Pub Date : 2013-01-01Epub Date: 2013-05-08DOI: 10.1159/000350744
Elisabeth Thifault, Hubert Cormier, Annie Bouchard-Mercier, Iwona Rudkowska, Ann-Marie Paradis, Veronique Garneau, Catherine Ouellette, Simone Lemieux, Patrick Couture, Marie-Claude Vohl
Objectives: To test whether age, sex, body mass index (BMI), and the apolipoprotein E (APOE) genotype are associated with the metabolic response to an n-3 polyunsaturated fatty acid (PUFA) supplementation.
Methods: 210 subjects followed a 2-week run-in period based on Canada's Food Guide and underwent a 6-week 5 g/day fish oil supplementation (1.9 g of eicosapentaenoic acid and 1.1 g of docosahexaenoic acid). Cardiovascular disease risk factors were measured.
Results: n-3 PUFA supplementation was associated with a decrease of plasma triglyceride levels (p = 0.0002) as well as with an increase of fasting glucose (FG) levels (p = 0.02). Age was associated with post-intervention plasma total cholesterol (p = 0.01), low-density lipoprotein cholesterol (p = 0.007), apolipoprotein B (p = 0.04), and insulin (p = 0.002) levels. Sex was associated with post-intervention plasma high-density lipoprotein cholesterol levels (p = 0.02). BMI was associated with plasma FG (p = 0.02) and insulin levels (p < 0.0001) after the supplementation. APOE genotype was associated with FG (p = 0.001) and C-reactive protein levels (p = 0.03) after the supplementation.
Conclusion: Results suggest that age, sex, BMI, and the APOE genotype contribute to the inter-individual variability observed in the metabolic response to an n-3 PUFA supplementation.
{"title":"Effects of age, sex, body mass index and APOE genotype on cardiovascular biomarker response to an n-3 polyunsaturated fatty acid supplementation.","authors":"Elisabeth Thifault, Hubert Cormier, Annie Bouchard-Mercier, Iwona Rudkowska, Ann-Marie Paradis, Veronique Garneau, Catherine Ouellette, Simone Lemieux, Patrick Couture, Marie-Claude Vohl","doi":"10.1159/000350744","DOIUrl":"https://doi.org/10.1159/000350744","url":null,"abstract":"<p><strong>Objectives: </strong>To test whether age, sex, body mass index (BMI), and the apolipoprotein E (APOE) genotype are associated with the metabolic response to an n-3 polyunsaturated fatty acid (PUFA) supplementation.</p><p><strong>Methods: </strong>210 subjects followed a 2-week run-in period based on Canada's Food Guide and underwent a 6-week 5 g/day fish oil supplementation (1.9 g of eicosapentaenoic acid and 1.1 g of docosahexaenoic acid). Cardiovascular disease risk factors were measured.</p><p><strong>Results: </strong>n-3 PUFA supplementation was associated with a decrease of plasma triglyceride levels (p = 0.0002) as well as with an increase of fasting glucose (FG) levels (p = 0.02). Age was associated with post-intervention plasma total cholesterol (p = 0.01), low-density lipoprotein cholesterol (p = 0.007), apolipoprotein B (p = 0.04), and insulin (p = 0.002) levels. Sex was associated with post-intervention plasma high-density lipoprotein cholesterol levels (p = 0.02). BMI was associated with plasma FG (p = 0.02) and insulin levels (p < 0.0001) after the supplementation. APOE genotype was associated with FG (p = 0.001) and C-reactive protein levels (p = 0.03) after the supplementation.</p><p><strong>Conclusion: </strong>Results suggest that age, sex, BMI, and the APOE genotype contribute to the inter-individual variability observed in the metabolic response to an n-3 PUFA supplementation.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 2","pages":"73-82"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000350744","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31536937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01Epub Date: 2013-08-10DOI: 10.1159/000354081
Camila S Silva, Thaís H Monteiro, Lívia M C Simões-Ambrósio, Daniele Y Sunaga, João F R Cardoso, Kelly S Furtado, Thomas P Ong, Fernando S Moreno, Sérgio Zucoloto, Helio Vannucchi
Background/aims: Chronic alcoholism is characterized by hepatotoxicity associated with antioxidant and redox status imbalance. Continuous ethanol intake induces free radical synthesis, resulting in the depletion of antioxidants, especially α-tocopherol, which has an important role in lipid peroxidation. This study aimed to evaluate if α-tocopherol supplementation can restore liver phenotype in rats chronically exposed to ethanol.
