Pub Date : 1985-01-01DOI: 10.1007/978-1-4613-2529-1_6
R P Bird, N J Mercer, H H Draper
{"title":"Animal models for the study of nutrition and human disease: colon cancer, atherosclerosis, and osteoporosis.","authors":"R P Bird, N J Mercer, H H Draper","doi":"10.1007/978-1-4613-2529-1_6","DOIUrl":"https://doi.org/10.1007/978-1-4613-2529-1_6","url":null,"abstract":"","PeriodicalId":50856,"journal":{"name":"Advances in Nutritional Research","volume":"7 ","pages":"155-86"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-1-4613-2529-1_6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"15029893","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 : 1985-01-01DOI: 10.1007/978-1-4613-2529-1_9
P D Whanger
{"title":"Metabolic interactions of selenium with cadmium, mercury, and silver.","authors":"P D Whanger","doi":"10.1007/978-1-4613-2529-1_9","DOIUrl":"https://doi.org/10.1007/978-1-4613-2529-1_9","url":null,"abstract":"","PeriodicalId":50856,"journal":{"name":"Advances in Nutritional Research","volume":"7 ","pages":"221-50"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-1-4613-2529-1_9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"15029895","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 : 1984-01-01DOI: 10.1007/978-1-4613-2801-8_4
G L Klein, J W Coburn
Patients receiving long-term treatment with total parenteral nutrition often develop bony abnormalities characterized by patchy osteomalacia and low bone turnover. The patients present evidence of physiologic hypoparathyroidism, although low levels of iPTH cannot entirely explain the osteomalacia. Abnormally low serum levels of 1,25(OH)2-vitamin D have been demonstrated, but the significance of these reduced levels in the pathogenesis of the bone lesions is not defined. Aluminum has been detected in large quantities in the plasma, urine, and bone of some patients treated with TPN, and there is mounting evidence that aluminum may be associated with skeletal pathology, particularly osteomalacia. There is, however, no clear documentation that aluminum accumulation produces the skeletal lesions observed, although it could be a contributing factor. There has been the unusual empiric observation that the removal of vitamin D2 from the infusate is associated with a decrease in the quantity of unmineralized osteoid in TPN patients. A possible role of vitamin D2 in producing osteomalacia is not easy to understand since normal serum levels of 25(OH)-D2, the circulating form of vitamin D2, have been reported. The long-term consequences of intravenous nutritional support for many aspects of metabolism remain unknown. Administration into the systemic circulation of predetermined quantities of calcium and phosphorus via a route that bypasses their passage across the intestinal mucosa, the portal system and the liver may have adverse consequences. It is possible that bypassing homeostatic mechanisms may affect bone formation and metabolism or lead to alterations in vitamin D sterols. Alternatively, a deficiency of an essential trace metal or the accumulation of a toxic trace substance could be responsible for the bony abnormalities. Much remains to be clarified concerning calcium homeostasis and bone disease during total parenteral nutrition. Among various possible factors, it seems likely that the significance of the low levels of 1,25(OH)2-vitamin D and of the accumulation of aluminum in this condition will soon be clarified.
{"title":"Metabolic bone disease associated with total parenteral nutrition.","authors":"G L Klein, J W Coburn","doi":"10.1007/978-1-4613-2801-8_4","DOIUrl":"https://doi.org/10.1007/978-1-4613-2801-8_4","url":null,"abstract":"<p><p>Patients receiving long-term treatment with total parenteral nutrition often develop bony abnormalities characterized by patchy osteomalacia and low bone turnover. The patients present evidence of physiologic hypoparathyroidism, although low levels of iPTH cannot entirely explain the osteomalacia. Abnormally low serum levels of 1,25(OH)2-vitamin D have been demonstrated, but the significance of these reduced levels in the pathogenesis of the bone lesions is not defined. Aluminum has been detected in large quantities in the plasma, urine, and bone of some patients treated with TPN, and there is mounting evidence that aluminum may be associated with skeletal pathology, particularly osteomalacia. There is, however, no clear documentation that aluminum accumulation produces the skeletal lesions observed, although it could be a contributing factor. There has been the unusual empiric observation that the removal of vitamin D2 from the infusate is associated with a decrease in the quantity of unmineralized osteoid in TPN patients. A possible role of vitamin D2 in producing osteomalacia is not easy to understand since normal serum levels of 25(OH)-D2, the circulating form of vitamin D2, have been reported. The long-term consequences of intravenous nutritional support for many aspects of metabolism remain unknown. Administration into the systemic circulation of predetermined quantities of calcium and phosphorus via a route that bypasses their passage across the intestinal mucosa, the portal system and the liver may have adverse consequences. It is possible that bypassing homeostatic mechanisms may affect bone formation and metabolism or lead to alterations in vitamin D sterols. Alternatively, a deficiency of an essential trace metal or the accumulation of a toxic trace substance could be responsible for the bony abnormalities. Much remains to be clarified concerning calcium homeostasis and bone disease during total parenteral nutrition. Among various possible factors, it seems likely that the significance of the low levels of 1,25(OH)2-vitamin D and of the accumulation of aluminum in this condition will soon be clarified.</p>","PeriodicalId":50856,"journal":{"name":"Advances in Nutritional Research","volume":"6 ","pages":"67-92"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17496962","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 : 1984-01-01DOI: 10.1007/978-1-4613-2801-8_1
