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Special Issue "Nutrigenomics of Risk Factors for Disease"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 March 2017)

Special Issue Editor

Guest Editor
Prof. Marica Bakovic

Department of Human Health and Nutritional Sciences, University of Guelph, ANNU Bldg Rm 346, 50 Stone Road East, Guelph, ON, N1G 2W1 Canada
Website | E-Mail
Phone: 15198244120 Ex 53764
Interests: genomics of lipid disorders; micronutrients; diabetes; metabolic syndrome

Special Issue Information

Dear Colleagues,

Over the past two decades, the focus of nutrition has shifted from traditional epidemiological approaches of investigating the effects of diet on general population health towards a better understanding of the main processes through which dietary components regulate biological functions. The completion of the human genome project revealed significant individual and population differences in response to diets that now need to be seriously considered when new nutritional strategies are to be developed.

The new era of nutrition (nutragenomics) became of particular importance when applied to the increased global epidemics of predominantly diet related diseases. Using tools of nutragenomics we begin to appreciate better the dualistic role of diet, not only in the propagation but also in the prevention of debilitating diseases of obesity, diabetes and cardiovascular disease, as well as the most influential factor in the epigenetic adaptations during fetal development and ageing. 

Another important aspect of modern nutrition is to develop personalized diets and this great concept has yet to be fully developed. We need to learn more how to optimally combine traditional and bioinformatics’ information in our search for alternative approaches, with the processes of identification of responders and no responders as the primary goal in the applied nutragenomics.

This Special Issue, "Nutrigenomics of Risk Factors for Disease", will focus on the nutragenomic role of diet in development and prevention of chronic diseases.

Prof. Dr. Marica Bakovic
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • nutragenomics
  • epigenetics
  • metabolic phenotyping
  • preventive health
  • dietary interventions

Related Special Issue

Published Papers (13 papers)