Methods: α-Tocopherol levels were determined and histologic analysis of liver was performed. Hepatic gene expression was analyzed through oligonucleotide microarray and real-time PCR.
Results: Alcohol exposure for 6 weeks did not decrease hepatic α-tocopherol levels; however, both groups exposed to ethanol (supplemented or not with α-tocopherol) displayed fatty liver. The antioxidant supplementation prevented Mallory bodies and inflammatory infiltration, but not apoptosis, in liver of the rats exposed to ethanol. Gene expression analysis showed evidence of adaptive response to chronic alcohol consumption, where antioxidant components were not regulated. Nevertheless, differentially expressed genes reflected the change in cellular homeostasis.
Conclusion: The hepatic α-tocopherol content was coherent with the antioxidant gene expression in this study. Cells are likely to have adapted and restored their antioxidant status after long-term ethanol exposure, which might be the reason for such conflicting reports concerning α-tocopherol status in chronic alcoholism.
{"title":"Effects of α-tocopherol supplementation on liver of rats chronically exposed to ethanol.","authors":"Camila S Silva, Thaís H Monteiro, Lívia M C Simões-Ambrósio, Daniele Y Sunaga, João F R Cardoso, Kelly S Furtado, Thomas P Ong, Fernando S Moreno, Sérgio Zucoloto, Helio Vannucchi","doi":"10.1159/000354081","DOIUrl":"https://doi.org/10.1159/000354081","url":null,"abstract":"<p><strong>Background/aims: </strong>Chronic alcoholism is characterized by hepatotoxicity associated with antioxidant and redox status imbalance. Continuous ethanol intake induces free radical synthesis, resulting in the depletion of antioxidants, especially α-tocopherol, which has an important role in lipid peroxidation. This study aimed to evaluate if α-tocopherol supplementation can restore liver phenotype in rats chronically exposed to ethanol.</p><p><strong>Methods: </strong>α-Tocopherol levels were determined and histologic analysis of liver was performed. Hepatic gene expression was analyzed through oligonucleotide microarray and real-time PCR.</p><p><strong>Results: </strong>Alcohol exposure for 6 weeks did not decrease hepatic α-tocopherol levels; however, both groups exposed to ethanol (supplemented or not with α-tocopherol) displayed fatty liver. The antioxidant supplementation prevented Mallory bodies and inflammatory infiltration, but not apoptosis, in liver of the rats exposed to ethanol. Gene expression analysis showed evidence of adaptive response to chronic alcohol consumption, where antioxidant components were not regulated. Nevertheless, differentially expressed genes reflected the change in cellular homeostasis.</p><p><strong>Conclusion: </strong>The hepatic α-tocopherol content was coherent with the antioxidant gene expression in this study. Cells are likely to have adapted and restored their antioxidant status after long-term ethanol exposure, which might be the reason for such conflicting reports concerning α-tocopherol status in chronic alcoholism.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 3","pages":"125-36"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000354081","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31654564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01Epub Date: 2013-09-24DOI: 10.1159/000355340
Jing X Kang
As an increasingly prevalent disease and a leading cause of death, cancer is a major threat to human health. Although cancer research has provided us with a better understanding of cancer biology, we still face numerous challenges in cancer treatment and prevention. Current therapies are largely limited to surgery, radiation therapy, and chemotherapy, which remain unsatisfactory. In particular, there are many problems in chemotherapy, such as low response rate, poor specificity, drug resistance, and severe side effects. Thus, we still have much to do in order to improve the current situation. It is our priority to identify and develop alternative treatment options that can increase efficacy, reduce side effects, and improve quality of life for cancer patients. In this context, nutrigenomics is emerging as a field that holds great promise for this endeavor because of its capability to modulate cancer metabolism and tumorigenesis through nutritional intervention. Cancer metabolism has gained unprecedented attention due to its involvement in every stage of cancer development. Cancer cells are characterized by an altered metabolism to sustain their rapid growth. One well-recognized alteration is the reprogramming of cellular energy production, known as the Warburg effect: unlike normal cells that primarily utilize oxidative phosphorylation, cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation, and thus require a large supply of glucose [1] . Recent studies have revealed that changes in gene expression, such as phosphofructokinase 1 [2] and pyruvate kinase type M2 [3] , are implicated in this altered pathway. Cancer cells also exhibit an