N J Benevenga
{"title":"Evidence for alternative pathways of methionine catabolism.","authors":"N J Benevenga","doi":"10.1007/978-1-4613-2801-8_1","DOIUrl":"https://doi.org/10.1007/978-1-4613-2801-8_1","url":null,"abstract":"","PeriodicalId":50856,"journal":{"name":"Advances in Nutritional Research","volume":"6 ","pages":"1-18"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17274513","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 : 1984-01-01DOI: 10.1007/978-1-4613-2801-8_5
P J Reeds, P J Garlick
{"title":"Nutrition and protein turnover in man.","authors":"P J Reeds, P J Garlick","doi":"10.1007/978-1-4613-2801-8_5","DOIUrl":"https://doi.org/10.1007/978-1-4613-2801-8_5","url":null,"abstract":"","PeriodicalId":50856,"journal":{"name":"Advances in Nutritional Research","volume":"6 ","pages":"93-138"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17496963","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 : 1984-01-01DOI: 10.1007/978-1-4613-2801-8_3
C Mettlin
Data derived from epidemiologic studies on human populations are consistent with the protection from cancer afforded by vitamin A seen in animal studies. The populations studied are diverse, including groups living in India, Singapore, Norway, the United Kingdom, and the United States. The methodologies brought to bear on the question have been equally varied. Although there are inconsistencies in findings, and instances in which an association has not been observed, the weight of evidence suggests that the intake of vitamin A from dietary or other sources may inhibit the onset of lung cancer and possibly other cancers. However, the evidence from human populations is not experimental and it is conceivable that the associations observed are not causal. Additional epidemiologic research is needed to determine what sites of cancer may be inhibited by vitamin A and whether cancer growth at any other site is enhanced by high vitamin A intakes. It is also important that controlled trials using vitamin A as a chemopreventive agent be considered as a means of determining whether the epidemiologic findings are of clinical significance.
{"title":"Epidemiologic studies on vitamin A and cancer.","authors":"C Mettlin","doi":"10.1007/978-1-4613-2801-8_3","DOIUrl":"https://doi.org/10.1007/978-1-4613-2801-8_3","url":null,"abstract":"<p><p>Data derived from epidemiologic studies on human populations are consistent with the protection from cancer afforded by vitamin A seen in animal studies. The populations studied are diverse, including groups living in India, Singapore, Norway, the United Kingdom, and the United States. The methodologies brought to bear on the question have been equally varied. Although there are inconsistencies in findings, and instances in which an association has not been observed, the weight of evidence suggests that the intake of vitamin A from dietary or other sources may inhibit the onset of lung cancer and possibly other cancers. However, the evidence from human populations is not experimental and it is conceivable that the associations observed are not causal. Additional epidemiologic research is needed to determine what sites of cancer may be inhibited by vitamin A and whether cancer growth at any other site is enhanced by high vitamin A intakes. It is also important that controlled trials using vitamin A as a chemopreventive agent be considered as a means of determining whether the epidemiologic findings are of clinical significance.</p>","PeriodicalId":50856,"journal":{"name":"Advances in Nutritional Research","volume":"6 ","pages":"47-65"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17449806","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 : 1984-01-01DOI: 10.1007/978-1-4613-2801-8_6
B Lönnerdal, C L Keen, L S Hurley
{"title":"Zinc binding ligands and complexes in zinc metabolism.","authors":"B Lönnerdal, C L Keen, L S Hurley","doi":"10.1007/978-1-4613-2801-8_6","DOIUrl":"https://doi.org/10.1007/978-1-4613-2801-8_6","url":null,"abstract":"","PeriodicalId":50856,"journal":{"name":"Advances in Nutritional Research","volume":"6 ","pages":"139-67"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17450903","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 : 1984-01-01DOI: 10.1007/978-1-4613-2801-8_8
G Q Yang, J S Chen, Z M Wen, K Y Ge, L Z Zhu, X C Chen, X S Chen
{"title":"The role of selenium in Keshan disease.","authors":"G Q Yang, J S Chen, Z M Wen, K Y Ge, L Z Zhu, X C Chen, X S Chen","doi":"10.1007/978-1-4613-2801-8_8","DOIUrl":"https://doi.org/10.1007/978-1-4613-2801-8_8","url":null,"abstract":"","PeriodicalId":50856,"journal":{"name":"Advances in Nutritional Research","volume":"6 ","pages":"203-31"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-1-4613-2801-8_8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17565639","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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