Journal of Nutrigenetics and Nutrigenomics最新文献

{"title":"Short-term folate supplementation in physiological doses has no effect on ESR1 and MLH1 methylation in colonic mucosa of individuals with adenoma.","authors":"Reyad Al-Ghnaniem Abbadi,&nbsp;Peter Emery,&nbsp;Maria Pufulete","doi":"10.1159/000345819","DOIUrl":"https://doi.org/10.1159/000345819","url":null,"abstract":"<p><strong>Background/aims: </strong>Low folate intake may increase risk of colorectal cancer by altering gene-specific methylation in the colon. We determined whether supplementation with physiological doses of folate could alter methylation in the oestrogen receptor 1 (ESR1) and mutL homolog 1 (MLH1) genes in colonic mucosa of subjects with colorectal adenoma.</p><p><strong>Methods: </strong>This was a randomised, double-blind, placebo-controlled trial. Subjects received either 400 µg/day folic acid (n = 15) or placebo (n = 14) for 10 weeks. Blood and colonic tissue samples were collected at baseline and after intervention to determine biomarkers of folate and vitamin B12 status, MTHFR C677T and MS A2756G genotypes, and ESR1 and MLH1 methylation.</p><p><strong>Results: </strong>Although serum and red cell folate increased (p < 0.001 vs. placebo) and plasma homocysteine decreased (p = 0018 vs. placebo) in the folic acid group, there were no significant changes in ESR1 (p = 0.649 vs. placebo) or MLH1 (p = 0.211 vs. placebo) methylation. There was a significant effect of gender on ESR1 methylation (p = 0.004) and significant gender and genotype (MTHFR C677T and MS A2756G) interactions (p = 0.04 and p = 0.014, respectively) that were independent of treatment group allocation.</p><p><strong>Conclusions: </strong>Short-term folate supplementation in physiological doses decreases plasma homocysteine but has no effect on ESR1 and MLH1 methylation in colonic mucosa of individuals with adenoma. Further studies to investigate the interactions between gender, genotype and DNA methylation suggested in this study are warranted.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":" ","pages":"327-38"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000345819","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31169074","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}

{"title":"Associations between polymorphisms in genes involved in fatty acid metabolism and dietary fat intakes.","authors":"Annie Bouchard-Mercier,&nbsp;Ann-Marie Paradis,&nbsp;Louis Pérusse,&nbsp;Marie-Claude Vohl","doi":"10.1159/000336511","DOIUrl":"https://doi.org/10.1159/000336511","url":null,"abstract":"<p><strong>Background: </strong>Obesity prevalence is growing in our population. Twin studies have estimated the heritability of dietary intakes to about 30%. The objective of this study was to verify whether polymorphisms in genes involved in fatty acid metabolism are associated with dietary fat intakes.</p><p><strong>Methods: </strong>Seven hundred participants were recruited. A validated food frequency questionnaire was used to assess dietary intakes. PCR-RFLP and TAQMAN methodology were used to genotype PPARα Leu162Val, PPARγ Pro12Ala, PPARδ -87T>C, PPARGC1α Gly482Ser, FASN Val1483Ile and SREBF1 c.*619C>G. Statistical analyses were executed with SAS statistical package.</p><p><strong>Results: </strong>Carriers of the Ala12 allele of PPARγ Pro12Ala polymorphism had higher intakes of total fat (p = 0.04). For FASN Val1483Ile polymorphism, significant gene-sex interaction effects were found for total fat and saturated fat intakes (p = 0.02 and p = 0.002, respectively). No significant difference in fat intakes was observed for PPARα Leu162Val, PPARδ -87T>C, PPARGC1α Gly482Ser and SREBF1 c.*619C>G polymorphisms.</p><p><strong>Conclusions: </strong>Polymorphisms in PPARγ and FASN seem to be associated with dietary fat intakes. Genetic variants are important to take into account when studying dietary intakes.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":" ","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000336511","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40161866","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}

