirus infection, no norovirus-specific antiviral drugs or vaccines are available. Conventional intervention methods used to inactivate norovirus, such as treatment with disinfecting agents (e.g., ethanol, hypochlorite, and quaternary ammonium formulations), have shown a lack of efficacy against human norovirus when they are applied to foods and in food preparation processes. Therefore, alternative antiviral or inactivating agents such as phytochemicals have received attention as potential norovirus inhibitors due to their relatively low toxicity and lack of side effects, which allows them to be prepared as food-safe formulations. Evidence from studies using viral surrogates suggests that numerous phytochemicals and foods containing flavonoids and polyphenols have anti-norovirus activity, and future studies will be necessary to confirm the effectiveness of such compounds against human norovirus and the molecular mechanisms through which they produce antiviral effects.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Scope: We investigated whether a combination of two promising chemopreventive agents arctigenin and quercetin increases the anti-carcinogenic potency at lower concentrations than necessary when used individually in prostate cancerMethods and results: Androgen-dependent LAPC-4 and LNCaP prostate cancer cells were treated with low doses of arctigenin and quercetin alone or in combination for 48h. The anti-proliferative activity of arctigenin was 10–20 fold stronger than quercetin in both cell lines. Their combination synergistically enhanced the anti-proliferative effect, with a stronger effect in androgen receptor (AR) wild-type LAPC-4 cells than in AR mutated LNCaP cells. Arctigenin demonstrated a strong ability to inhibit AR protein expression in LAPC-4 cells. The combination treatment significantly inhibited both AR and PI3K/Akt pathways compared to control. A protein array analysis revealed that the mixture targets multiple pathways particularly in LAPC-4 cells including Stat3 pathway. The mixture significantly inhibited the expression of several oncogenic microRNAs including miR-21, miR-19b, and miR-148a compared to control. The mixture also enhanced the inhibition of cell migration in both cell lines compared to individual compounds testedConclusion: The combination of arctigenin and quercetin, that target similar pathways, at low physiological doses, provides a novel regimen with enhanced chemoprevention in prostate cancer.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Scope: Bone homeostasis is ensured by the balance between bone formation and resorption. Thus, control of the recruitment, proliferation, and differentiation of bone cells is essential to maintain bone mass. The aim of this study was to elucidate the effects of rosmarinic acid as a potential therapeutic agent on bone metabolism using bone cells and a mouse model.Methods and Results: Rosmarinic acid increased alkaline phosphatase activity and induced mineralization in osteoblasts. Addition of rosmarinic acid to cultures of calvarial osteoblastic cells prepared from TCF/β-catenin TOP-GAL mutant mice strongly induced the expression of LacZ and promoted stabilization of β-catenin in the cytoplasm of ST2 cells, suggesting that rosmarinic acid affects the canonical Wnt signaling pathway. Moreover, rosmarinic acid inhibited not only osteoclast formation in cocultures of mouse bone marrow cells and osteoblasts, but also RANKL-induced osteoclastic differentiation in bone marrow-derived macrophages. RANKL-induced p38 MAPK and the expression of NFATc1, c-Jun, and c-Fos were inhibited by rosmarinic acid in bone marrow macrophages. Finally, we confirmed that rosmarinic acid improved bone mass in a soluble RANKL-induced bone loss mouse model.Conclusion: Rosmarinic acid has dual regulatory effects on bone metabolism and may control the bone functions by controlling osteoblastic and osteoclastic differentiation.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Aims: The present meta-analysis aimed to investigate fiber consumption and all-cause mortality, and cause-specific mortality.Methods: Medline and web of science database were searched for cohort studies published from inception to August 2014.Studies were included if they provided a hazard ratio (HR) and corresponding 95% CI for mortality in relation to fiber consumption.Results: Compared with those who consumed lowest fiber, for individuals who ate highest fiber, mortality rate was lower by 23% (HR, 0.77; 95% CI, 0.72-0.81) for CVD, by 17% (HR, 0.83; 95% CI, 0.74- 0.91) for cancer, by 23% (HR, 0.77; 95% CI, 0.73-0.81) for all-cause mortality. For each 10 gram/day increase in fiber intake, the pooled HR was estimated to be 0.89 (95% CI, 0.86-0.93) for all-cause mortality, 0.80 (95% CI, 0.72-0.88) for CHD mortality, and 0.66 (95% CI, 0.40-0.92) for IHD mortality, 0.91 (95% CI, 0.88-0.94) for cancer. Dietary fiber and CVD mortality showed a strong dose-response relation.Conclusions: Fiber consumption is inversely associated with all-cause mortality and CVD, IHD, cancer mortality.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 11/2014;
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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
    Molecular Nutrition & Food Research 11/2014;
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    ABSTRACT: Scope: Activation of endothelial adenosine monophosphate-activated protein kinase (AMPK) contributes to increase nitric oxide (NO) availability. The aim of this study was to assess if high fat diet (HFD)-induced endothelial dysfunction is linked to AMPK deregulation.Methods and Results: Twelve-week old Sprague Dawley male rats were assigned either to control (10 kcal % from fat) or to HFD (45 kcal % from fat) for 8 weeks. HFD rats segregated in obesity-prone (OP) or obesity-resistant (OR) rats according to body weight. HFD triggered an impaired glucose management together with impaired endothelium-dependent relaxation, reduced endothelial AMPK activity and lower NO availability in aortic rings of OP and OR cohorts. Relaxation evoked by AMPK activator, AICAR was reduced in both OP and OR rings, which exhibited lower p-AMPKα-Thr172/AMPKα ratios that negatively correlated with plasma non-esterified fatty acids (NEFA) and triglycerides (TG). Inhibition of PI3K (wortmannin, 10−7 M) or Akt (triciribine, 10−5 M) reduced relaxation to AICAR only in the control group (p<0.001). Akt (p-Akt-Ser473) and eNOS phosphorylation (p-eNOS-Ser1177) were significantly reduced in OP and OR (p<0.01).Conclusion: Endothelial dysfunction caused by HFD is related to a dysfunctional endothelial AMPK-PI3K-Akt-eNOS pathway correlating with the increase of plasma NEFA, TG and an impaired glucose management.This article is protected by copyright. All rights reserved
    Molecular Nutrition & Food Research 11/2014;