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Research

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Open AccessArticle Ontogeny of Sex-Related Differences in Foetal Developmental Features, Lipid Availability and Fatty Acid Composition
Int. J. Mol. Sci. 2017, 18(6), 1171; https://doi.org/10.3390/ijms18061171
Received: 13 February 2017 / Revised: 5 May 2017 / Accepted: 25 May 2017 / Published: 31 May 2017
Cited by 1 | PDF Full-text (1188 KB) | HTML Full-text | XML Full-text
Abstract
Sex-related differences in lipid availability and fatty acid composition during swine foetal development were investigated. Plasma cholesterol and triglyceride concentrations in the mother were strongly related to the adequacy or inadequacy of foetal development and concomitant activation of protective growth in some organs
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Sex-related differences in lipid availability and fatty acid composition during swine foetal development were investigated. Plasma cholesterol and triglyceride concentrations in the mother were strongly related to the adequacy or inadequacy of foetal development and concomitant activation of protective growth in some organs (brain, heart, liver and spleen). Cholesterol and triglyceride availability was similar in male and female offspring, but female foetuses showed evidence of higher placental transfer of essential fatty acids and synthesis of non-essential fatty acids in muscle and liver. These sex-related differences affected primarily the neutral lipid fraction (triglycerides), which may lead to sex-related postnatal differences in energy partitioning. These results illustrate the strong influence of the maternal lipid profile on foetal development and homeorhesis, and they confirm and extend previous reports that female offspring show better adaptive responses to maternal malnutrition than male offspring. These findings may help guide dietary interventions to ensure adequate fatty acid availability for postnatal development. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessArticle A Systems Biology Approach Using Transcriptomic Data Reveals Genes and Pathways in Porcine Skeletal Muscle Affected by Dietary Lysine
Int. J. Mol. Sci. 2017, 18(4), 885; https://doi.org/10.3390/ijms18040885
Received: 10 March 2017 / Revised: 8 April 2017 / Accepted: 18 April 2017 / Published: 21 April 2017
Cited by 1 | PDF Full-text (2478 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Nine crossbred finishing barrows (body weight 94.4 ± 6.7 kg) randomly assigned to three dietary treatments were used to investigate the effects of dietary lysine on muscle growth related metabolic and signaling pathways. Muscle samples were collected from the longissimus dorsi of individual
[...] Read more.
Nine crossbred finishing barrows (body weight 94.4 ± 6.7 kg) randomly assigned to three dietary treatments were used to investigate the effects of dietary lysine on muscle growth related metabolic and signaling pathways. Muscle samples were collected from the longissimus dorsi of individual pigs after feeding the lysine-deficient (4.30 g/kg), lysine-adequate (7.10 g/kg), or lysine-excess (9.80 g/kg) diet for five weeks, and the total RNA was extracted afterwards. Affymetrix Porcine Gene 1.0 ST Array was used to quantify the expression levels of 19,211 genes. Statistical ANOVA analysis of the microarray data showed that 674 transcripts were differentially expressed (at p ≤ 0.05 level); 60 out of 131 transcripts (at p ≤ 0.01 level) were annotated in the NetAffx database. Ingenuity pathway analysis showed that dietary lysine deficiency may lead to: (1) increased muscle protein degradation via the ubiquitination pathway as indicated by the up-regulated DNAJA1, HSP90AB1 and UBE2B mRNA; (2) reduced muscle protein synthesis via the up-regulated RND3 and ZIC1 mRNA; (3) increased serine and glycine synthesis via the up-regulated PHGDH and PSPH mRNA; and (4) increased lipid accumulation via the up-regulated ME1, SCD, and CIDEC mRNA. Dietary lysine excess may lead to: (1) decreased muscle protein degradation via the down-regulated DNAJA1, HSP90AA1, HSPH1, and UBE2D3 mRNA; and (2) reduced lipid biosynthesis via the down-regulated CFD and ME1 mRNA. Collectively, dietary lysine may function as a signaling molecule to regulate protein turnover and lipid metabolism in the skeletal muscle of finishing pigs. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessArticle The Angiogenesis Inhibitor ALS-L1023 from Lemon-Balm Leaves Attenuates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease through Regulating the Visceral Adipose-Tissue Function
Int. J. Mol. Sci. 2017, 18(4), 846; https://doi.org/10.3390/ijms18040846
Received: 3 March 2017 / Revised: 31 March 2017 / Accepted: 12 April 2017 / Published: 17 April 2017
Cited by 6 | PDF Full-text (3831 KB) | HTML Full-text | XML Full-text
Abstract
