Scandinavian Journal of Food & Nutrition最新文献

{"title":"Grapefruit juice and serum lipids in healthy adults","authors":"Christina E. Jonsson, L. Ellegård","doi":"10.3402/FNR.V50I3.1590","DOIUrl":"https://doi.org/10.3402/FNR.V50I3.1590","url":null,"abstract":"Background: Grapefruit juice has been reported to decrease serum cholesterol in patients with hyperlipidaemia. Whether grapefruit juice can influence serum lipids in healthy people had not been investigated. Objective: To investigate the effect of grapefruit juice on serum lipid levels in healthy adults by comparing grapefruit juice with apple juice in the same individuals. Design: In a cross-over study, 28 healthy volunteers took 250 ml grapefruit juice or apple juice daily for 3 weeks followed by a 3 week washout, and then the juices were swapped for the second intervention period. Serum samples for total, low-density lipoprotein (LDL)-, high-density lipoprotein (HDL)-cholesterol and triglycerides were collected before and after each period, and analysed batchwise after the study. Results: In the grapefruit juice period LDL-cholesterol decreased by 6% (p=0.04). Serum lipids were not significantly affected by apple juice. There were no differences in lipid levels\u0000 between grapefruit juice and apple juice periods. During the whole 9 week study total and LDL-cholesterol decreased by 8% (p<0.0001) and 14% (p<0.0001), respectively, whereas HDL-cholesterol increased by 6% (p=0.028). Conclusions: Consumption of grapefruit juice decreased LDL-cholesterol by 6%, but with no significant differences compared with the apple juice or washout periods. Thus, the hypocholesterolaemic effect of grapefruit juice cannot be separated from the general time effect encountered in this study. Keywords: apple juice; cholesterol; cross-over; grapefruit juice; HDL; LDL; triglycerides","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"29 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128546410","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":"Phospholipid signals and intestinal carcinogenesis","authors":"R. Duan","doi":"10.1080/17482970601075703","DOIUrl":"https://doi.org/10.1080/17482970601075703","url":null,"abstract":"Phospholipids are an important constituent of the cell plasma membrane and are also present in most common dietary products, being particularly abundant in milk, egg, meat and beans. Phospholipids are hydrolysed by different phospholipases to generate multiple breakdown products that affect the fate of the cells. Most phospholipids such as phosphatidylcholine, lysophosphatidylcholine, phosphatidylinositol and platelet activating factor are important for cell survival and thus may promote tumorigenesis and inflammation. Sphingomyelin is unique in the sense that its hydrolysis by sphingomyelinase and ceramidase generates several lipid messengers such as ceramide and sphingosine that inhibit cell proliferation and induce apoptosis. In the intestinal tract there is a specific type of sphingomyelinase called alkaline sphingomyelinase, which can hydrolyse sphingomyelin in both the cell membrane and the diet. The enzyme may play important roles in preventing colon cancer\u0000 development and inflammation by hydrolysing sphingomyelin to generate anticancer molecules, and by counteracting the cancer-promoting effects of other phospholipids such as lysophosphatidylcholine and platelet activating factor. This mini-review highlights the signal transduction pathways activated by different phospholipids, with special attention being paid to potential implications in the development of colon cancer. Keywords: colon cancer; inflammatory bowel disease; phospholipids; signal transduction pathway; sphingomyelin; sphingomyelinase","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"159 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133007514","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":"Validation study of fatty acid consumption assessed with a short food frequency questionnaire against plasma concentration in middle-aged Japanese people","authors":"C. Goto, Y. Tokudome, N. Imaeda, K. Takekuma, K. Kuriki, Fukuyo Igarashi, M. Ikeda, S. Tokudome","doi":"10.1080/11026480600568720","DOIUrl":"https://doi.org/10.1080/11026480600568720","url":null,"abstract":"Objective: To assess the relative validity of data for consumption of fatty acids (FAs) measured with a short food frequency questionnaire (FFQ) in comparison with plasma concentration of FAs. Design: In this