{"title":"Identification of metabolic biomarkers for personalized nutrition.","authors":"Jing X Kang","doi":"10.1159/000342702","DOIUrl":"https://doi.org/10.1159/000342702","url":null,"abstract":"Now more than ever, we have begun to appreciate the roles of individual physical and genetic variation in health and medicine. A great deal of research attention has recently been devoted toward personalized medicine, in which technologies like medical genetics are used to determine information such as how a patient is likely to respond to a treatment or the optimal dose of a drug. While drug therapy will undoubtedly advance as a result of this new focus, it is critical that we not overlook the importance of personalized nutrition in disease management and health promotion. Indeed, personalized nutrition may be even more critical than personalized medicine given that dietary intake is a fundamental part of everyday life that affects our health. The fields of nutrigenetics and nutrigenomics present uniquely powerful sources of information for implementing personalized nutrition. Nutrigenetics specifies how individual genetic variance impacts response to nutrients such that an individual can avoid negative metabolic consequences by choosing appropriate foods. One classic example is lactose intolerance, in which one lacks the lactase persistence allele and therefore cannot digest lactose [1] . Thus, this person’s health would benefit from avoiding foods containing lactose. On the other hand, nutrigenomics explores how nutrients affect gene expression, so that ingesting certain nutrients according to an individual’s health condition can normalize their diseaserelated gene expression. For example, increased systemic inflammation is linked to an upregulation of inflammatory cytokines (e.g. TNF\u0002 , IL-1, IL-6), which can in turn be suppressed by some nutrients (e.g. omega-3 fatty acids [2] ). The key element linking these ‘sister’ fields is the concept that nutrients interact with an individual’s genetic profile to impact their health. Thus, as each individual has their own unique genetic profile, this knowledge is essential for developing personalized nutrition. The critical prerequisite for personalized nutrition is the ability to precisely detect and interpret an individual’s metabolic and health status by way of metabolic biomarkers. These","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":" ","pages":"I-II"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000342702","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30894932","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}

{"title":"Rat chromosome 8 confers protection against dyslipidemia caused by a high-fat/low-carbohydrate diet.","authors":"Leah C Solberg Woods,&nbsp;Brett C Woods,&nbsp;Caroline M Leitschuh,&nbsp;Sonia J Laurie,&nbsp;Howard J Jacob","doi":"10.1159/000338848","DOIUrl":"https://doi.org/10.1159/000338848","url":null,"abstract":"<p><strong>Background/aims: </strong>Recent studies have highlighted the importance of gene by diet interactions in contributing to risk factors of metabolic syndrome. We used a consomic rat panel, in which a chromosome of the Brown Norway (BN) strain is introgressed onto the background of the Dahl salt-sentitive (SS) strain, to test the hypothesis that these animals will be useful for dissecting gene by diet interactions involved in metabolic syndrome.</p><p><strong>Methods: </strong>We placed the parental SS and BN strains on a low-fat/high-carbohydrate (LF) or high-fat/low-carbohydrate (HF) diet for 22 weeks and measured several indices of metabolic syndrome. We then investigated the effect of diet in eight consomic rat strains.</p><p><strong>Results: </strong>We show that the HF diet resulted in significantly increased levels of fasting plasma cholesterol and triglycerides in the SS strain, with no effect in the BN. Both strains responded to the HF diet with slight increases in body weight. SSBN8 was the only consomic strain that resembled that of the BN, with low levels of fasting cholesterol and triglycerides even on the HF diet.</p><p><strong>Conclusions: </strong>These results indicate that BN chromosome 8 harbors a gene or genes that confer protection against dyslipidemia caused by the HF diet.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":" ","pages":"81-93"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000338848","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30710078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cannabinoid type 1 receptor gene polymorphism and macronutrient intake.","authors":"Maria Gabriella Caruso,&nbsp;Patrizia Gazzerro,&nbsp;Maria Notarnicola,&nbsp;Anna Maria Cisternino,&nbsp;Vito Guerra,&nbsp;Giovanni Misciagna,&nbsp;Chiara Laezza,&nbsp;Maurizio Bifulco","doi":"10.1159/000343563","DOIUrl":"https://doi.org/10.1159/000343563","url":null,"abstract":"<p><strong>Background: </strong>Cannabinoid type 1 receptor (CB1-R) is a key mediator in the control of food intake and is linked to obesity.</p><p><strong>Aim: </strong>To evaluate the relationship between CB1-R gene polymorphism and dietary macronutrient intake in elderly subjects.