Similar to neoplastic tissues, growth and development of adipose tissue are thought to be angiogenesis-dependent. Since visceral adipose tissue (VAT) is associated with development and progression of nonalcoholic fatty liver disease (NAFLD), we hypothesized that angiogenesis inhibition would attenuate obesity-induced NAFLD. We fed
[...] Read more.
Similar to neoplastic tissues, growth and development of adipose tissue are thought to be angiogenesis-dependent. Since visceral adipose tissue (VAT) is associated with development and progression of nonalcoholic fatty liver disease (NAFLD), we hypothesized that angiogenesis inhibition would attenuate obesity-induced NAFLD. We fed C57BL/6J mice a low-fat diet (LFD, chow 10% kcal fat), a high-fat diet (HFD, 45% kcal fat) or HFD supplemented with the lemon-balm extract ALS-L1023 (HFD-ALS) for 15 weeks. ALS-L1023 reduced endothelial cell-tube formation in vitro. HFD increased VAT angiogenesis and induced weight gains including body weight, VAT mass and visceral adipocyte size compared with LFD. However, HFD-ALS led to weight reductions without affecting calorie intake compared with HFD. HFD-ALS also reduced serum ALT and AST levels and improved lipid metabolism. HFD-ALS suppressed steatosis, infiltration of inflammatory cells, and accumulation of collagen in livers. HFD-ALS modulated hepatic expression of genes involved in lipid metabolism, inflammation, fibrosis, antioxidation, and apoptosis. Concomitantly, analysis of VAT function revealed that HFD-ALS led to fewer CD68-positive macrophage numbers and lower expression of inflammatory cytokines compared with HFD. Our findings show that the anti-angiogenic herbal extract ALS-L1023 attenuates NAFLD by targeting VAT during obesity, suggesting that angiogenesis inhibitors could aid in the treatment and prevention of obesity-induced human NAFLD. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessArticle Hepatic Transcriptome Profiles of Mice with Diet-Induced Nonalcoholic Steatohepatitis Treated with Astaxanthin and Vitamin E
Int. J. Mol. Sci. 2017, 18(3), 593; https://doi.org/10.3390/ijms18030593
Received: 19 January 2017 / Accepted: 4 March 2017 / Published: 8 March 2017
Cited by 6 | PDF Full-text (2768 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Astaxanthin alleviates hepatic lipid accumulation and peroxidation, inflammation, and fibrosis in mice with high-cholesterol, high-cholate, and high-fat (CL) diet-induced nonalcoholic steatohepatitis (NASH) [...] Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessArticle Genetic Variation in Choline-Metabolizing Enzymes Alters Choline Metabolism in Young Women Consuming Choline Intakes Meeting Current Recommendations
Int. J. Mol. Sci. 2017, 18(2), 252; https://doi.org/10.3390/ijms18020252
Received: 24 December 2016 / Revised: 14 January 2017 / Accepted: 17 January 2017 / Published: 26 January 2017
Cited by 6 | PDF Full-text (6462 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Single nucleotide polymorphisms (SNPs) in choline metabolizing genes are associated with disease risk and greater susceptibility to organ dysfunction under conditions of dietary choline restriction. However, the underlying metabolic signatures of these variants are not well characterized and it is unknown whether genotypic
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Single nucleotide polymorphisms (SNPs) in choline metabolizing genes are associated with disease risk and greater susceptibility to organ dysfunction under conditions of dietary choline restriction. However, the underlying metabolic signatures of these variants are not well characterized and it is unknown whether genotypic differences persist at recommended choline intakes. Thus, we sought to determine if common genetic risk factors alter choline dynamics in pregnant, lactating, and non-pregnant women consuming choline intakes meeting and exceeding current recommendations. Women (n = 75) consumed 480 or 930 mg choline/day (22% as a metabolic tracer, choline-d9) for 10–12 weeks in a controlled feeding study. Genotyping was performed for eight variant SNPs and genetic differences in metabolic flux and partitioning of plasma choline metabolites were evaluated using stable isotope methodology. CHKA rs10791957, CHDH rs9001, CHDH rs12676, PEMT rs4646343, PEMT rs7946, FMO3 rs2266782, SLC44A1 rs7873937, and SLC44A1 rs3199966 altered the use of choline as a methyl donor; CHDH rs9001 and BHMT rs3733890 altered the partitioning of dietary choline between betaine and phosphatidylcholine synthesis via the cytidine diphosphate (CDP)-choline pathway; and CHKA rs10791957, CHDH rs12676, PEMT rs4646343, PEMT rs7946 and SLC44A1 rs7873937 altered the distribution of dietary choline between the CDP-choline and phosphatidylethanolamine N-methyltransferase (PEMT) denovo pathway. Such metabolic differences may contribute to disease pathogenesis and prognosis over the long-term. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessArticle Fto-Deficiency Affects the Gene and MicroRNA Expression Involved in Brown Adipogenesis and Browning of White Adipose Tissue in Mice
Int. J. Mol. Sci. 2016, 17(11), 1851; https://doi.org/10.3390/ijms17111851