increased production of certain metabolites that serve as building blocks to meet proliferation requirements. In particular, lipid synthesis is enhanced in cancer cells by the upregulation of fatty acid-metabolizing enzymes, such as fatty acid synthase [4] , stearoyl-CoA desaturase-1 [5] , and delta-6 desaturase [6] . Furthermore, the production of factors that support the tumor microenvironment is augmented in cancer cells. For example, one well-known metabolic biomarker of cancer is the overexpression of cyclooxygenase-2, which is responsible for converting omega-6 arachidonic acid into tumor-promoting eicosanoids [7] . It is clear that nutrient metabolism is critical for cancer biology, and thus modulation of the metabolic pathways would have profound effects on cancer development. Certain nutrients have been shown to be capable of modulating gene expression related to cancer hallmarks, such as inflammation, angiogenesis, and proliferation, through multiple mechanisms. For example, polyunsaturated fatty acids (PUFA) can influence gene expression
{"title":"Nutrigenomics and cancer therapy.","authors":"Jing X Kang","doi":"10.1159/000355340","DOIUrl":"https://doi.org/10.1159/000355340","url":null,"abstract":"As an increasingly prevalent disease and a leading cause of death, cancer is a major threat to human health. Although cancer research has provided us with a better understanding of cancer biology, we still face numerous challenges in cancer treatment and prevention. Current therapies are largely limited to surgery, radiation therapy, and chemotherapy, which remain unsatisfactory. In particular, there are many problems in chemotherapy, such as low response rate, poor specificity, drug resistance, and severe side effects. Thus, we still have much to do in order to improve the current situation. It is our priority to identify and develop alternative treatment options that can increase efficacy, reduce side effects, and improve quality of life for cancer patients. In this context, nutrigenomics is emerging as a field that holds great promise for this endeavor because of its capability to modulate cancer metabolism and tumorigenesis through nutritional intervention. Cancer metabolism has gained unprecedented attention due to its involvement in every stage of cancer development. Cancer cells are characterized by an altered metabolism to sustain their rapid growth. One well-recognized alteration is the reprogramming of cellular energy production, known as the Warburg effect: unlike normal cells that primarily utilize oxidative phosphorylation, cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation, and thus require a large supply of glucose [1] . Recent studies have revealed that changes in gene expression, such as phosphofructokinase 1 [2] and pyruvate kinase type M2 [3] , are implicated in this altered pathway. Cancer cells also exhibit an increased production of certain metabolites that serve as building blocks to meet proliferation requirements. In particular, lipid synthesis is enhanced in cancer cells by the upregulation of fatty acid-metabolizing enzymes, such as fatty acid synthase [4] , stearoyl-CoA desaturase-1 [5] , and delta-6 desaturase [6] . Furthermore, the production of factors that support the tumor microenvironment is augmented in cancer cells. For example, one well-known metabolic biomarker of cancer is the overexpression of cyclooxygenase-2, which is responsible for converting omega-6 arachidonic acid into tumor-promoting eicosanoids [7] . It is clear that nutrient metabolism is critical for cancer biology, and thus modulation of the metabolic pathways would have profound effects on cancer development. Certain nutrients have been shown to be capable of modulating gene expression related to cancer hallmarks, such as inflammation, angiogenesis, and proliferation, through multiple mechanisms. For example, polyunsaturated fatty acids (PUFA) can influence gene expression","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 3","pages":"I-II"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000355340","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31770979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01Epub Date: 2013-06-12DOI: 10.1159/000350751
Frédéric Capel, Gaëlle Rolland-Valognes, Catherine Dacquet, Manuel Brun, Michel Lonchampt, Alain Ktorza, Brian Lockhart, Jean-Pierre Galizzi
Background: The sterol regulatory element-binding protein (SREBP) 1c contributes to the transcriptional coordination of cholesterol, fatty acid, and carbohydrate metabolisms. Alterations in these processes accelerate the progression of hepatic steatosis and insulin resistance during aging and obesity.
Methods: Using an ex vivo chromatin immunoprecipitation coupled to microarray (ChIP-on-chip) technique combined with genome-wide gene expression analysis, we analyzed the transcriptomic adaptations mediated by Srebp-1c binding to gene promoters in the liver of mice fed with a low-fat diet or a high-fat diet (HFD) for either 1 or 12 months.