</p><p><strong>Methods: </strong>This study included 118 subjects (60 males, 58 females) from a population survey carried out in southern Italy in 1992-1993 who were older than 65 years and previously characterized for CB1-R polymorphism (75 with GG wild-type genotype, 41 with heterozygous polymorphic allele AG, and 2 with genotype AA). All subjects completed a validated semi-quantitative food frequency questionnaire. Statistical methods included multiple logistic regression to model macronutrient intake to genotype, controlling for potential confounders.</p><p><strong>Results: </strong>When controlled for age, gender, and body mass index, the intake of dietary cholesterol and saturated fats corrected for calories was inversely associated with the CB1-R 1359 G/A polymorphism, while the intake of starchy carbohydrates was directly associated with this polymorphism.</p><p><strong>Conclusion: </strong>In our unselected elderly population, the 1359 G/A polymorphism is linked with a specific macronutrient intake. This could be explained by the role of the cannabinoid system as a determinant of food intake and eating behavior.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":" ","pages":"305-13"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000343563","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31094915","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}

{"title":"The coming of age of nutrigenetics and nutrigenomics.","authors":"Jing X Kang","doi":"10.1159/000339375","DOIUrl":"https://doi.org/10.1159/000339375","url":null,"abstract":"In recent years, human health has begun to face a new type of crisis. While the greatest risks of mortality in previous centuries were attributed to acute infectious disease, chronic metabolic disease is rapidly becoming a more significant concern, particularly in developed nations. According to the World Health Organization [1] , 65% of the world’s population now live in countries where obesity kills more people than diseases related to malnourishment. Medical advancements may have enabled us to outwit many of the pathogens that harmed us in the past, but now our most serious concerns are the diseases that arise from how we live. To address the rising prevalence of chronic diseases such as diabetes, obesity, heart disease, and cancer, it is imperative that we continue to develop our knowledge of the biological mechanisms that underlie these diseases and seek safer and more effective prevention and treatment. Needless to say, contributions from the fields of nutrigenetics and nutrigenomics are more critical now than ever before. Our understanding of genetics has progressed in leaps and bounds over the past decades, the apex of which was the completion of the Human Genome Project in 2004 [2] . Genetics play an integral role in every type of disease, whether the relationship is one of inheritance or the product of gene-environment interactions. This greater understanding of genetics has provided insight into the etiology of many diseases as well as the types of interventions that may be successful. We now understand that a variety of environmental stimuli trigger changes in gene expression, and that these changes underlie disease; for example, a decrease in global DNA methylation can upregulate genes involved in disease, such as cancer-promoting genes, thereby heightening the risk of developing cancer [3–5] . Clearly, nutrition and diet constitute a major source of environmental input, and there is reason to believe that increases in metabolic disease are associated with recent changes to the human diet and its impact on the genome. Published online: June 14, 2012","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"5 1","pages":"I-II"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000339375","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30691729","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}

{"title":"Prostate disease risk factors among a New Zealand cohort.","authors":"Nishi Karunasinghe,&nbsp;Dug Yeo Han,&nbsp;Megan Goudie,&nbsp;Shuoton Zhu,&nbsp;Karen Bishop,&nbsp;Alice Wang,&nbsp;He Duan,&nbsp;Katja Lange,&nbsp;Sarah Ko,&nbsp;Roxanne Medhora,&nbsp;Shiu Theng Kan,&nbsp;Jonathan Masters,&nbsp;Lynnette R Ferguson","doi":"10.1159/000346279","DOIUrl":"https://doi.org/10.1159/000346279","url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer is a leading public health burden worldwide, and in New Zealand it is the most commonly registered cancer and the third leading cause of cancer deaths among males. Genetic variability and its associations with diet, demographic and lifestyle factors could influence the risk of this disease.