cross-sectional study, completed FFQs were secured from 177 (92 male and 85 female) employees working for a company in August 2001. Intake of FAs was assessed with the FFQ, and the values were validated against FA concentration in plasma in overnight-fasting blood. Results: Mean9/SD daily intakes of total fatty acids (TFAs) were 44.49/8.0 g day-1 for men and 42.99/7.2 g day-1 for women. Plasma concentration of TFAs were 12.739/3.78 mmol l-1 for men and 10.549/1.75 mmol l-1 for women. Spearman’s rank correlation coefficients, unadjusted and energy-adjusted by the energy-density method and residual method, for n-3 highly unsaturated fatty acids (HUFAs) were 0.37 (p<0.001), 0.38 (p<0.001) and 0.40 (p<0.001) for men, and 0.41 (p<0.001), 0.26 (p<0\u0000 .01) and 0.29 (p<0.01) for women, respectively. Conclusions: Relative validity values of data for intake of n-3 polyunsaturated fatty acids (PUFAs) for women and n-3 HUFAs in both genders, assessed with the FFQ compared with FA concentration in plasma, were moderate, but no significant associations were found for saturated fatty acids, monounsaturated fatty acids or n-6 PUFAs. Keywords: fatty acids; food frequency questionnaire; plasma concentration; relative validity","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"386 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116643396","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":"Reply: Breast-feeding and allergy","authors":"B. Björkstén, B. Lundbäck","doi":"10.1080/17482970600767847","DOIUrl":"https://doi.org/10.1080/17482970600767847","url":null,"abstract":"We would once again like to comment the paper by Kull et al. (1), in which the authors suggest that breast-feeding decreases the risk for development of eczema and discuss in general terms that breastfeeding protects against the development of allergy. Our criticism was based on the fact that exclusive breast-feeding for 4 months or more did not reduce the risk for eczema at the age of 4 years [odds ratio (OR) 0.88, not significant) [2]. In order to avoid all possible disease-related modification of exposure, the authors excluded all children who developed eczema or asthma during the period of breastfeeding. By excluding those children who developed symptoms while they were breast-fed and by creating an arbitrary group with ‘‘severe allergic disease’’, the authors found support for a protective role of breast-feeding yielding a slightly lower OR of 0.78. The authors have now replied to our comments (3) by referring to two meta-analyses, one about breastfeeding and asthma (4) and another about breastfeeding and eczema (5). It is well known from several studies that breast-feeding protects against wheezing, at least during infancy. However, the problem is that recurrent wheezing has different phenotypes. The evidence quoted by Kull et al. refers to the non-allergic phenotype. This has also been shown in studies in Sweden by Ronmark et al. (6). In her reply (3) to our initial critical remarks, Kull exemplifies the previous results by pooling asthma and eczema together and makes a point of the fact that there is no statistically significant difference between the association of breast-feeding and eczema whether children with an overlap and exposure are excluded or not. Such secondary analyses are open to critique, particularly in the absence of any power calculations. Non-allergic asthma is particularly common in very small children. By including non-allergic asthmatics, the results become biased when discussing protection against allergy. The fact is that there is little or no support for any major impact of breast-feeding on allergy development. The study by Kull et al. (1) has not contributed novel data on that point. There is a problem with the meta-analysis related to eczema (5) quoted by Kull in that five of the papers providing low odds ratios for childhood eczema to be associated with breast-feeding were conducted by Chandra, whose work has been revealed to be fraudulent (7). Obviously Kull could not possibly have known this at the time of writing her paper, but the fact nevertheless provides further reason for our argument that there is little support for any significant allergy-preventive effect of breast-feeding. We would like to reaffirm our initial statement that preventive measures and information should be based on solid scientific ground, just as other medical therapies and interventions.","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"5 