Pub Date : 2014-01-01Epub Date: 2014-06-21DOI: 10.1159/000363138
Candace E Cuthbert, D Dan Ramdath, Jerome E Foster
Background: The fat mass and obesity-associated gene (FTO) rs9939609 and peroxisome proliferator-activated receptor gamma 2 gene (PPARG2) rs1801282 polymorphisms are type 2 diabetes mellitus susceptibility gene variants associated with obesity. This study examined whether these variants are associated with anthropometry at birth among a representative multi-ethnic sample of Trinidadian neonates.
Methods: Cord blood was obtained from consecutive term live births and DNA was genotyped for FTO and PPARG2 variants using polymerase chain reaction. Associations between neonate anthropometry at birth and genotype frequency were assessed using the χ(2) test and linear regression.
Results: Significant associations were observed between neonate ethnicity and PPARG2 (p = 0.005) and FTO (p = 0.017) variants: high-risk alleles were more prevalent among African than South Asian neonates for both variants. The allelic and genotypic frequencies for mixed neonates were between those for the African and those for the South Asian neonates. No significant relationship was observed between rs9939609 and rs1801282 and anthropometric measures. For both variants, the allelic and genotypic frequencies among the African and South Asian neonates mirrored those found elsewhere for similar ethnic groups.
Conclusions: Neonates of African ethnicity possess the highest frequency of rs9939609 and rs1801282 alleles and genotypes; this may be associated with ethnic differences in the risk of lifestyle diseases.
{"title":"Frequency of fat mass and obesity-associated gene rs9939609 and peroxisome proliferator-activated receptor gamma 2 gene rs1801282 polymorphisms among Trinidadian neonates of different ethnicities and their relationship to anthropometry at birth.","authors":"Candace E Cuthbert, D Dan Ramdath, Jerome E Foster","doi":"10.1159/000363138","DOIUrl":"https://doi.org/10.1159/000363138","url":null,"abstract":"<p><strong>Background: </strong>The fat mass and obesity-associated gene (FTO) rs9939609 and peroxisome proliferator-activated receptor gamma 2 gene (PPARG2) rs1801282 polymorphisms are type 2 diabetes mellitus susceptibility gene variants associated with obesity. This study examined whether these variants are associated with anthropometry at birth among a representative multi-ethnic sample of Trinidadian neonates.</p><p><strong>Methods: </strong>Cord blood was obtained from consecutive term live births and DNA was genotyped for FTO and PPARG2 variants using polymerase chain reaction. Associations between neonate anthropometry at birth and genotype frequency were assessed using the χ(2) test and linear regression.</p><p><strong>Results: </strong>Significant associations were observed between neonate ethnicity and PPARG2 (p = 0.005) and FTO (p = 0.017) variants: high-risk alleles were more prevalent among African than South Asian neonates for both variants. The allelic and genotypic frequencies for mixed neonates were between those for the African and those for the South Asian neonates. No significant relationship was observed between rs9939609 and rs1801282 and anthropometric measures. For both variants, the allelic and genotypic frequencies among the African and South Asian neonates mirrored those found elsewhere for similar ethnic groups.</p><p><strong>Conclusions: </strong>Neonates of African ethnicity possess the highest frequency of rs9939609 and rs1801282 alleles and genotypes; this may be associated with ethnic differences in the risk of lifestyle diseases.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"7 1","pages":"39-47"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000363138","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32459543","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 : 2014-01-01Epub Date: 2015-05-27DOI: 10.1159/000381777
Catia L Amaral, Amanda R Crisma, Laureane N Masi, Amanda R Martins, Sandro M Hirabara, Rui Curi
Background/aims: To investigate the global changes in DNA methylation and methylation of the promoter region of the peroxisome proliferator-activated receptor gamma transcript variant 2 (Pparg2) gene resulting from a high-fat diet (HFD) and/or fish oil supplementation.
Methods: Fish oil, rich in omega-3 polyunsaturated fatty acids, or water was orally administered to male mice for 12 weeks. After the first 4 weeks, the animals were fed a control diet or an HFD until the end of the experimental protocol, when the epididymal fat, gastrocnemius muscle and liver were excised.
Results: Pparg2 mRNA expression was upregulated by obesity and downregulated by fish oil supplementation in the liver. In the gastrocnemius muscle, diet-induced obesity increased global DNA methylation. Fish oil prevented the decrease in Pparg2 promoter methylation induced by obesity in the gastrocnemius muscle. Regardless of the diet given, fish oil supplementation increased Pparg2 promoter methylation at CpG-263 in muscle and adipose tissue.
