Forum of NutritionPub Date : 2009-01-01Epub Date: 2009-04-07DOI: 10.1159/000212740
Werner Siems, Costantino Salerno, Carlo Crifò, Olaf Sommerburg, Ingrid Wiswedel
{"title":"Beta-carotene degradation products - formation, toxicity and prevention of toxicity.","authors":"Werner Siems, Costantino Salerno, Carlo Crifò, Olaf Sommerburg, Ingrid Wiswedel","doi":"10.1159/000212740","DOIUrl":"https://doi.org/10.1159/000212740","url":null,"abstract":"<p><p>Carotenoids are widely used as important micronutrients in food. Furthermore, carotenoid supplementation has been used in the treatment of diseases associated with oxidative stress such as various types of cancer, inflammatory diseases or cystic fibrosis. However, in some clinical studies harmful effects have been observed, e.g. a higher incidence of lung cancer in individuals exposed to extraordinary oxidative stress. The causal mechanisms of harmful effects are still unclear. Carotenoid breakdown products (CBPs) including highly reactive aldehydes and epoxides are formed during oxidative attacks in the course of antioxidative action. We investigated the formation of CBPs by stimulated neutrophils (and at further conditions), tested the hypothesis that CBPs may exert mitochondriotoxicity and tried to prevent toxicity in the presence of members of the antioxidative network. Stimulated neutrophils are able to degrade beta-carotene and to generate a number of CBPs. Concerning mitochondriotoxicity, we found that CBPs strongly inhibit state 3 respiration of rat liver mitochondria at concentrations between 0.5 and 20 microM. This was true for retinal, beta-ionone, and for mixtures of cleavage/breakdown products. The inhibition of mitochondrial respiration was accompanied by a reduction in protein sulfhydryl content, decreasing GSH levels and redox state, and elevated accumulation of malondialdehyde. Changes in mitochondrial membrane potential favor functional deterioration in the adenine nucleotide translocator as a sensitive target. The presence of additional antioxidants such as alpha-tocopherol, ascorbic acid, N-acetyl-cysteine or others could mitigate mitochondriotoxicity. The findings reflect a basic mechanism of increasing the risk of cancer induced by carotenoid degradation products.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"75-86"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212740","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28184569","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}
Forum of NutritionPub Date : 2009-01-01Epub Date: 2009-09-21DOI: 10.1159/000242367
I Elmadfa, A Meyer, V Nowak, V Hasenegger, P Putz, R Verstraeten, A M Remaut-DeWinter, P Kolsteren, J Dostálová, P Dlouhý, E Trolle, S Fagt, A Biltoft-Jensen, J Mathiessen, M Velsing Groth, L Kambek, N Gluskova, N Voutilainen, A Erkkilä, M Vernay, C Krems, A Strassburg, A L Vasquez-Caicedo, C Urban, A Naska, E Efstathopoulou, E Oikonomou, K Tsiotas, V Bountziouka, V Benetou, A Trichopoulou, G Zajkás, V Kovács, E Martos, P Heavey, C Kelleher, J Kennedy, A Turrini, G Selga, M Sauka, J Petkeviciene, J Klumbiene, T Holm Totland, L F Andersen, E Halicka, K Rejman, B Kowrygo, S Rodrigues, S Pinhão, L S Ferreira, C Lopes, E Ramos, M D Vaz Almeida, M Vlad, M Simcic, K Podgrajsek, L Serra Majem, B Román Viñas, J Ngo, L Ribas Barba, V Becker, H Fransen, C Van Rossum, M Ocké, B Margetts
{"title":"European Nutrition and Health Report 2009.","authors":"I Elmadfa, A Meyer, V Nowak, V Hasenegger, P Putz, R Verstraeten, A M Remaut-DeWinter, P Kolsteren, J Dostálová, P Dlouhý, E Trolle, S Fagt, A Biltoft-Jensen, J Mathiessen, M Velsing Groth, L Kambek, N Gluskova, N Voutilainen, A Erkkilä, M Vernay, C Krems, A Strassburg, A L Vasquez-Caicedo, C Urban, A Naska, E Efstathopoulou, E Oikonomou, K Tsiotas, V Bountziouka, V Benetou, A Trichopoulou, G Zajkás, V Kovács, E Martos, P Heavey, C Kelleher, J Kennedy, A Turrini, G Selga, M Sauka, J Petkeviciene, J Klumbiene, T Holm Totland, L F Andersen, E Halicka, K Rejman, B Kowrygo, S Rodrigues, S Pinhão, L S Ferreira, C Lopes, E Ramos, M D Vaz Almeida, M Vlad, M Simcic, K Podgrajsek, L Serra Majem, B Román Viñas, J Ngo, L Ribas Barba, V Becker, H Fransen, C Van Rossum, M Ocké, B Margetts","doi":"10.1159/000242367","DOIUrl":"https://doi.org/10.1159/000242367","url":null,"abstract":"The aim of the European Nutrition and Health Report (ENHR) 2009 is to provide a comprehensive view of the nutrition and health status in the European Union (EU). It is not intended to generate new data, but rather to collect available and authorised data, published or unpublished, on the nutrition and health situation in the countries of the EU","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"62 ","pages":"1-405"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000242367","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28654473","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}
Forum of NutritionPub Date : 2009-01-01Epub Date: 2009-04-07DOI: 10.1159/000212746
Kazuo Miyashita