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114283666","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":"Fatty acids and gene transcription","authors":"D. Jump, D. Botolin, Yun Wang, Jinghua Xu, Barbara D. Christian","doi":"10.1080/17482970601069318","DOIUrl":"https://doi.org/10.1080/17482970601069318","url":null,"abstract":"The type and quantity of dietary fat ingested contributes to the onset and progression of chronic diseases, such as diabetes and atherosclerosis. The liver plays a central role in whole-body lipid metabolism and responds rapidly to changes in dietary fat composition. In rodents, n-3 polyunsaturated fatty acids (PUFAs) enhance hepatic fatty acid oxidation and inhibit fatty acid synthesis and very low-density lipoprotein secretion, in part, by regulating key transcription factors, including peroxisome proliferator activated receptor-? (PPAR-?), sterol regulatory element binding protein-1 (SREBP-1), carbohydrate regulatory element binding protein (ChREBP) and Max-like factor X (MLX). These transcription factors control the expression of multiple genes involved in lipid synthesis and oxidation. Changes in PPAR-? target genes correlate well with changes in intracellular non-esterified fatty acids. Insulin stimulates hepatic de novo lipogenesis by rapidly inducing SR\u0000 EBP-1 nuclear abundance (nSREBP-1). This mechanism is linked to insulin-induced protein kinase B (Akt) and glycogen synthase kinase (Gsk)-3? phosphorylation and inhibition of 26S proteasomal degradation of nSREBP-1. n-3 PUFAs, particularly 22:6 n-3, inhibit lipid synthesis by suppressing nSREBP-1. A major action of 22:6 n-3 is to stimulate the loss of nSREBP-1 through 26S proteasomal and extracellular regulated kinase (Erk)-dependent pathways. 22:6 n-3 is the only n-3 PUFA accumulating in livers of rodents or humans ingesting essential fatty acid-sufficient or n-3 PUFA-enriched diets. As such, 22:6 n-3 is a major feedback regulator of hepatic lipid synthesis. Finally, insulin-stimulated glucose metabolism augments de novo lipogenesis by elevating nuclear levels of ChREBP, a key regulator of glycolytic and lipogenic genes. ChREBP binding to promoters requires MLX. n-3 PUFAs repress expression of the glycolytic gene, L-pyruvate kinase and lipogenic genes by suppressing MLX nu\u0000 c\u0000 lear abundance. In summary, n-3 PUFAs control the activity or abundance of several hepatic transcription factors that impact hepatic carbohydrate and lipid metabolism. Recent studies have identified Erk, Gsk-3? and MLX as novel targets of fatty acid-regulated gene expression. Keywords: gene transcription; hepatic fatty acid metabolism","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"229 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130769139","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":"Sugars or sweeteners: towards guidelines for their use in practice report from an expert consultation +","authors":"P. Nowicka, S. Bryngelsson","doi":"10.1080/17482970600774736","DOIUrl":"https://doi.org/10.1080/17482970600774736","url":null,"abstract":"With the aim of suggesting recommendations regarding the practical implementation of sweeteners from a nutritional point of view for different groups of consumers, based on present scientific knowledge, the Swedish Nutrition Foundation (SNF) arranged a workshop focusing on the use of sugars and sweeteners in relation to obesity, diabetes, dental health, appetite, reward and addiction. The discussions and conclusions are summarized in this article. It was concluded that restrictions to keep the intake of refined sugars within the recommendations (10E%) should be achieved by limited intake of foods high in sugars, e.g. sweet drinks and candies, rather than other foods that provide less significant amounts of sugars. From a practical point of view it may be useful to restrict the intake of foods high in sugars, especially drinks, to a small amount and to a limited number of occasions, e.g. once or twice a week. Regarding sweeteners, the present intake is considered t\u0000 o be safe from a toxicological point of view. Non-caloric intense sweeteners may be useful for lowering the energy content of liquid and semi-solid foods. Sweeteners may also provide tooth-friendly alternatives within certain food categories, but do not reduce the erosive potential of acidic foods. Keywords: appetite; dental health; diabetes; obesity; reward; weight regulation","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"9 