Conclusion: HFD and fish oil modified global and Pparg2 promoter DNA methylation in a tissue-specific manner. Fish oil supplementation attenuated body weight gain, abolished the increase in Pparg2 expression in the liver and prevented the decrease in Pparg2 promoter methylation in the muscle induced by the HFD.
{"title":"DNA Methylation Changes Induced by a High-Fat Diet and Fish Oil Supplementation in the Skeletal Muscle of Mice.","authors":"Catia L Amaral, Amanda R Crisma, Laureane N Masi, Amanda R Martins, Sandro M Hirabara, Rui Curi","doi":"10.1159/000381777","DOIUrl":"https://doi.org/10.1159/000381777","url":null,"abstract":"<p><strong>Background/aims: </strong>To investigate the global changes in DNA methylation and methylation of the promoter region of the peroxisome proliferator-activated receptor gamma transcript variant 2 (Pparg2) gene resulting from a high-fat diet (HFD) and/or fish oil supplementation.</p><p><strong>Methods: </strong>Fish oil, rich in omega-3 polyunsaturated fatty acids, or water was orally administered to male mice for 12 weeks. After the first 4 weeks, the animals were fed a control diet or an HFD until the end of the experimental protocol, when the epididymal fat, gastrocnemius muscle and liver were excised.</p><p><strong>Results: </strong>Pparg2 mRNA expression was upregulated by obesity and downregulated by fish oil supplementation in the liver. In the gastrocnemius muscle, diet-induced obesity increased global DNA methylation. Fish oil prevented the decrease in Pparg2 promoter methylation induced by obesity in the gastrocnemius muscle. Regardless of the diet given, fish oil supplementation increased Pparg2 promoter methylation at CpG-263 in muscle and adipose tissue.</p><p><strong>Conclusion: </strong>HFD and fish oil modified global and Pparg2 promoter DNA methylation in a tissue-specific manner. Fish oil supplementation attenuated body weight gain, abolished the increase in Pparg2 expression in the liver and prevented the decrease in Pparg2 promoter methylation in the muscle induced by the HFD.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"7 4-6","pages":"314-26"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000381777","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33343883","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 : 2014-01-01Epub Date: 2015-03-04DOI: 10.1159/000375495
Artemis P Simopoulos
The Bellagio Report on Healthy Agriculture, Healthy Nutrition, Healthy People was the result of a meeting held at the Rockefeller Foundation Bellagio Center in the fall of 2012. The meeting was science based but policy oriented. The Bellagio Report concluded that: (1) sugar consumption, especially in the form of high-energy fructose in soft drinks, poses a major and insidious health threat, particularly for children; (2) current diets in most populations, albeit with regional differences, are deficient in omega-3 fatty acids but too high in omega-6 fatty acid intake, and (3) not all calories are the same since calories from different sources (i.e. glucose or fructose or omega-6 or omega-3 fatty acids) have different metabolic and neurohormonal effects. This paper summarizes the scientific progress and policy actions that have occurred in these three areas. Genetic variation in populations and gene-nutrient interactions are fundamental concepts that need to be taken into consideration in growth and development and in the prevention and management of chronic noncommunicable diseases since there is enormous variation in both the frequency of genetic variants and dietary composition worldwide. Furthermore, this paper updates the Bellagio Report in terms of the scientific and policy aspects, both of which have expanded over the past 2 years, and describes the progress made in establishing an International Network of Centers for Genetics, Nutrition and Fitness for Health.