{"title":"Function of marine carotenoids.","authors":"Kazuo Miyashita","doi":"10.1159/000212746","DOIUrl":"https://doi.org/10.1159/000212746","url":null,"abstract":"<p><p>Although an effort is made to review marine carotenoids as important bioactive compounds with reference to their presence, and chemical and biofunctional benefits, there has been a relatively little information on the impact of these carotenoids on human health. The potential beneficial effects of marine carotenoids have been studied particularly in astaxanthin and fucoxanthin as they are major marine carotenoids. Both carotenoids show strong antioxidant activity which is attributed to quenching singlet oxygen and scavenging free radicals. The potential role of the carotenoids as dietary anti-oxidants has been suggested to be one of the main mechanisms for their preventive effects against cancer and inflammatory diseases. However, it would be difficult to explain their biological activities only by their antioxidant activity. We have found the antiobesity and antidiabetic effects as specific and novel bio-functions of fucoxanthin. A nutrigenomic study revealed that fucoxanthin induces uncoupling protein 1 expression in white adipose tissue (WAT) mitochondria to lead to oxidation of fatty acids and heat production in WAT. Fucoxanthin improves insulin resistance and decreases blood glucose level, at least in part, through the downregulation of tumor necrosis factor-alpha in WAT of animals. Thus, the specific regulation of fucoxanthin on a particular bio-molecule will be responsible for the characteristic chemical structures which differ depending on the length of the polyene, nature of the end group and various substituents they contain. The key structure of carotenoids for the expression of antiobesity effect was suggested to be carotenoid end of the polyene chromophore containing an allenic bond and two hydroxyl groups.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"136-146"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212746","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28108799","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}
Forum of NutritionPub Date : 2009-01-01Epub Date: 2009-04-07DOI: 10.1159/000212751
Akira Murakami
{"title":"Chemoprevention with phytochemicals targeting inducible nitric oxide synthase.","authors":"Akira Murakami","doi":"10.1159/000212751","DOIUrl":"https://doi.org/10.1159/000212751","url":null,"abstract":"<p><p>A regulated low level of nitric oxide (NO) production in the body is essential for maintaining homeostasis (neuroprotection, vasorelaxation, etc.), though certain pathophysiological conditions associated with inflammation involve de novo synthesis of inducible NO synthase (iNOS) in immune cells, including macrophages. A large body of evidence indicates that many inflammatory diseases, such as colitis and gastritis, as well as many types of cancer, occur through sustained and elevated activation of this particular enzyme. The biochemical process of iNOS protein expression is tightly regulated and complex, in which the endotoxin lipopolysaccharide selectively binds to toll-like receptor 4 and thereby activates its adaptor protein MyD88, which in turn targets downstream proteins such as IRAK and TRAF6. This leads to functional activation of key protein kinases, including IkB kinases and mitogen-activated protein kinases (MAPKs), such as p38 MAPK, JNK1/2, and ERK1/2, all of which are involved in activating key transcription factors, including nuclear factor-kappaB and activator protein-1. In addition, the production of proinflammatory cytokines such as interferon-gamma and interleukin-12 potentiates iNOS induction in autocrine fashions. Meanwhile, an LPS-stimulated p38 MAPK pathway plays a pivotal role in the stabilization of iNOS mRNA, which has the AU-rich element in its 3'-untranslated region, for rapid NO production. Thus, suppression and/or inhibition of the above-mentioned signaling molecules may have a great potential for the prevention and treatment of inflammation-associated carcinogenesis. In fact, there have been numerous reports of phytochemicals found capable of targeting NO production by unique mechanisms, including polyphenols, terpenoids, and others. This review article briefly highlights the molecular mechanisms underlying endotoxin-induced iNOS expression in macrophages, and also focuses on promising natural agents that may be useful for anti-inflammation and anticarcinogenesis strategies.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"193-203"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212751","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28108804","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}
Forum of NutritionPub Date : 2009-01-01Epub Date: 2009-04-07DOI: 10.1159/000212733
Keiko Abe
{"title":"Genomics for food functionality and palatability.","authors":"Keiko Abe","doi":"10.1159/000212733","DOIUrl":"https://doi.org/10.1159/000212733","url":null,"abstract":"<p><p>In the 1980s, Japan proposed the terminology of 'functional food' and its concept [1], and since then the importance of conducting basic and applied studies on food functionality has been emphasized globally. Functional foods in particular as well as common foods in general are constituted with a variety of components including functional factors, and it has been recognized as difficult to evaluate their functionalities by usual chemical, biochemical and physiological methodologies [2]. Against this backdrop, nutrigenomics came into being as a new method of evaluating functional foods, as well as nutrients, in a holistic manner. Meanwhile the endowed chair, Functional Food Genomics, was established at the University of Tokyo with the aegis of 32 