Results: Aging had a higher transcriptional impact than HFD and modified the expression of genes involved in fatty acid oxidation and oxidative stress. HFD was associated with a marked induction of genes involved in lipid and cholesterol metabolism. The prolonged high-fat feeding together with the aging effects stimulates inflammatory pathways. ChIP-on-chip applied to aging and HFD analyses revealed that the binding of SREBP-1c to a series of promoters accompanied a paralleled modification of gene expression. Therefore, SREBP-1c could play a role in aging and high-fat feeding through the regulation of genes involved in lipid metabolism and inflammatory response.
Conclusions: This study represents an original ex vivo experiment to elucidate the molecular events involved in metabolic disorders.
{"title":"Analysis of sterol-regulatory element-binding protein 1c target genes in mouse liver during aging and high-fat diet.","authors":"Frédéric Capel, Gaëlle Rolland-Valognes, Catherine Dacquet, Manuel Brun, Michel Lonchampt, Alain Ktorza, Brian Lockhart, Jean-Pierre Galizzi","doi":"10.1159/000350751","DOIUrl":"https://doi.org/10.1159/000350751","url":null,"abstract":"<p><strong>Background: </strong>The sterol regulatory element-binding protein (SREBP) 1c contributes to the transcriptional coordination of cholesterol, fatty acid, and carbohydrate metabolisms. Alterations in these processes accelerate the progression of hepatic steatosis and insulin resistance during aging and obesity.</p><p><strong>Methods: </strong>Using an ex vivo chromatin immunoprecipitation coupled to microarray (ChIP-on-chip) technique combined with genome-wide gene expression analysis, we analyzed the transcriptomic adaptations mediated by Srebp-1c binding to gene promoters in the liver of mice fed with a low-fat diet or a high-fat diet (HFD) for either 1 or 12 months.</p><p><strong>Results: </strong>Aging had a higher transcriptional impact than HFD and modified the expression of genes involved in fatty acid oxidation and oxidative stress. HFD was associated with a marked induction of genes involved in lipid and cholesterol metabolism. The prolonged high-fat feeding together with the aging effects stimulates inflammatory pathways. ChIP-on-chip applied to aging and HFD analyses revealed that the binding of SREBP-1c to a series of promoters accompanied a paralleled modification of gene expression. Therefore, SREBP-1c could play a role in aging and high-fat feeding through the regulation of genes involved in lipid metabolism and inflammatory response.</p><p><strong>Conclusions: </strong>This study represents an original ex vivo experiment to elucidate the molecular events involved in metabolic disorders.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 2","pages":"107-22"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000350751","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31512626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01Epub Date: 2014-03-15DOI: 10.1159/000360422
Mohamed A Abu El Maaty, Sally I Hassanein, Hameis M Sleem, Mohamed Z Gad
Background/aims: Recent genome-wide association studies have identified the rs1790349 and rs12785878 single-nucleotide polymorphisms (SNPs), present in the NADSYN1/DHCR7 locus, as an influential player on circulating 25-hydroxyvitamin D [25(OH)D] levels, which itself has been linked to various diseases including cardiovascular disease (CVD). This study investigated the association of these SNPs with CVD and 25(OH)D levels.
Methods: Sixty- three male patients with verified coronary artery disease (CAD) were recruited, as well as 31 age- and sex-matched controls. Genotyping was performed by sequencing, whereas plasma 25(OH)D levels were assessed by HPLC-UV.
Results: Statistical insignificance was observed in comparing the genotype distribution of patients and controls for both the rs12785878 (NADSYN1) polymorphism (p = 0.097) and the rs1790349 (DHCR7; p = 0.9). Comparison of allelic distributions of rs1790349 and rs12785878 yielded insignificant results (p = 0.7, OR: 0.58-2.6 and p = 0.14, OR: 0.88-2.85, respectively). Taking together patients and controls, both SNPs were found to influence total 25(OH)D levels (p = 0.001 and p < 0.0001) as well as 25(OH)D3 levels only in controls.
Conclusion: This study further supports the evidence of the ability of the investigated SNPs to predict circulating 25(OH)D levels, nonetheless opposing their use as genetic markers for CAD.