{"title":"The impact of the Bellagio Report on healthy agriculture, healthy nutrition, healthy people: scientific and policy aspects and the International Network of Centers for Genetics, Nutrition and Fitness for Health.","authors":"Artemis P Simopoulos","doi":"10.1159/000375495","DOIUrl":"https://doi.org/10.1159/000375495","url":null,"abstract":"<p><p>The Bellagio Report on Healthy Agriculture, Healthy Nutrition, Healthy People was the result of a meeting held at the Rockefeller Foundation Bellagio Center in the fall of 2012. The meeting was science based but policy oriented. The Bellagio Report concluded that: (1) sugar consumption, especially in the form of high-energy fructose in soft drinks, poses a major and insidious health threat, particularly for children; (2) current diets in most populations, albeit with regional differences, are deficient in omega-3 fatty acids but too high in omega-6 fatty acid intake, and (3) not all calories are the same since calories from different sources (i.e. glucose or fructose or omega-6 or omega-3 fatty acids) have different metabolic and neurohormonal effects. This paper summarizes the scientific progress and policy actions that have occurred in these three areas. Genetic variation in populations and gene-nutrient interactions are fundamental concepts that need to be taken into consideration in growth and development and in the prevention and management of chronic noncommunicable diseases since there is enormous variation in both the frequency of genetic variants and dietary composition worldwide. Furthermore, this paper updates the Bellagio Report in terms of the scientific and policy aspects, both of which have expanded over the past 2 years, and describes the progress made in establishing an International Network of Centers for Genetics, Nutrition and Fitness for Health.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"7 4-6","pages":"191-211"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000375495","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33001864","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}
Obesity can result from the disequilibrium between energy intake and expenditure associated with alterations of many metabolic pathways [1] . As many cellular functions related to energy homeostasis are regulated by gene expression and gene-environment interactions, individual variation in body weight/composition and adipose metabolism could be influenced by genetic makeup and nutrient intake. Nutritional outcomes can also be determined by gene-mediated biochemical pathways that regulate nutrient absorption, distribution, metabolism, and excretion as well as other cellular energy processes [2] . Indeed, the interplay between nutrients and genetic variation could be a key factor influencing obesity risk and development as well as associated conditions. About 25–70% of body weight variability is thought to be controlled by genes that affect energy homeostasis through the modulation of nuclear transcription factors, signalling molecules and receptors, adipogenesis and fat deposition, thermogenesis, hypothalamic networks, and other cellular functions related to energy efficiency [3, 4] . More than 50 genes have been implicated in obesity phenotypes, and adiposity traits have been identified in both animal and human studies [5] . For example, monogenic obesity is attributed to the mutation of specific alleles with profound effects, namely in the leptin, leptin receptor, pro-opiomelanocortin, proprotein convertase/kexin type 1, melanocortin-4 receptor, and single-minded homolog 1 genes. However, monogenic obesity is relatively uncommon, and studies on polygenic obesity support the notion that the modern prevalence of obesity has resulted from the interactions of unfavourable lifestyles with specific gene variants or single-nucleotide polymorphisms (SNPs) with less profound but converging effects [6] . Individuals susceptible to excessive fat gain may therefore carry gene variants that influence appetite control (CNR1, NPY, POMC, MC4R, etc.), nuclear and cytoplasm regulatory machinery (FTO, TFAPB2, TCF7L2, SCAP, DRD2, etc.), adipogenesis and lipid metabolism (ADRB3, PPAR, APOs, PLIN, etc.), energy expenditure (UCPs), insulin signalling (ISR-2, INSIG2, GIPR), and inflammation (ADIPOQ, IL-6, RESISTIN, etc.) [6] . Over 500 SNPs or chromosomal regions have been directly or indirectly associated with obesity [7] . Published online: July 24, 2014
{"title":"Perspectives on personalized nutrition for obesity.","authors":"J Alfredo Martínez","doi":"10.1159/000365158","DOIUrl":"https://doi.org/10.1159/000365158","url":null,"abstract":"Obesity can result from the disequilibrium between energy intake and expenditure associated with alterations of many metabolic pathways [1] . As many cellular functions related to energy homeostasis are regulated by gene expression and gene-environment interactions, individual variation in body weight/composition and adipose metabolism could be influenced by genetic makeup and nutrient intake. Nutritional outcomes can also be determined by gene-mediated biochemical pathways that regulate nutrient absorption, distribution, metabolism, and excretion as well as other cellular energy processes [2] . Indeed, the interplay between nutrients and genetic variation could be a key factor influencing obesity risk and development as well as associated conditions. About 25–70% of body weight variability is thought to be controlled by genes that affect energy homeostasis through the modulation of nuclear transcription factors, signalling molecules and receptors, adipogenesis and fat deposition, thermogenesis, hypothalamic networks, and other cellular functions related