</p><p><strong>Methods: </strong>The single nucleotide polymorphisms (SNPs) within a group of antioxidant genes and related markers were tested between patient and control cohorts, adjusted for significant differences between basic lifestyle and demographic characteristics.</p><p><strong>Results: </strong>Increasing age, smoking and low serum selenium levels were significantly associated with an increased risk for prostate disease. Alcohol consumption increased the glutathione peroxidase (GPx) activity. A significant reduction in alcohol consumption was recorded with prostate disease. Three SNPs, namely GPx1 rs1050450, SEL15 rs5845 and CAT rs1001179, were significantly associated with prostate disease risk. A cumulative risk of prostate cancer was noted with 6 risk alleles. A lower GPx activity was recorded with prostate disease compared to the controls. However, the GPx1 rs1050450 allele T in association with prostate cancer recorded a significantly higher GPx activity compared to the controls.</p><p><strong>Conclusions: </strong>These data point to a possibility of identifying individuals at risk of prostate cancer for better management purposes.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"5 6","pages":"339-51"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000346279","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10379364","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}

{"title":"High-amylose resistant starch increases hormones and improves structure and function of the gastrointestinal tract: a microarray study.","authors":"Michael J Keenan, Roy J Martin, Anne M Raggio, Kathleen L McCutcheon, Ian L Brown, Anne Birkett, Susan S Newman, Jihad Skaf, Maren Hegsted, Richard T Tulley, Eric Blair, June Zhou","doi":"10.1159/000335319","DOIUrl":"10.1159/000335319","url":null,"abstract":"<p><strong>Background/aims: </strong>Type 2 resistant starch from high-amylose maize (HAM-RS2) is associated with increased fermentation, increased expression of proglucagon (gene for GLP-1) and peptide YY (PYY) genes in the large intestine, and improved health. To determine what other genes are up- or downregulated with feeding of HAM-RS2, a microarray was performed.</p><p><strong>Methods: </strong>Adult, male Sprague Dawley rats were fed one of the following three diets for a 4-week study period: cornstarch control (CC, 3.74 kcal/g), dietary energy density control (EC, 3.27 kcal/g), and 30% HAM-RS2 (RS, 3.27 kcal/g). Rat microarray with ∼27,000 genes and validation of 94 representative genes with multiple qPCR were used to determine gene expression in total RNA extracts of cecal cells from rats. The RS versus EC comparison tested effects of fermentation as energy density of the diet was controlled.</p><p><strong>Results: </strong>For the RS versus EC comparison, 86% of the genes were validated from the microarray and the expression indicates promotion of cell growth, proliferation, differentiation, and apoptosis. Gut hormones GLP-1 and PYY were increased.</p><p><strong>Conclusions: </strong>Gene expression results predict improved structure and function of the GI tract. Production of gut hormones may promote healthy functions beyond the GI tract.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"5 1","pages":"26-44"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4030412/pdf/nihms393630.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30586471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin E alters inflammatory gene expression in alcoholic chronic pancreatitis.","authors":"Thaís Helena Monteiro,&nbsp;Camila Siqueira Silva,&nbsp;Livia Maria Cordeiro Simões Ambrosio,&nbsp;Sergio Zucoloto,&nbsp;Helio Vannucchi","doi":"10.1159/000336076","DOIUrl":"https://doi.org/10.1159/000336076","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the effect of vitamin E supplementation on pancreatic gene expression of inflammatory markers in rats with alcoholic chronic pancreatitis.</p><p><strong>Methods: </strong>Wistar rats were divided into 3 groups: control (1), alcoholic chronic pancreatitis without (2) and with (3) vitamin E supplementation. Pancreatitis was induced by a liquid diet containing ethanol, cyclosporin A and cerulein. α-tocopherol content in plasma and liver and pancreas histopathology were analyzed. Gene expression of inflammatory biomarkers was analyzed by the quantitative real-time PCR technique.