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121768926","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 importance of dietary antioxidants on plasma antioxidant capacity and lipid peroxidation in vivo in middle-aged men","authors":"C. Nälsén, S. Basu, A. Wolk, B. Vessby","doi":"10.1080/11026480600717202","DOIUrl":"https://doi.org/10.1080/11026480600717202","url":null,"abstract":"Background: High intake of foods rich in antioxidants is associated with a reduced risk of several diseases, including coronary heart disease and some cancers. Objective: To study associations between dietary antioxidants and antioxidant-rich food items and antioxidant capacity (AOC), as well as lipid peroxidation in vivo. Design: A total of 86 men, with a mean age of 60 years, who were part of a larger population-based study in Sweden, participated. Fourteen 24 h recalls were collected by telephone, evenly distributed during 1 year. AOC was measured in plasma using an enhanced chemiluminescence assay and biomarkers of non-enzymic in vivo lipid peroxidation were determined by measuring F2-isoprostanes (8-iso-prostaglandin F2a) in plasma. Results: Higher intakes of ascorbic acid, tocopherols and b-carotene, and of the combined intake of different antioxidant-rich foods, were related to a higher plasma AOC. The levels of F2-isoprostanes were related neither to dieta\u0000 ry intake of antioxidants nor to antioxidant-rich foods. Conclusions: Individuals with a higher intake of several different antioxidant-rich foods and of dietary antioxidants had a higher plasma AOC than those with the lowest intake, supporting the importance of a balanced diet rich in various antioxidants. Moreover, the results indicate that non-enzymic lipid peroxidation in vivo, measured as F2-isoprostanes in plasma, is not easily affected by the diet. Keywords: antioxidant status; diet; food habits; isoprostanes; oxidative stress","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"28 2 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134490127","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":"Dietary fatty acids and insulin secretion","authors":"G. Mingrone","doi":"10.1080/17482970601076354","DOIUrl":"https://doi.org/10.1080/17482970601076354","url":null,"abstract":"It is well known that free fatty acids (FFAs) play a central role in insulin resistance. However, increasing evidence suggests that they are also implicated in the control of pancreatic insulin secretion. Simultaneous exposure of pancreatic b-cells to high levels of glucose and to saturated FFAs results in a substantial increase in insulin release, whereas chronic exposure may lead to a desensitization and suppression of secretion. A source of fatty acid, either exogenous or endogenous, is necessary to support normal insulin secretion. A rapid increase in fatty acids potentiates glucose-stimulated secretion by increasing the concentration of fatty acyl-coenzyme A or complex lipids, which act indirectly by modulating key enzymes, such as protein kinase C, or directly by modulating the exocytotic machinery. Mathematical models including FFAs in controlling insulin secretion are devised. Finally, insulin secretion in a human model of very low-fat diet, the malabsorpt\u0000 ive bariatric surgery for morbid obesity, is described. Keywords: fatty acids; insulin secretion; mathematical models; bariatric surgery","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"14 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126730171","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":"Promoting breast-feeding with weak arguments","authors":"Bengt Bjo¨rkste´n, Bo Lundba¨ck","doi":"10.1080/11026480600601125","DOIUrl":"https://doi.org/10.1080/11026480600601125","url":null,"abstract":"","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"46 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130236200","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":"Nutrients, stress, and medical disorders: Shloma Yehuda and David I. Mostofsky, eds. Totowa, NJ: Humana Press; 2006. 448 pp.ISBN 1-58829-432-3. US $145","authors":"A. Duttaroy","doi":"10.1080/11026480600568902","DOIUrl":"https://doi.org/10.1080/11026480600568902","url":null,"abstract":"","PeriodicalId":225599,"journal":{"name":"Scandinavian Journal of Food & Nutrition","volume":"40 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2006-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116977395","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}