to energy efficiency [3, 4] . More than 50 genes have been implicated in obesity phenotypes, and adiposity traits have been identified in both animal and human studies [5] . For example, monogenic obesity is attributed to the mutation of specific alleles with profound effects, namely in the leptin, leptin receptor, pro-opiomelanocortin, proprotein convertase/kexin type 1, melanocortin-4 receptor, and single-minded homolog 1 genes. However, monogenic obesity is relatively uncommon, and studies on polygenic obesity support the notion that the modern prevalence of obesity has resulted from the interactions of unfavourable lifestyles with specific gene variants or single-nucleotide polymorphisms (SNPs) with less profound but converging effects [6] . Individuals susceptible to excessive fat gain may therefore carry gene variants that influence appetite control (CNR1, NPY, POMC, MC4R, etc.), nuclear and cytoplasm regulatory machinery (FTO, TFAPB2, TCF7L2, SCAP, DRD2, etc.), adipogenesis and lipid metabolism (ADRB3, PPAR, APOs, PLIN, etc.), energy expenditure (UCPs), insulin signalling (ISR-2, INSIG2, GIPR), and inflammation (ADIPOQ, IL-6, RESISTIN, etc.) [6] . Over 500 SNPs or chromosomal regions have been directly or indirectly associated with obesity [7] . Published online: July 24, 2014","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"7 1","pages":"I-III"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000365158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32533757","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 : 2014-01-01Epub Date: 2014-12-02DOI: 10.1159/000368833
Azahara I Rupérez, Josune Olza, Mercedes Gil-Campos, Rosaura Leis, María Dolores Mesa, Rafael Tojo, Ramón Cañete, Ángel Gil, Concepción M Aguilera
Background/aims: Altered expression and activity of the antioxidant enzymes glutathione peroxidases (GPXs) have been observed in obesity in human and animal studies. We aimed to study 59 single nucleotide polymorphisms (SNPs) for GPX1-7 genes and to characterize their association with prepubertal childhood obesity and its associated biomarkers.
Methods: This case-control study included 193 obese and 191 normal-weight prepubertal Spanish children, in whom anthropometry, biochemical parameters, adipokines, antioxidant enzyme erythrocyte activities and biomarkers of oxidative stress, inflammation and cardiovascular risk were measured. The genotype analysis was performed in the Illumina platform. PLINK and SPSS were used for statistical analyses.
Results: We found SNPs rs757228 and rs8103188 (GPX4) to be negatively associated and rs445870 (GPX5) and rs406113 (GPX6) to be positively associated with obesity in children. The variant rs2074451 (GPX4) increased GPX activity in erythrocytes. Although we did not find significant differences in erythrocyte GPX activity between obese and normal-weight children, GPX activity was found to be positively and significantly correlated with blood pressure, adipocyte fatty acid-binding protein and high-sensitivity C-reactive protein.
Conclusions: The GPX variants rs757228, rs8103188, rs445870 and rs406113 were associated with prepubertal childhood obesity. However, erythrocyte GPX activity was not altered in obese prepubertal Spanish children.
{"title":"Association of genetic polymorphisms for glutathione peroxidase genes with obesity in Spanish children.","authors":"Azahara I Rupérez, Josune Olza, Mercedes Gil-Campos, Rosaura Leis, María Dolores Mesa, Rafael Tojo, Ramón Cañete, Ángel Gil, Concepción M Aguilera","doi":"10.1159/000368833","DOIUrl":"https://doi.org/10.1159/000368833","url":null,"abstract":"<p><strong>Background/aims: </strong>Altered expression and activity of the antioxidant enzymes glutathione peroxidases (GPXs) have been observed in obesity in human and animal studies. We aimed to study 59 single nucleotide polymorphisms (SNPs) for GPX1-7 genes and to characterize their association with prepubertal childhood obesity and its associated biomarkers.</p><p><strong>Methods: </strong>This case-control study included 193 obese and 191 normal-weight prepubertal Spanish children, in whom anthropometry, biochemical parameters, adipokines, antioxidant enzyme erythrocyte activities and biomarkers of oxidative stress, inflammation and cardiovascular risk were measured. The genotype analysis was performed in the Illumina platform. PLINK and SPSS were used for statistical analyses.</p><p><strong>Results: </strong>We found SNPs rs757228 and rs8103188 (GPX4) to be negatively associated and rs445870 (GPX5) and rs406113 (GPX6) to be positively associated with obesity in children. The variant rs2074451 (GPX4) increased GPX activity in erythrocytes. Although we did not find significant differences in erythrocyte GPX activity between obese and normal-weight children, GPX activity was found to be positively and significantly correlated with blood pressure, adipocyte fatty acid-binding protein and high-sensitivity C-reactive protein.</p><p><strong>Conclusions: </strong>The GPX variants rs757228, rs8103188, rs445870 and rs406113 were associated with prepubertal childhood obesity. However, erythrocyte GPX activity was not altered in obese prepubertal Spanish children.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"7 3","pages":"130-42"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000368833","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32875048","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: 2013-08-15DOI: 10.1159/000353703
Y Z Pan, S G Wu, H C Dai, H J Zhang, H Y Yue, G H Qi
Aim: The aim of this study was to determine the effect of chromium picolinate (CrPic) on the differential expression of the known microRNAs (miRNAs) in broiler skeletal muscle.