food companies in Japan. This academia-industry collaboration has been working well to disclose why and how some particular functional foods elicit their effects in the body. These include soy protein isolate, cocoa polyphenol, sesamin as a lignan of sesame origin, and many others. On the other hand, food safety has been gaining public attention, and we applied genomics for assessment of the wholesomeness of newly developed hypoallergenic wheat flour compared with normal flour. The application of this way of holistic evaluation suggested that the new product was basically the same as the normal product in terms of all-gene expression profiles. The same method was applied to a new sweet protein, neoculin, which resembled toxic lectins in conformation. The result indicated that neoculin had lost its lectin activity, possessing no particular toxic effect. It is thus likely that genomics can be applied to a variety of foods in general for the purpose of simultaneously assessing their functionality.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212733","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28183566","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":"Genome science of lipid metabolism and obesity.","authors":"Nobuyuki Takahashi, Tsuyoshi Goto, Shizuka Hirai, Taku Uemura, Teruo Kawada","doi":"10.1159/000212736","DOIUrl":"https://doi.org/10.1159/000212736","url":null,"abstract":"<p><p>Abnormalities in lipid metabolism cause obesity leading to metabolic syndrome. Thus, improvement of the abnormalities is significant for the treatment of metabolic syndrome. Nuclear receptors activated by specific ligands regulate lipid metabolism at the genomic level. The expression of lipid metabolism-related enzymes is increased or decreased by the activity of various nuclear receptors. The regulation of enzyme expression is mediated by specific response elements to each nuclear receptor in promoters of target genes. Many food factors acting as agonists or antagonists control the activities of nuclear receptors. Here, we provide several examples of food factors acting as agonists or antagonists, which are useful for the management of obesity accompanied by lipid metabolism abnormalities.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"25-38"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212736","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28183568","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}
Forum of NutritionPub Date : 2009-01-01Epub Date: 2009-04-07DOI: 10.1159/000212745
Xuebo Liu, Toshihiko Osawa
{"title":"Astaxanthin protects neuronal cells against oxidative damage and is a potent candidate for brain food.","authors":"Xuebo Liu, Toshihiko Osawa","doi":"10.1159/000212745","DOIUrl":"https://doi.org/10.1159/000212745","url":null,"abstract":"<p><p>Astaxanthin (AST) is a powerful antioxidant that occurs naturally in a wide variety of living organisms. Based on the report claiming that AST could cross the brain-blood barrier, the aim of this study was to investigate the neuroprotective effect of AST by using an oxidative stress-induced neuronal cell damage system. The treatment with DHA hydroperoxide (DHA-OOH) or 6-hydroxydopamine (6-OHDA), either of which is a reactive oxygen species (ROS)-inducing neurotoxin, led to a significant decrease in viable dopaminergic SH-SY5Y cells by the MTT assay, whereas a significant protection was shown when the cells were pretreated with AST. Moreover, 100 nM AST pretreatment significantly inhibited intracellular ROS generation that occurred in either DHA-OOH- or 6-OHDA-treated cells. The neuroprotective effect of AST is suggested to be dependent upon its antioxidant potential and mitochondria protection; therefore, it is strongly suggested that treatment with AST may be effective for oxidative stress-associated neurodegeneration and a potential candidate for natural brain food.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"129-135"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212745","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28184574","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}
Forum of NutritionPub Date : 2009-01-01Epub Date: 2009-04-07DOI: 10.1159/000212752
Sayori Wada
{"title":"Chemoprevention of tocotrienols: the mechanism of antiproliferative effects.","authors":"Sayori Wada","doi":"10.1159/000212752","DOIUrl":"https://doi.org/10.1159/000212752","url":null,"abstract":"<p><p>Tocotrienols have been reported as antitumor agents and widely commercialized as an antioxidant dietary supplement. Tocotrienols have more significant biological activity than tocopherols, although serum level of tocotrienols is much lower than that of tocopherols. This may be because intracellular concentration of tocotrienols was revealed to be significantly higher compared with tocopherols, and tocotrienol accumulation is observed in tumor. Previous reports have suggested antiproliferative effect, induction of apoptosis, modulation of cell cycle, antioxidant activity, inhibition of angiogenesis, and suppression of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase activity as anticarcinogenesis mechanisms of tocotrienols both in vivo and in vitro. Extension of the duration of host survival was observed in tumor-implanted mice treated with tocotrienol. Tocotrienols induce apoptosis mainly via mitochondria-mediated pathway. Cell