Received: 30 August 2016 / Revised: 1 November 2016 / Accepted: 2 November 2016 / Published: 7 November 2016
Cited by 5 | PDF Full-text (2122 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Genetic variants in the fat mass- and obesity-associated gene Fto are linked to the onset of obesity in humans. The causal role of the FTO protein in obesity is supported by evidence obtained from transgenic mice; however, the underlying molecular pathways pertaining to
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Genetic variants in the fat mass- and obesity-associated gene Fto are linked to the onset of obesity in humans. The causal role of the FTO protein in obesity is supported by evidence obtained from transgenic mice; however, the underlying molecular pathways pertaining to the role of FTO in obesity have yet to be established. In this study, we investigate the Fto gene in mouse brown adipose tissue and in the browning process of white adipose tissue. We analyze distinct structural and molecular factors in brown and white fat depots of Fto-deficient mice under normal and obesogenic conditions. We report significant alterations in the morphology of adipose tissue depots and the expression of mRNA and microRNA related to brown adipogenesis and metabolism in Fto-deficient mice. Furthermore, we show that high-fat feeding does not attenuate the browning process of Fto-deficient white adipose tissue as observed in wild-type tissue, suggesting a triggering effect of the FTO pathways by the dietary environment. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessArticle Vitamin D-Related Gene Polymorphisms, Plasma 25-Hydroxy-Vitamin D, Cigarette Smoke and Non-Small Cell Lung Cancer (NSCLC) Risk
Int. J. Mol. Sci. 2016, 17(10), 1597; https://doi.org/10.3390/ijms17101597
Received: 29 June 2016 / Revised: 22 August 2016 / Accepted: 13 September 2016 / Published: 22 September 2016
Cited by 12 | PDF Full-text (646 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Epidemiological studies regarding the relationship between vitamin D, genetic polymorphisms in the vitamin D metabolism, cigarette smoke and non-small cell lung cancer (NSCLC) risk have not been investigated comprehensively. To search for additional evidence, the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique
[...] Read more.
Epidemiological studies regarding the relationship between vitamin D, genetic polymorphisms in the vitamin D metabolism, cigarette smoke and non-small cell lung cancer (NSCLC) risk have not been investigated comprehensively. To search for additional evidence, the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique and radioimmunoassay method were utilized to evaluate 5 single-nucleotide polymorphisms (SNPs) in vitamin D receptor (VDR), 6 SNPs in 24-hydroxylase (CYP24A1), 2 SNPs in 1α-hydroxylase (CYP27B1) and 2 SNPs in vitamin D-binding protein (group-specific component, GC) and plasma vitamin D levels in 426 NSCLC cases and 445 controls from China. Exposure to cigarette smoke was ascertained through questionnaire information. Multivariable linear regressions and mixed effects models were used in statistical analysis. The results showed that Reference SNP rs6068816 in CYP24A1, rs1544410 and rs731236 in VDR and rs7041 in GC were statistically significant in relation to reduction in NSCLC risk (p < 0.001–0.05). No significant connection was seen between NSCLC risk and overall plasma 25-hydroxyvitamin D [25(OH)D] concentrations, regardless of smoking status. However, the mutation genotype of CYP24A1 rs6068816 and VDR rs1544410 were also significantly associated with increased 25(OH)D levels only in both the smoker and non-smoker cases (p < 0.01–0.05). Meanwhile, smokers and non-smokers with mutated homozygous rs2181874 in CYP24A1 had significantly increased NSCLC risk (odds ratio (OR) = 2.14, 95% confidence interval (CI) 1.47–3.43; p = 0.031; OR = 3.57, 95% CI 2.66–4.74; p = 0.019, respectively). Smokers with mutated homozygous rs10735810 in VDR had significantly increased NSCLC risk (OR = 1.93, 95% CI 1.41–2.76; p = 0.015). However, smokers with mutated homozygous rs6068816 in CYP24A1 had significantly decreased NSCLC risk (OR = 0.43, 95% CI 0.27–1.02; p = 0.006); and smokers and non-smokers with mutated homozygous rs1544410 in VDR had significantly decreased NSCLC risk (OR = 0.51, 95% CI 0.34–1.17; p = 0.002; OR = 0.26, 95% CI 0.20–0.69; p = 0.001, respectively). There are significant joint effects between smoking and CYP24A1 rs2181874, CYP24A1 rs6068816, VDR rs10735810, and VDR rs1544410 (p < 0.01–0.05). Smokers with mutated homozygous rs10735810 in VDR had significantly increased NSCLC risk (OR = 1.93, 95% CI 1.41–2.76; p = 0.015). In summary, the results suggested that the lower the distribution of vitamin D concentration, the more the genetic variations in CYP24A1, VDR and GC genes may be associated with NSCLC risk. In addition, there are significant joint associations of cigarette smoking and vitamin D deficiency on NSCLC risk. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Review