Methods and results: A total of 288 1-day-old male Arbor Acres broilers were randomly assigned to one of four dietary treatments supplemented with 0, 0.4, 2.0, or 10.0 mg·kg(-1) CrPic, respectively. Dietary CrPic supplementation at 10.0 mg·kg(-1) increased the average daily feed intake in broilers (p < 0.05). On day 42, the serum total protein level was highest in animals treated with 2.0 mg·kg(-1) (p < 0.05) and 10.0 mg·kg(-1) CrPic (p < 0.05). Dietary supplementation with 10.0 mg·kg(-1) CrPic decreased the levels of serum glucose (p < 0.05) on day 42 and of serum triglyceride (p < 0.05) on days 21 and 42. To further identify miRNAs from broiler skeletal muscles, we sequenced two small RNA libraries using the Solexa sequencing approach, and 57 miRNAs were found to be significantly differentially expressed (p < 0.05). Among them, 6 upregulated and 2 downregulated miRNAs were validated by real-time qPCR (p < 0.05).
Conclusions: The results of the present study provide a valuable clue regarding the role of miRNA target genes in the mechanism of the dietary CrPic effect on protein synthesis in skeletal muscles of broilers.
{"title":"Solexa sequencing of microRNAs on chromium metabolism in broiler chicks.","authors":"Y Z Pan, S G Wu, H C Dai, H J Zhang, H Y Yue, G H Qi","doi":"10.1159/000353703","DOIUrl":"https://doi.org/10.1159/000353703","url":null,"abstract":"<p><strong>Aim: </strong>The aim of this study was to determine the effect of chromium picolinate (CrPic) on the differential expression of the known microRNAs (miRNAs) in broiler skeletal muscle.</p><p><strong>Methods and results: </strong>A total of 288 1-day-old male Arbor Acres broilers were randomly assigned to one of four dietary treatments supplemented with 0, 0.4, 2.0, or 10.0 mg·kg(-1) CrPic, respectively. Dietary CrPic supplementation at 10.0 mg·kg(-1) increased the average daily feed intake in broilers (p < 0.05). On day 42, the serum total protein level was highest in animals treated with 2.0 mg·kg(-1) (p < 0.05) and 10.0 mg·kg(-1) CrPic (p < 0.05). Dietary supplementation with 10.0 mg·kg(-1) CrPic decreased the levels of serum glucose (p < 0.05) on day 42 and of serum triglyceride (p < 0.05) on days 21 and 42. To further identify miRNAs from broiler skeletal muscles, we sequenced two small RNA libraries using the Solexa sequencing approach, and 57 miRNAs were found to be significantly differentially expressed (p < 0.05). Among them, 6 upregulated and 2 downregulated miRNAs were validated by real-time qPCR (p < 0.05).</p><p><strong>Conclusions: </strong>The results of the present study provide a valuable clue regarding the role of miRNA target genes in the mechanism of the dietary CrPic effect on protein synthesis in skeletal muscles of broilers.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 3","pages":"137-53"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000353703","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31660070","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/aim: Plant phenolics can inhibit, retard or reverse carcinogenesis, and may thus help prevent or treat cancer. Oil palm phenolics (OPP) previously showed anti-tumour activities in vivo via a cytostatic mechanism at 1,500 ppm gallic acid equivalent. Here, we report other possible molecular mechanisms by which this extract attenuates cancer, especially those concerning the immune response.
Methods: We subcutaneously injected J558 myeloma cells in BALB/c mice and supplemented OPP orally at 1,500 ppm gallic acid equivalent. We observed the physiology parameters of these animals and harvested their spleens and livers after 18 h, 1 week and 4 weeks for microarray gene expression analysis using Illumina MouseRef-8 BeadChips.
Results: Time course microarray analysis on spleens after injecting J558 myeloma cells in mice revealed that the immune response of tumour-bearing mice supplemented with OPP was lower compared to controls, thus suggesting delayed inflammation in response to OPP. In livers, cholesterol biosynthesis genes were upregulated while inflammatory genes were downregulated through time, further suggesting attenuation of systemic inflammation and cachexia. These effects correlated with the delayed in vivo development of syngeneic tumours in mice given OPP.
Conclusions: This study suggests the possible utilisation of OPP as an anti-tumour and anti-cachexia agent.