cycle arrest is due to suppression of cyclin D by tocotrienols. Tocotrienols also inhibit vascularization-reducing proliferation, migration and tube formation. Malignant proliferation demands elevation of HMG CoA reductase activity, and tocotrienols suppress its activity. Tocotrienol treatment decreases oncogene expression and increases the level of tumor suppressors. Only a few clinical trials to determine the effects of tocotrienol on cancer prevention or treatment have been carried out. There is no convincing or probable evidence of the role of tocotrienols in cancer prevention, while alpha-tocopherol has been suggested to have a limited anti-prostate cancer potential. Neither beneficial activity nor adverse effect of tocotrienol has sufficiently been explored so far. The above-mentioned mechanisms of tocotrienols seem to be promising for cancer prevention; however, further clinical studies are warranted to assess the efficacy and safety of tocotrienol.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"204-216"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212752","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28108805","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":"Lipid metabolism and nutrigenomics - impact of sesame lignans on gene expression profiles and fatty acid oxidation in rat liver.","authors":"Takashi Ide, Yasutaka Nakashima, Hiroshi Iida, Satoko Yasumoto, Masumi Katsuta","doi":"10.1159/000212735","DOIUrl":"https://doi.org/10.1159/000212735","url":null,"abstract":"<p><p>The impact of sesamin, episesamin and sesamolin (sesame lignans) on hepatic gene expression profiles was compared with a DNA microarray. Male Sprague-Dawley rats were fed experimental diets containing 0.2% sesamin, episesamin or sesamolin, and a control diet free of lignans for 15 days. Compared to a lignan-free diet, a diet containing sesamin, episesamin and sesamolin caused more than 1.5- and 2-fold changes in the expression of 128 and 40, 526 and 152, and 516 and 140 genes, respectively. The lignans modified the mRNA levels of not only many enzymes involved in hepatic fatty acid oxidation, but also proteins involved in the transportation of fatty acids into hepatocytes and their organelles, and in the regulation of hepatic concentrations of carnitine, CoA and malonyl-CoA. It is apparent that sesame lignans stimulate hepatic fatty acid oxidation by affecting the gene expression of various proteins regulating hepatic fatty acid metabolism. The changes in the gene expression were generally greater with episesamin and sesamolin than with sesamin. In terms of amounts accumulated in serum and the liver, the lignans ranked in the order sesamolin, episesamin and sesamin. The differences in bioavailability among these lignans appear to be important to their divergent physiological activities. We also confirmed that dietary sesame seed affected the expression of genes related to fatty acid oxidation in a manner similar to isolated lignan compounds.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"10-24"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212735","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28183567","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}
Forum of NutritionPub Date : 2009-01-01Epub Date: 2009-04-07DOI: 10.1159/000212738
Akihiko Nagao
{"title":"Absorption and function of dietary carotenoids.","authors":"Akihiko Nagao","doi":"10.1159/000212738","DOIUrl":"https://doi.org/10.1159/000212738","url":null,"abstract":"<p><p>Carotenoids are highly hydrophobic pigments with yellow to red color and their major dietary sources are fruits and vegetables. They have an essential physiological function as a vitamin A precursor and also have antioxidant, anticancer, immune enhancement and antiobesity activities related to prevention of degenerative diseases. The release of carotenoids from food matrix, their dispersion within the digestive tract, and their solubilization in mixed micelles are important steps for carotenoid bioaccessibility. Solubilized carotenoids are taken up by epithelial cells of the small intestine by simple diffusion and/or transporter-mediated processes and then secreted to lymph as chylomicron. Carotenoids accumulated in tissues are thought to be metabolized to small molecules by enzymatic cleavage and/or chemical oxidation with active oxygen species at conjugated double bonds. The hydroxyl group of xanthophylls can be oxidatively metabolized to carbonyl group. Carotenoids with long chain of conjugated double bonds physically quench singlet oxygen and scavenge oxygen radicals, particularly under low oxygen pressure, and thereby they have been thought to work as lipophilic antioxidants for human health. In addition to antioxidant activities, each carotenoid has characteristic functions such as cell cycle inhibition, induction of cell differentiation and apoptosis, and enhancement of gap-junctional communication. However, the detailed mechanisms of these biological actions have not been fully revealed yet and deserve future studies.</p>","PeriodicalId":55148,"journal":{"name":"Forum of Nutrition","volume":"61 ","pages":"55-63"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000212738","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28184567","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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