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Open AccessReview A Nutrigenomic Approach to Non-Alcoholic Fatty Liver Disease
Int. J. Mol. Sci. 2017, 18(7), 1534; https://doi.org/10.3390/ijms18071534
Received: 9 June 2017 / Revised: 7 July 2017 / Accepted: 13 July 2017 / Published: 16 July 2017
Cited by 7 | PDF Full-text (1088 KB) | HTML Full-text | XML Full-text
Abstract
Following the epidemics of obesity due to the consumption of high-calorie diet and sedentary lifestyle, nonalcoholic fatty liver disease (NAFLD) is now the leading cause of liver disease in Western countries. NAFLD is epidemiologically associated with metabolic syndrome and insulin resistance, and in
[...] Read more.
Following the epidemics of obesity due to the consumption of high-calorie diet and sedentary lifestyle, nonalcoholic fatty liver disease (NAFLD) is now the leading cause of liver disease in Western countries. NAFLD is epidemiologically associated with metabolic syndrome and insulin resistance, and in susceptible individuals it may progress to cirrhosis and hepatocellular carcinoma. Genetic factors play a key role in NAFLD predisposition by interacting with nutritional and other environmental factors. To date, there is no drug therapy for the treatment of NAFLD, and the main clinical recommendation is lifestyle modification. In the last years, nutrigenomics is promoting an increased understanding of how nutrition affects the switch from health to disease by altering the expression of an individual’s genetic makeup. The present review tries to summarize the most recent data evidencing how the interactions between nutrients and genetic factors can influence NAFLD development. The final goal should be to develop tools to quantify these complex interactions. The definition of a “nutrigenomic risk score” for each individual may represent a novel therapeutic approach for the management of NAFLD patients. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessReview Gut–CNS-Axis as Possibility to Modulate Inflammatory Disease Activity—Implications for Multiple Sclerosis
Int. J. Mol. Sci. 2017, 18(7), 1526; https://doi.org/10.3390/ijms18071526
Received: 7 June 2017 / Revised: 10 July 2017 / Accepted: 11 July 2017 / Published: 14 July 2017
Cited by 7 | PDF Full-text (797 KB) | HTML Full-text | XML Full-text
Abstract
In the last decade the role of environmental factors as modulators of disease activity and progression has received increasing attention. In contrast to classical environmental modulators such as exposure to sun-light or fine dust pollution, nutrition is an ideal tool for a personalized
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In the last decade the role of environmental factors as modulators of disease activity and progression has received increasing attention. In contrast to classical environmental modulators such as exposure to sun-light or fine dust pollution, nutrition is an ideal tool for a personalized human intervention. Various studies demonstrate a key role of dietary factors in autoimmune diseases including Inflammatory Bowel Disease (IBD), rheumatoid arthritis or inflammatory central nervous system (CNS) diseases such as Multiple Sclerosis (MS). In this review we discuss the connection between diet and inflammatory processes via the gut–CNS-axis. This axis describes a bi-directional communication system and comprises neuronal signaling, neuroendocrine pathways and modulation of immune responses. Therefore, the gut–CNS-axis represents an emerging target to modify CNS inflammatory activity ultimately opening new avenues for complementary and adjunctive treatment of autoimmune diseases such as MS. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessReview Maternal Macronutrient Consumption and the Developmental Origins of Metabolic Disease in the Offspring
Int. J. Mol. Sci. 2017, 18(7), 1451; https://doi.org/10.3390/ijms18071451
Received: 8 March 2017 / Revised: 14 June 2017 / Accepted: 30 June 2017 / Published: 6 July 2017
Cited by 8 | PDF Full-text (300 KB) | HTML Full-text | XML Full-text
Abstract
Recent research aimed at understanding the rise in obesity and cardiometabolic disease in children suggests that suboptimal maternal nutrition conditions organ systems and physiological responses in the offspring contributing to disease development. Understanding the mechanisms by which the macronutrient composition of the maternal
[...] Read more.
Recent research aimed at understanding the rise in obesity and cardiometabolic disease in children suggests that suboptimal maternal nutrition conditions organ systems and physiological responses in the offspring contributing to disease development. Understanding the mechanisms by which the macronutrient composition of the maternal diet during pregnancy or lactation affects health outcomes in the offspring may lead to new maternal nutrition recommendations, disease prevention strategies and therapies that reduce the increasing incidence of cardiometabolic disease in children. Recent mechanistic animal model research has identified how excess fats and sugars in the maternal diet alter offspring glucose tolerance, insulin signaling and metabolism. Maternal nutrition appears to influence epigenetic alterations in the offspring and the programming of gene expression in key metabolic pathways. This review is focused on experimental studies in animal models that have investigated mechanisms of how maternal consumption of macronutrients affects cardiometabolic disease development in the offspring. Future research using “-omic” technologies is essential to elucidate the mechanisms of how altered maternal macronutrient consumption influences the development of disease in the offspring. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessReview A Review of the Impact of Maternal Obesity on the Cognitive Function and Mental Health of the Offspring