{"title":"Gene expression changes in spleens and livers of tumour-bearing mice suggest delayed inflammation and attenuated cachexia in response to oil palm phenolics.","authors":"Soon-Sen Leow, Shamala Devi Sekaran, Kalyana Sundram, Yewai Tan, Ravigadevi Sambanthamurthi","doi":"10.1159/000357948","DOIUrl":"https://doi.org/10.1159/000357948","url":null,"abstract":"<p><strong>Background/aim: </strong>Plant phenolics can inhibit, retard or reverse carcinogenesis, and may thus help prevent or treat cancer. Oil palm phenolics (OPP) previously showed anti-tumour activities in vivo via a cytostatic mechanism at 1,500 ppm gallic acid equivalent. Here, we report other possible molecular mechanisms by which this extract attenuates cancer, especially those concerning the immune response.</p><p><strong>Methods: </strong>We subcutaneously injected J558 myeloma cells in BALB/c mice and supplemented OPP orally at 1,500 ppm gallic acid equivalent. We observed the physiology parameters of these animals and harvested their spleens and livers after 18 h, 1 week and 4 weeks for microarray gene expression analysis using Illumina MouseRef-8 BeadChips.</p><p><strong>Results: </strong>Time course microarray analysis on spleens after injecting J558 myeloma cells in mice revealed that the immune response of tumour-bearing mice supplemented with OPP was lower compared to controls, thus suggesting delayed inflammation in response to OPP. In livers, cholesterol biosynthesis genes were upregulated while inflammatory genes were downregulated through time, further suggesting attenuation of systemic inflammation and cachexia. These effects correlated with the delayed in vivo development of syngeneic tumours in mice given OPP.</p><p><strong>Conclusions: </strong>This study suggests the possible utilisation of OPP as an anti-tumour and anti-cachexia agent.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 6","pages":"305-26"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000357948","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32186897","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: 2014-04-04DOI: 10.1159/000362481
Jing X Kang
It is increasingly recognized that nutritional intervention holds great potential for the management of modern chronic disease. Understanding the relationship between nutrient metabolism and disease development is an important foundation for nutritional intervention. To maximize the utility of nutritional intervention, it is critical that we identify the factors underlying chronic disease that can be modulated by nutrients. Based on recent research, I consider the following three areas to be among the frontiers of nutritional intervention: chronic low-grade inflammation, gut microbiota, and epigenetics. Chronic low-grade inflammation is known to be a common mechanism underlying the pathology of many chronic diseases, including obesity, diabetes, heart disease, cancer, and neurodegenerative diseases [1] . Interventions that suppress the development of chronic lowgrade inflammation could therefore be of great utility in addressing these diseases. In fact, much of the current research on the prevention and treatment of these diseases has targeted chronic inflammation. Inflammatory response involves multiple processes, including lipid mediator formation, cytokine expression, immune cell migration, etc., which can be modulated directly or indirectly by nutrients and/or their metabolites in differential manners. Certain nutrients exhibit opposing effects on inflammation. For example, omega-6 polyunsaturated fatty acids and their metabolites generally promote inflammatory processes, while omega-3 fatty acids and their metabolites largely suppress them [2] . Thus, a full understanding of the specific nutrients’ effect on chronic inflammation should be an important area of nutritional research. Given the complexity of the diet and the numerous interactions that occur between nutrients in different compositions, there remains much to be investigated about the overall effect of a diet on chronic low-grade inflammation. Future studies to elucidate how the steps of chronic low-grade inflammation are influenced by the type and quantity of nutrients and their metabolites will allow us to formulate effective interventions to modulate chronic low-grade inflammation. The gut microbiota, which is highly variable among individuals, has recently been shown to play a key role in human health and disease [3] . More and more studies have shown that alterations in the gut microbiota can influence many physiological and pathological processes, Published online: April 4, 2014
{"title":"Frontiers of nutritional intervention.","authors":"Jing X Kang","doi":"10.1159/000362481","DOIUrl":"https://doi.org/10.1159/000362481","url":null,"abstract":"It is increasingly recognized that nutritional intervention holds great potential for the management of modern chronic disease. Understanding the relationship between nutrient metabolism and disease development is an important foundation for nutritional intervention. To maximize the utility of nutritional intervention, it is critical that we identify the factors underlying chronic disease that can be modulated by nutrients. Based on recent research, I consider the following three areas to be among the frontiers of nutritional intervention: chronic low-grade inflammation, gut microbiota, and epigenetics. Chronic low-grade inflammation is known to be a common mechanism underlying the pathology of many chronic diseases, including obesity, diabetes, heart disease, cancer, and neurodegenerative diseases [1] . Interventions that suppress the development of chronic lowgrade inflammation could therefore be of great utility in