P Rose, E Fraine, L P Hunt, D W Acheson, J M Braganza
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When the selenium intakes were examined alongside the results of theophylline tests--which reflect cytochromes P450 activities and, thereby, provide an index of antioxidant demand--a line of discrimination separated the majority of patients (with faster drug clearances and lower selenium intakes) and controls. There were no differences in the intakes of individual unsaturated fatty acids, C14:1 through to C24:6, between the two groups. However, amongst six subjects in the overlap zone, three with chronic pancreatitis habitually ate greater amounts of highly unsaturated fatty acids C20:4 to C24:6 inclusive (1970, 1049, 750 mg/d) than did three controls (329, 320, 82 mg/d). Animal experiments show that suboptimal intakes of dietary antioxidants and/or excessive intakes of highly unsaturated fatty acids and/or induction of cytochromes P450 facilitate peroxidation of cellular lipid membranes by free radicals. Our dietary data, taken in conjunction with pharmacokinetic data, thus suggest that a similar situation--favouring lipid peroxidation--may underlie human chronic pancreatitis.</p>","PeriodicalId":13078,"journal":{"name":"Human nutrition. Clinical nutrition","volume":"40 2","pages":"151-64"},"PeriodicalIF":0.0000,"publicationDate":"1986-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Dietary antioxidants and chronic pancreatitis.\",\"authors\":\"P Rose, E Fraine, L P Hunt, D W Acheson, J M Braganza\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Fifteen patients with idiopathic chronic pancreatitis (aged 17-78 years), who had not altered their diet since their first symptoms, completed 7-d weighed dietary records at home. The computed information was compared with that from 15 age- and sex-matched volunteers. Attention was focussed on the intakes of antioxidants and unsaturated fatty acids. The patients ingested less selenium, vitamin E, vitamin C and riboflavin than did controls (P less than 0.001, P less than 0.02, P less than 0.001 and P less than 0.05 respectively, using paired t-tests): selenium was by far the best discriminator on step-wise analysis. When the selenium intakes were examined alongside the results of theophylline tests--which reflect cytochromes P450 activities and, thereby, provide an index of antioxidant demand--a line of discrimination separated the majority of patients (with faster drug clearances and lower selenium intakes) and controls. There were no differences in the intakes of individual unsaturated fatty acids, C14:1 through to C24:6, between the two groups. 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引用次数: 0
摘要
15例特发性慢性胰腺炎患者(年龄17-78岁),自首次出现症状以来未改变饮食习惯,在家中完成了7天的称重饮食记录。计算出的信息与15名年龄和性别匹配的志愿者的信息进行了比较。注意力集中在抗氧化剂和不饱和脂肪酸的摄入上。与对照组相比,患者硒、维生素E、维生素C和核黄素的摄入较少(P < 0.001, P < 0.02, P < 0.001, P < 0.05,采用配对t检验):在逐步分析中,硒是迄今为止最好的鉴别指标。当将硒摄入量与茶碱测试结果(反映细胞色素P450活性,从而提供抗氧化剂需求指数)一起检查时,一条区分线将大多数患者(药物清除率更快,硒摄入量更低)与对照组分开。两组之间的不饱和脂肪酸(C14:1至C24:6)的摄入量没有差异。然而,在重叠区域的6名受试者中,有3名慢性胰腺炎患者习惯性地摄入更多的高不饱和脂肪酸C20:4至C24:6(包括1970、1049、750 mg/d),而对照组为329、320、82 mg/d。动物实验表明,膳食抗氧化剂摄入量不足和/或过量摄入高度不饱和脂肪酸和/或细胞色素P450的诱导会促进自由基对细胞脂质膜的过氧化。我们的饮食数据,结合药代动力学数据,因此表明类似的情况——有利于脂质过氧化——可能是人类慢性胰腺炎的基础。
Fifteen patients with idiopathic chronic pancreatitis (aged 17-78 years), who had not altered their diet since their first symptoms, completed 7-d weighed dietary records at home. The computed information was compared with that from 15 age- and sex-matched volunteers. Attention was focussed on the intakes of antioxidants and unsaturated fatty acids. The patients ingested less selenium, vitamin E, vitamin C and riboflavin than did controls (P less than 0.001, P less than 0.02, P less than 0.001 and P less than 0.05 respectively, using paired t-tests): selenium was by far the best discriminator on step-wise analysis. When the selenium intakes were examined alongside the results of theophylline tests--which reflect cytochromes P450 activities and, thereby, provide an index of antioxidant demand--a line of discrimination separated the majority of patients (with faster drug clearances and lower selenium intakes) and controls. There were no differences in the intakes of individual unsaturated fatty acids, C14:1 through to C24:6, between the two groups. However, amongst six subjects in the overlap zone, three with chronic pancreatitis habitually ate greater amounts of highly unsaturated fatty acids C20:4 to C24:6 inclusive (1970, 1049, 750 mg/d) than did three controls (329, 320, 82 mg/d). Animal experiments show that suboptimal intakes of dietary antioxidants and/or excessive intakes of highly unsaturated fatty acids and/or induction of cytochromes P450 facilitate peroxidation of cellular lipid membranes by free radicals. Our dietary data, taken in conjunction with pharmacokinetic data, thus suggest that a similar situation--favouring lipid peroxidation--may underlie human chronic pancreatitis.