Int. J. Mol. Sci. 2017, 18(5), 1093; https://doi.org/10.3390/ijms18051093
Received: 31 March 2017 / Revised: 3 May 2017 / Accepted: 16 May 2017 / Published: 19 May 2017
Cited by 9 | PDF Full-text (213 KB) | HTML Full-text | XML Full-text
Abstract
Globally, more than 20% of women of reproductive age are currently estimated to be obese. Children born to obese mothers are at higher risk of developing obesity, coronary heart disease, diabetes, stroke, and asthma in adulthood. Increasing clinical and experimental evidence suggests that
[...] Read more.
Globally, more than 20% of women of reproductive age are currently estimated to be obese. Children born to obese mothers are at higher risk of developing obesity, coronary heart disease, diabetes, stroke, and asthma in adulthood. Increasing clinical and experimental evidence suggests that maternal obesity also affects the health and function of the offspring brain across the lifespan. This review summarizes the current findings from human and animal studies that detail the impact of maternal obesity on aspects of learning, memory, motivation, affective disorders, attention-deficit hyperactivity disorder, autism spectrum disorders, and neurodegeneration in the offspring. Epigenetic mechanisms that may contribute to this mother–child interaction are also discussed. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessReview The Roles of Glutamine in the Intestine and Its Implication in Intestinal Diseases
Int. J. Mol. Sci. 2017, 18(5), 1051; https://doi.org/10.3390/ijms18051051
Received: 25 March 2017 / Revised: 9 May 2017 / Accepted: 10 May 2017 / Published: 12 May 2017
Cited by 7 | PDF Full-text (543 KB) | HTML Full-text | XML Full-text
Abstract
Glutamine, the most abundant free amino acid in the human body, is a major substrate utilized by intestinal cells. The roles of glutamine in intestinal physiology and management of multiple intestinal diseases have been reported. In gut physiology, glutamine promotes enterocyte proliferation, regulates
[...] Read more.
Glutamine, the most abundant free amino acid in the human body, is a major substrate utilized by intestinal cells. The roles of glutamine in intestinal physiology and management of multiple intestinal diseases have been reported. In gut physiology, glutamine promotes enterocyte proliferation, regulates tight junction proteins, suppresses pro-inflammatory signaling pathways, and protects cells against apoptosis and cellular stresses during normal and pathologic conditions. As glutamine stores are depleted during severe metabolic stress including trauma, sepsis, and inflammatory bowel diseases, glutamine supplementation has been examined in patients to improve their clinical outcomes. In this review, we discuss the physiological roles of glutamine for intestinal health and its underlying mechanisms. In addition, we discuss the current evidence for the efficacy of glutamine supplementation in intestinal diseases. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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Open AccessReview Pro-Resolving Molecules—New Approaches to Treat Sepsis?
Int. J. Mol. Sci. 2017, 18(3), 476; https://doi.org/10.3390/ijms18030476
Received: 9 November 2016 / Revised: 15 February 2017 / Accepted: 15 February 2017 / Published: 23 February 2017
Cited by 6 | PDF Full-text (3069 KB) | HTML Full-text | XML Full-text
Abstract
Inflammation is a complex response of the body to exogenous and endogenous insults. Chronic and systemic diseases are attributed to uncontrolled inflammation. Molecules involved in the initiation of inflammation are very well studied while pathways regulating its resolution are insufficiently investigated. Approaches to
[...] Read more.
Inflammation is a complex response of the body to exogenous and endogenous insults. Chronic and systemic diseases are attributed to uncontrolled inflammation. Molecules involved in the initiation of inflammation are very well studied while pathways regulating its resolution are insufficiently investigated. Approaches to down-modulate mediators relevant for the onset and duration of inflammation are successful in some chronic diseases, while all of them have failed in sepsis patients. Inflammation and immune suppression characterize sepsis, indicating that anti-inflammatory strategies alone are inappropriate for its therapy. Heme oxygenase 1 is a sensitive marker for oxidative stress and is upregulated in inflammation. Carbon monoxide, which is produced by this enzyme, initiates multiple anti-inflammatory and pro-resolving activities with higher production of omega-3 fatty acid-derived lipid metabolites being one of its protective actions. Pro-resolving lipids named maresins, resolvins and protectins originate from the omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid while lipoxins are derived from arachidonic acid. These endogenously produced lipids do not simply limit inflammation but actively contribute to its resolution, and thus provide an opportunity to combat chronic inflammatory diseases and eventually sepsis. Full article
(This article belongs to the Special Issue Nutrigenomics of Risk Factors for Disease)
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