addressing these diseases. In fact, much of the current research on the prevention and treatment of these diseases has targeted chronic inflammation. Inflammatory response involves multiple processes, including lipid mediator formation, cytokine expression, immune cell migration, etc., which can be modulated directly or indirectly by nutrients and/or their metabolites in differential manners. Certain nutrients exhibit opposing effects on inflammation. For example, omega-6 polyunsaturated fatty acids and their metabolites generally promote inflammatory processes, while omega-3 fatty acids and their metabolites largely suppress them [2] . Thus, a full understanding of the specific nutrients’ effect on chronic inflammation should be an important area of nutritional research. Given the complexity of the diet and the numerous interactions that occur between nutrients in different compositions, there remains much to be investigated about the overall effect of a diet on chronic low-grade inflammation. Future studies to elucidate how the steps of chronic low-grade inflammation are influenced by the type and quantity of nutrients and their metabolites will allow us to formulate effective interventions to modulate chronic low-grade inflammation. The gut microbiota, which is highly variable among individuals, has recently been shown to play a key role in human health and disease [3] . More and more studies have shown that alterations in the gut microbiota can influence many physiological and pathological processes, Published online: April 4, 2014","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 6","pages":"I-II"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000362481","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32247378","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: 2013-03-27DOI: 10.1159/000348839
Cornelie Nienaber-Rousseau, Pedro T Pisa, Christine S Venter, Suria M Ellis, Annamarie Kruger, Sarah J Moss, Alida Melse-Boonstra, G Wayne Towers
Background/aims: It is unknown whether the effect of alcohol consumption on homocysteine (Hcy) is modulated by the methylenetetrahydrofolate reductase (MTHFR) C677T. We explored this hypothesized effect by analyzing cross-sectional data of 1,827 black South Africans.
Methods: Total Hcy concentrations were determined by fluorescence polarization immunoassay and the genotype through polymerase chain reaction-based RFLP analysis.
Results: Subjects harboring the 677 TT genotype had the highest Hcy. Among subjects harboring the 677 CC genotype, men had higher Hcy (p = 0.04). Age and gamma-glutamyltransferase (GGT) correlated best (r = 0.26 and r = 0.27; p < 0.05), while the percentage carbohydrate-deficient transferrin and the B vitamins correlated weakly (r < 0.1; p < 0.05) with Hcy. Hcy was positively associated with the reported alcohol intake (p ≤ 0.01). There was no interaction between alcohol consumption and the MTHFR 677 CC or CT genotypes (p > 0.05) for Hcy concentrations; however, an interaction was determined for GGT and the MTHFR genotype (p = 0.02). Age, GGT, gender, MTHFR and vitamin B6 explained 16.8% of the variation in Hcy (p < 0.01).
Conclusion: The determined interactions might result in differences in the risk conveyed through Hcy with regard to disease development in those with unfavorable GGT concentrations.
{"title":"Nutritional genetics: the case of alcohol and the MTHFR C677T polymorphism in relation to homocysteine in a black South African population.","authors":"Cornelie Nienaber-Rousseau, Pedro T Pisa, Christine S Venter, Suria M Ellis, Annamarie Kruger, Sarah J Moss, Alida Melse-Boonstra, G Wayne Towers","doi":"10.1159/000348839","DOIUrl":"https://doi.org/10.1159/000348839","url":null,"abstract":"<p><strong>Background/aims: </strong>It is unknown whether the effect of alcohol consumption on homocysteine (Hcy) is modulated by the methylenetetrahydrofolate reductase (MTHFR) C677T. We explored this hypothesized effect by analyzing cross-sectional data of 1,827 black South Africans.</p><p><strong>Methods: </strong>Total Hcy concentrations were determined by fluorescence polarization immunoassay and the genotype through polymerase chain reaction-based RFLP analysis.</p><p><strong>Results: </strong>Subjects harboring the 677 TT genotype had the highest Hcy. Among subjects harboring the 677 CC genotype, men had higher Hcy (p = 0.04). Age and gamma-glutamyltransferase (GGT) correlated best (r = 0.26 and r = 0.27; p < 0.05), while the percentage carbohydrate-deficient transferrin and the B vitamins correlated weakly (r < 0.1; p < 0.05) with Hcy. Hcy was positively associated with the reported alcohol intake (p ≤ 0.01). There was no interaction between alcohol consumption and the MTHFR 677 CC or CT genotypes (p > 0.05) for Hcy concentrations; however, an interaction was determined for GGT and the MTHFR genotype (p = 0.02). Age, GGT, gender, MTHFR and vitamin B6 explained 16.8% of the variation in Hcy (p < 0.01).</p><p><strong>Conclusion: </strong>The determined interactions might result in differences in the risk conveyed through Hcy with regard to disease development in those with unfavorable GGT concentrations.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":" ","pages":"61-72"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000348839","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40243306","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/aims: Numerous studies have shown that epigallocatechin-3-gallate (EGCG), a polyphenol component extracted from green tea, can inhibit the growth and induce apoptosis of various types of human tumor cells. In this study, we evaluated the inhibitory effects of EGCG on the proangiogenic capabilities of A549 cells.