{"title":"Effect of polymorphisms in the NADSYN1/DHCR7 locus (rs12785878 and rs1790349) on plasma 25-hydroxyvitamin D levels and coronary artery disease incidence.","authors":"Mohamed A Abu El Maaty, Sally I Hassanein, Hameis M Sleem, Mohamed Z Gad","doi":"10.1159/000360422","DOIUrl":"https://doi.org/10.1159/000360422","url":null,"abstract":"<p><strong>Background/aims: </strong>Recent genome-wide association studies have identified the rs1790349 and rs12785878 single-nucleotide polymorphisms (SNPs), present in the NADSYN1/DHCR7 locus, as an influential player on circulating 25-hydroxyvitamin D [25(OH)D] levels, which itself has been linked to various diseases including cardiovascular disease (CVD). This study investigated the association of these SNPs with CVD and 25(OH)D levels.</p><p><strong>Methods: </strong>Sixty- three male patients with verified coronary artery disease (CAD) were recruited, as well as 31 age- and sex-matched controls. Genotyping was performed by sequencing, whereas plasma 25(OH)D levels were assessed by HPLC-UV.</p><p><strong>Results: </strong>Statistical insignificance was observed in comparing the genotype distribution of patients and controls for both the rs12785878 (NADSYN1) polymorphism (p = 0.097) and the rs1790349 (DHCR7; p = 0.9). Comparison of allelic distributions of rs1790349 and rs12785878 yielded insignificant results (p = 0.7, OR: 0.58-2.6 and p = 0.14, OR: 0.88-2.85, respectively). Taking together patients and controls, both SNPs were found to influence total 25(OH)D levels (p = 0.001 and p < 0.0001) as well as 25(OH)D3 levels only in controls.</p><p><strong>Conclusion: </strong>This study further supports the evidence of the ability of the investigated SNPs to predict circulating 25(OH)D levels, nonetheless opposing their use as genetic markers for CAD.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 6","pages":"327-35"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000360422","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32188702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01Epub Date: 2013-06-14DOI: 10.1159/000353144
Jing X Kang
The gut microbiota has recently attracted unprecedented attention from the biomedical community for the mounting evidence supporting its central role in human health and disease [1] . The gut microbiota consists of the trillions of bacterial microorganisms, spanning over 500 species, that inhabit our gastrointestinal tracts. We now know that these bacteria are not simply commensal organisms in our bodies, but instead serve as an important ‘organ’ that regulates metabolic processes, including the digestion and absorption of nutrients, synthesis of vitamins, modulation of mucosal immunity, as well as production of toxins and carcinogens [1, 2] . The composition of the gut microbial community – whether the bacterial numbers are balanced or in dysbiosis – determines the nature of its influence on numerous physiological and pathological conditions. Since the gut microbial profile is unique to each individual, evolves over a lifetime, and can be altered by internal and external factors (especially the diet), the gut microbiome presents us with further complexities as well as new opportunities for nutrigenomics and personalized nutrition. When we study the effects of dietary nutrients on gene expression, we must be aware that these effects can be mediated by gut bacteria. The gut microbiota can influence gene expression both locally and systemically. Through interactions with the intestinal mucosal tissue, certain species of bacteria can influence the expression of genes involved in nutrient absorption or immune function [3] , while some substances generated by gut bacteria can enter the bloodstream; for example, short-chain fatty acids (produced by fermentation of polysaccharides) can regulate lipogenesis gene expression in the liver, and toxins like lipopolysaccharides (LPS) can affect inflammation-related genes [4] . The quantities of these bacteria, such as the LPS-producing Escherichia coli , can be significantly altered by dietary nutrients. For example, a diet high in saturated fat has been shown to increase E. coli and subsequent LPS production [5] , while a laminarin-supplemented diet can suppress E. coli numbers and result in lower levels of inflammatory cytokines [6] . These findings illustrate a new interface for the regulation of gene expression by dietary nutrients, and also reveal an alternative pathway for regulating gene expression through the manipulation of the gut microbiota.