</p><p><strong>Results: </strong>The animals that received vitamin E supplementation had higher α-tocopherol amounts in plasma and liver. The pancreas in Group 1 showed normal histology, whereas in Groups 2 and 3, mild to moderate tissue destruction foci and mononuclear cell infiltration were detected. Real-time PCR analysis showed an increased expression of all genes in Groups 2 and 3 compared to Group 1. Vitamin E supplementation decreased the transcript number of 5 genes (α-SMA, COX-2, IL-6, MIP-3α and TNF-α) and increased the transcript number of 1 gene (Pap).</p><p><strong>Conclusion: </strong>Vitamin E supplementation had anti-inflammatory and beneficial effects on the pancreatic gene expression of some inflammatory biomarkers in rats with alcoholic chronic pancreatitis, confirming its participation in the inflammatory response mechanisms in the pancreas.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":" ","pages":"94-105"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000336076","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30832346","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}

{"title":"Genomic and metabolic responses to methionine-restricted and methionine-restricted, cysteine-supplemented diets in Fischer 344 rat inguinal adipose tissue, liver and quadriceps muscle.","authors":"Carmen E Perrone,&nbsp;Dwight A L Mattocks,&nbsp;Jason D Plummer,&nbsp;Sridar V Chittur,&nbsp;Rob Mohney,&nbsp;Katie Vignola,&nbsp;David S Orentreich,&nbsp;Norman Orentreich","doi":"10.1159/000339347","DOIUrl":"https://doi.org/10.1159/000339347","url":null,"abstract":"<p><strong>Background/aims: </strong>Methionine restriction (MR) is a dietary intervention that increases lifespan, reduces adiposity and improves insulin sensitivity. These effects are reversed by supplementation of the MR diet with cysteine (MRC). Genomic and metabolomic studies were conducted to identify potential mechanisms by which MR induces favorable metabolic effects, and that are reversed by cysteine supplementation.</p><p><strong>Methods: </strong>Gene expression was examined by microarray analysis and TaqMan quantitative PCR. Levels of selected proteins were measured by Western blot and metabolic intermediates were analyzed by mass spectrometry.</p><p><strong>Results: </strong>MR increased lipid metabolism in inguinal adipose tissue and quadriceps muscle while it decreased lipid synthesis in liver. In inguinal adipose tissue, MR not only caused the transcriptional upregulation of genes associated with fatty acid synthesis but also of Lpin1, Pc, Pck1 and Pdk1, genes that are associated with glyceroneogenesis. MR also upregulated lipolysis-associated genes in inguinal fat and led to increased oxidation in this tissue, as suggested by higher levels of methionine sulfoxide and 13-HODE + 9-HODE compared to control-fed (CF) rats. Moreover, MR caused a trend toward the downregulation of inflammation-associated genes in inguinal adipose tissue. MRC reversed most gene and metabolite changes induced by MR in inguinal adipose tissue, but drove the expression of Elovl6, Lpin1, Pc, and Pdk1 below CF levels. In liver, MR decreased levels of a number of long-chain fatty acids, glycerol and glycerol-3-phosphate corresponding with the gene expression data. Although MR increased the expression of genes associated with carbohydrate metabolism, levels of glycolytic intermediates were below CF levels. MR, however, stimulated gluconeogenesis and ketogenesis in liver tissue. As previously reported, sulfur amino acids derived from methionine were decreased in liver by MR, but homocysteine levels were elevated. Increased liver homocysteine levels by MR were associated with decreased cystathionine β-synthase (CBS) protein levels and lowered vitamin B6 and 5-methyltetrahydrofolate (5MeTHF) content. Finally, MR upregulated fibroblast growth factor 21 (FGF21) gene and protein levels in both liver and adipose tissues. MRC reversed some of MR's effects in liver and upregulated the transcription of genes associated with inflammation and carcinogenesis such as Cxcl16, Cdh17, Mmp12, Mybl1, and Cav1 among others. In quadriceps muscle, MR upregulated lipid metabolism-associated genes and increased 3-hydroxybutyrate levels suggesting increased fatty acid oxidation as well as stimulation of gluconeogenesis and glycogenolysis in this tissue.</p><p><strong>Conclusion: </strong>Increased lipid metabolism in inguinal adipose tissue and quadriceps muscle, decreased triglyceride synthesis in liver and the downregulation of inflammation-associated genes are among the factors that","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"5 3","pages":"132-57"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000339347","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30965544","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}