Methods: A549 cells starved in serum-free culture medium for 24 h were pretreated with EGCG at various concentrations (0, 10, 25, 50, and 100 μmol/l) for 1 h, followed by the addition of insulin-like growth factor-I (IGF-I) at the final concentration of 40 ng/ml and continued culturing for an additional 16 h. The in vitro angiogenesis analyzing test kit with ECMatrix™ gel was used to detect the formation of capillary tube-like structures. The mRNA expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) was determined by real-time PCR. The protein expression of HIF-1α and VEGF was detected by Western blotting and ELISA, respectively.
Results: EGCG significantly inhibited the formation of capillary tube-like structures on the surface of ECMatrix induced by IGF-I both in vitro and in vivo and reduced the level of hemoglobin in Matrigel plugs. In addition, EGCG was shown to significantly inhibit the IGF-I-induced upregulation of HIF-1α protein expression. Meanwhile, EGCG at the concentration of 25 and 100 μmol/l exhibited obvious inhibitory effects on IGF-I-induced VEGF expression (p < 0.01).
Conclusion: Our results suggest that EGCG has potent inhibitory effects on tumor angiogenesis induced by IGF-I in human non-small cell lung cancer cells, which may possibly contribute to the downregulation of HIF-1α and VEGF expression.
{"title":"Epigallocatechin-3-gallate inhibits IGF-I-stimulated lung cancer angiogenesis through downregulation of HIF-1α and VEGF expression.","authors":"Xiangyong Li, Yun Feng, Jinhua Liu, Xiaowei Feng, Keyuan Zhou, Xudong Tang","doi":"10.1159/000354402","DOIUrl":"https://doi.org/10.1159/000354402","url":null,"abstract":"<p><strong>Background/aims: </strong>Numerous studies have shown that epigallocatechin-3-gallate (EGCG), a polyphenol component extracted from green tea, can inhibit the growth and induce apoptosis of various types of human tumor cells. In this study, we evaluated the inhibitory effects of EGCG on the proangiogenic capabilities of A549 cells.</p><p><strong>Methods: </strong>A549 cells starved in serum-free culture medium for 24 h were pretreated with EGCG at various concentrations (0, 10, 25, 50, and 100 μmol/l) for 1 h, followed by the addition of insulin-like growth factor-I (IGF-I) at the final concentration of 40 ng/ml and continued culturing for an additional 16 h. The in vitro angiogenesis analyzing test kit with ECMatrix™ gel was used to detect the formation of capillary tube-like structures. The mRNA expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) was determined by real-time PCR. The protein expression of HIF-1α and VEGF was detected by Western blotting and ELISA, respectively.</p><p><strong>Results: </strong>EGCG significantly inhibited the formation of capillary tube-like structures on the surface of ECMatrix induced by IGF-I both in vitro and in vivo and reduced the level of hemoglobin in Matrigel plugs. In addition, EGCG was shown to significantly inhibit the IGF-I-induced upregulation of HIF-1α protein expression. Meanwhile, EGCG at the concentration of 25 and 100 μmol/l exhibited obvious inhibitory effects on IGF-I-induced VEGF expression (p < 0.01).</p><p><strong>Conclusion: </strong>Our results suggest that EGCG has potent inhibitory effects on tumor angiogenesis induced by IGF-I in human non-small cell lung cancer cells, which may possibly contribute to the downregulation of HIF-1α and VEGF expression.</p>","PeriodicalId":54779,"journal":{"name":"Journal of Nutrigenetics and Nutrigenomics","volume":"6 3","pages":"169-78"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000354402","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31710955","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}