{"title":"Gut microbiota and personalized nutrition.","authors":"Jing X Kang","doi":"10.1159/000353144","DOIUrl":"https://doi.org/10.1159/000353144","url":null,"abstract":"The gut microbiota has recently attracted unprecedented attention from the biomedical community for the mounting evidence supporting its central role in human health and disease [1] . The gut microbiota consists of the trillions of bacterial microorganisms, spanning over 500 species, that inhabit our gastrointestinal tracts. We now know that these bacteria are not simply commensal organisms in our bodies, but instead serve as an important ‘organ’ that regulates metabolic processes, including the digestion and absorption of nutrients, synthesis of vitamins, modulation of mucosal immunity, as well as production of toxins and carcinogens [1, 2] . The composition of the gut microbial community – whether the bacterial numbers are balanced or in dysbiosis – determines the nature of its influence on numerous physiological and pathological conditions. Since the gut microbial profile is unique to each individual, evolves over a lifetime, and can be altered by internal and external factors (especially the diet), the gut microbiome presents us with further complexities as well as new opportunities for nutrigenomics and personalized nutrition. When we study the effects of dietary nutrients on gene expression, we must be aware that these effects can be mediated by gut bacteria. The gut microbiota can influence gene expression both locally and systemically. Through interactions with the intestinal mucosal tissue, certain species of bacteria can influence the expression of genes involved in nutrient absorption or immune function [3] , while some substances generated by gut bacteria can enter the bloodstream; for example, short-chain fatty acids (produced by fermentation of polysaccharides) can regulate lipogenesis gene expression in the liver, and toxins like lipopolysaccharides (LPS) can affect inflammation-related genes [4] . The quantities of these bacteria, such as the LPS-producing Escherichia coli , can be significantly altered by dietary nutrients. For example, a diet high in saturated fat has been shown to increase E. coli and subsequent LPS production [5] , while a laminarin-supplemented diet can suppress E. coli numbers and result in lower levels of inflammatory cytokines [6] . These findings illustrate a new interface for the regulation of gene expression by dietary nutrients, and also reveal an alternative pathway for regulating gene expression through the manipulation of the gut microbiota.","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 2","pages":"I-II"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000353144","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31605080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01Epub Date: 2013-08-31DOI: 10.1159/000354403
Giuseppe Astarita, James Langridge
Nutritional research is undergoing a remarkable transformation driven by new technological tools. Because of the complexity of the components present in food and how they may interact with the biochemical networks of living organisms, nutrition cannot be considered a reductionist discipline. More holistic approaches, which are capable of gathering comprehensive, high-throughput amounts of data, appear to best enhance our understanding of the role of food in health and disease. In this context, global metabolite analysis, or 'metabolomics', is becoming an appealing research tool for nutrigenomics and nutrigenetics scientists. The purpose of the present review is to highlight some potential applications of metabolomics in nutrition research.
{"title":"An emerging role for metabolomics in nutrition science.","authors":"Giuseppe Astarita, James Langridge","doi":"10.1159/000354403","DOIUrl":"https://doi.org/10.1159/000354403","url":null,"abstract":"<p><p>Nutritional research is undergoing a remarkable transformation driven by new technological tools. Because of the complexity of the components present in food and how they may interact with the biochemical networks of living organisms, nutrition cannot be considered a reductionist discipline. More holistic approaches, which are capable of gathering comprehensive, high-throughput amounts of data, appear to best enhance our understanding of the role of food in health and disease. In this context, global metabolite analysis, or 'metabolomics', is becoming an appealing research tool for nutrigenomics and nutrigenetics scientists. The purpose of the present review is to highlight some potential applications of metabolomics in nutrition research.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 4-5","pages":"181-200"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000354403","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31710735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01Epub Date: 2014-02-04DOI: 10.1159/000357947
Ieler Ferreira Ribeiro, Ana Luisa Miranda-Vilela, Maria de Nazaré Klautau-Guimarães, Cesar Koppe Grisolia
Background/aims: As diet can affect an individual's genes and these can affect response to supplementation, we aimed to investigate the influence of erythropoietin (EPO T→G) and α-actinin-3 (ACTN3 R577X) polymorphisms on plasma lipid peroxidation, hemogram and biochemical dosages of creatine kinase, aspartate aminotransferase, alanine aminotransferase and C-reactive protein (including high-sensitivity C-reactive protein) of runners (n = 123) before and after 14 days of 400 mg pequi oil supplementation, a natural carotenoid-rich oil, after races under closely comparable conditions.
Methods/results: Blood samples were taken immediately after racing to perform the tests. Before pequi oil supplementation, EPO polymorphism influenced erythrogram and plateletgram results, suggesting an aerobic advantage for the TG genotype and a disadvantage for the GG genotype as regards possible microvascular complications, while no association was found for ACTN3 polymorphism with endurance performance. Both polymorphisms influenced the runners' response to pequi oil: significant responses were observed for the EPO TT genotype in erythrocyte, hematocrit, mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration values, and for the TT and TG genotypes in red blood cell distribution width values. Significant differences were also observed in the plateletgram for the TT and TG genotypes. ACTN3 mainly influenced aspartate aminotransferase and creatine kinase values: heterozygotes had a significant reduction in aspartate aminotransferase values and homozygous individuals (XX) in creatine kinase values after pequi oil supplementation.
Conclusion: These results emphasize the importance of studying nutrigenomic effects on athletes' performance.
{"title":"The influence of erythropoietin (EPO T → G) and α-actinin-3 (ACTN3 R577X) polymorphisms on runners' responses to the dietary ingestion of antioxidant supplementation based on pequi oil ( Caryocar brasiliense Camb.): a before-after study.","authors":"Ieler Ferreira Ribeiro, Ana Luisa Miranda-Vilela, Maria de Nazaré Klautau-Guimarães, Cesar Koppe Grisolia","doi":"10.1159/000357947","DOIUrl":"https://doi.org/10.1159/000357947","url":null,"abstract":"<p><strong>Background/aims: </strong>As diet can affect an individual's genes and these can affect response to supplementation, we aimed to investigate the influence of erythropoietin (EPO T→G) and α-actinin-3 (ACTN3 R577X) polymorphisms on plasma lipid peroxidation, hemogram and biochemical dosages of creatine kinase, aspartate aminotransferase, alanine aminotransferase and C-reactive protein (including high-sensitivity C-reactive protein) of runners (n = 123) before and after 14 days of 400 mg pequi oil supplementation, a natural carotenoid-rich oil, after races under closely comparable conditions.</p><p><strong>Methods/results: </strong>Blood samples were taken immediately after racing to perform the tests. Before pequi oil supplementation, EPO polymorphism influenced erythrogram and plateletgram results, suggesting an aerobic advantage for the TG genotype and a disadvantage for the GG genotype as regards possible microvascular complications, while no association was found for ACTN3 polymorphism with endurance performance. Both polymorphisms influenced the runners' response to pequi oil: significant responses were observed for the EPO TT genotype in erythrocyte, hematocrit, mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration values, and for the TT and TG genotypes in red blood cell distribution width values. Significant differences were also observed in the plateletgram for the TT and TG genotypes. ACTN3 mainly influenced aspartate aminotransferase and creatine kinase values: heterozygotes had a significant reduction in aspartate aminotransferase values and homozygous individuals (XX) in creatine kinase values after pequi oil supplementation.</p><p><strong>Conclusion: </strong>These results emphasize the importance of studying nutrigenomic effects on athletes' performance.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 6","pages":"283-304"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000357947","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32096016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-01-01Epub Date: 2013-03-16DOI: 10.1159/000348442
Sinead A O'Brien, Emma L Feeney, Amalia G M Scannell, Anne Markey, Eileen R Gibney
Background/aims: Variations in bitter receptor gene TAS2R38 affect the perception of bitter-tasting compound 6-n-propylthiouracil (PROP). The perception of PROP has been associated, in some reports, with the perception of fat and sweet tastes, and various food preferences and intakes. The aim was to investigate nutrient intakes and food patterns in a group of Irish children, using K-means cluster analysis, and compare these with TAS2R38 genotype and PROP taster status.
Methods: Dietary intake was measured via a 3-day diet history in 483 children aged 7-13 years. Children were genotyped for TAS2R38 variation, and PROP taster status was assessed. Anthropometric and socioeconomic data were also obtained.
Results: No differences were observed in macronutrient, micronutrient, or food group consumption between the TAS2R38 genotype and PROP taster groups. K-means cluster analysis identified two distinct dietary patterns, termed 'more healthful' and 'less healthful' clusters. The clusters did not differ in frequencies of TAS2R38 genotype nor PROP taster status groups, suggesting that dietary patterns are not influenced by bitter taste perception.
Conclusion: Bitterness perception, as measured by either TAS2R38 genotype or PROP taster status, does not appear to exert a significant effect on patterns of dietary intakes.
{"title":"Bitter taste perception and dietary intake patterns in irish children.","authors":"Sinead A O'Brien, Emma L Feeney, Amalia G M Scannell, Anne Markey, Eileen R Gibney","doi":"10.1159/000348442","DOIUrl":"https://doi.org/10.1159/000348442","url":null,"abstract":"<p><strong>Background/aims: </strong>Variations in bitter receptor gene TAS2R38 affect the perception of bitter-tasting compound 6-n-propylthiouracil (PROP). The perception of PROP has been associated, in some reports, with the perception of fat and sweet tastes, and various food preferences and intakes. The aim was to investigate nutrient intakes and food patterns in a group of Irish children, using K-means cluster analysis, and compare these with TAS2R38 genotype and PROP taster status.</p><p><strong>Methods: </strong>Dietary intake was measured via a 3-day diet history in 483 children aged 7-13 years. Children were genotyped for TAS2R38 variation, and PROP taster status was assessed. Anthropometric and socioeconomic data were also obtained.</p><p><strong>Results: </strong>No differences were observed in macronutrient, micronutrient, or food group consumption between the TAS2R38 genotype and PROP taster groups. K-means cluster analysis identified two distinct dietary patterns, termed 'more healthful' and 'less healthful' clusters. The clusters did not differ in frequencies of TAS2R38 genotype nor PROP taster status groups, suggesting that dietary patterns are not influenced by bitter taste perception.</p><p><strong>Conclusion: </strong>Bitterness perception, as measured by either TAS2R38 genotype or PROP taster status, does not appear to exert a significant effect on patterns of dietary intakes.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":" ","pages":"43-58"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000348442","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40242336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Marine omega-3 (n-3) polyunsaturated fatty acids (PUFA) reduce plasma triglyceride (TG) levels. Genetic factors such as single nucleotide polymorphisms (SNPs) could be responsible for the variability of the plasma TG response to n-3 PUFA supplementation. Previous studies have demonstrated that n-3 PUFA supplementation using fish oil modified the expression levels of three genes involved in the TG synthesis pathway (GPAM, AGPAT3 and AGPAT4) in peripheral blood mononuclear cells.
Methods: A total of 210 subjects consumed 5 g/day of a fish oil supplement for 6 weeks. Plasma lipids were measured before and after the supplementation period. Three SNPs in GPAM, 13 SNPs in AGPAT3 and 35 SNPs in AGPAT4 were genotyped.
Results: In an ANOVA for repeated measures adjusted for age, sex and BMI, genotype effects on plasma TG levels were observed for rs1838452 in AGPAT3 as well as for rs746731 and rs2293286 in AGPAT4. Genotype × supplementation interaction effects on plasma TG levels were observed for rs2792751 and rs17129561 in GPAM as well as for rs3798943 and rs9458172 in AGPAT4 (p < 0.05).
Conclusion: These results suggest that SNPs in genes involved in the TG synthesis pathway may influence plasma TG levels after n-3 PUFA supplementation.
{"title":"Polymorphisms in genes involved in the triglyceride synthesis pathway and marine omega-3 polyunsaturated fatty acid supplementation modulate plasma triglyceride levels.","authors":"Catherine Ouellette, Hubert Cormier, Iwona Rudkowska, Frédéric Guénard, Simone Lemieux, Patrick Couture, Marie-Claude Vohl","doi":"10.1159/000357432","DOIUrl":"https://doi.org/10.1159/000357432","url":null,"abstract":"<p><strong>Background: </strong>Marine omega-3 (n-3) polyunsaturated fatty acids (PUFA) reduce plasma triglyceride (TG) levels. Genetic factors such as single nucleotide polymorphisms (SNPs) could be responsible for the variability of the plasma TG response to n-3 PUFA supplementation. Previous studies have demonstrated that n-3 PUFA supplementation using fish oil modified the expression levels of three genes involved in the TG synthesis pathway (GPAM, AGPAT3 and AGPAT4) in peripheral blood mononuclear cells.</p><p><strong>Methods: </strong>A total of 210 subjects consumed 5 g/day of a fish oil supplement for 6 weeks. Plasma lipids were measured before and after the supplementation period. Three SNPs in GPAM, 13 SNPs in AGPAT3 and 35 SNPs in AGPAT4 were genotyped.</p><p><strong>Results: </strong>In an ANOVA for repeated measures adjusted for age, sex and BMI, genotype effects on plasma TG levels were observed for rs1838452 in AGPAT3 as well as for rs746731 and rs2293286 in AGPAT4. Genotype × supplementation interaction effects on plasma TG levels were observed for rs2792751 and rs17129561 in GPAM as well as for rs3798943 and rs9458172 in AGPAT4 (p < 0.05).</p><p><strong>Conclusion: </strong>These results suggest that SNPs in genes involved in the TG synthesis pathway may influence plasma TG levels after n-3 PUFA supplementation.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 4-5","pages":"268-80"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000357432","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32011581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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