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Monkeys (Macaca nemestrina) were divided into four groups, and each group was fed a particular diet. The variables in the diets were as follows: diet A, 0.3 mg cholesterol/kcal nutrient; diet B, 1.0 mg cholesterol/kcal nutrient; diet C, 0.3 mg cholesterol/kcal nutrient, ethanol (36% of calories); diet D, i.O mg cholesterol/ kcal nutrient, ethanol (36% of calories). Monkeys on the diets containing ethanol developed fatty liver. Mitochondria from ethanol-fed animals demonstrated significant decreases in uncoupler-stimulated, state 3, and state 4 succinate oxidation activity; respiratory control ratio; and ATP content. Liver microsomes isolated from the ethanol-fed groups demonstrated increased ethanol oxidizing activity with either NADPH or H2O2 as cosubstrate. Aniline hydroxylase and ami-nopyrine-N-demethylase activities were also elevated in ethanol-fed animals. The alterations in these functional properties were related primarily to ethanol in the diets. Cholesterol, while being less of a perturbant than ethanol, did elicit a significant decrease in cytochrome oxidase activity of mitochondria and a small but statistically significant increase in microsomal-associated ethanol oxidation activity. It appeared to potentiate the effect of ethanol in lowering mitochondrial respiratory control and ATP concentrations.  相似文献   
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The effects of copper and zinc supplements on weight gains, plasma total and high density lipoprotein (HDL)-cholesterol levels and liver trace mineral levels were studied in young rats fed either coconut oil or corn oil. Dietary factors included 1.5 ppm and 6 ppm copper, 7.5 ppm and 30 ppm zinc, and the two fat sources. Weight gains and levels of total and HDL-cholesterol were higher in rats fed corn oil than in rats fed coconut oil. Increases in dietary zinc were associated with increases in total and HDL-cholesterol levels in rats fed corn oil, while increases in copper supplements were associated with decreases in total and HDL-cholesterol levels in rats fed either fat source. Supplements of 30 ppm zinc resulted in decreases in total cholesterol/HDL-cholesterol ratios in rats fed coconut oil but had no apparent effect on these ratios in rats fed corn oil. Thus, zinc may be a more important factor than copper in the reduction of this ratio, particularly if saturated fatty acids predominate in the diet. Increases in dietary copper were associated with increases in liver copper levels of rats fed either fat source. Increases in either dietary copper or zinc resulted in decreases in liver iron deposition in rats fed both fat sources. Results of this study indicate that a dietary zinc/copper ratio of 5 may be required for optimum growth of young rats.  相似文献   
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Weight loss is common in cancer patients underwent radiation therapy. However, the impact of pretreatment behavior on postradiation nutritional status was unknown. This prospective observational study was conducted in 31 Thai head and neck cancer patients to investigate the association between pretreatment dietary preference and weight change after radiotherapy. Pretreatment preferences on sweet, salty, sour, bitter, umami, spicy, and fatty food were evaluated using a validated questionnaire, TASTE26. Body weights were monitored at baseline, 1,000–2,000, 2,800–3,400, 4,000–4,400, and 5,000–7,000?cGy of radiations and 2?month-follow up after radiotherapy. The energy intakes were analyzed by using 3?day-dietary record and INMUCAL software. Spicy food preference was the only factor found positively correlated with weight loss after radiation (r?=?0.64, P?=?0.007). Consistently, strong spicy lovers had more pronounced reduction of energy intake and body weight, and higher needs of tube feeding than those of mild or moderate lovers (P?<?0.05). This study suggested that stronger preference on spicy food may be associated with less energy intake and more severe weight loss after radiation therapy. A large-scale study is warranted to confirm such findings. Then, preradiation screening for spicy preference may be useful to predict weight loss during radiation therapy.  相似文献   
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Monkeys (Macaca nemestrina) were divided into four groups, and each group was fed a particular diet. The variables in the diets were as follows: diet A, 0.3 mg cholesterol/kcal nutrient; diet B, 1.0 mg cholesterol/kcal nutrient; diet C, 0.3 mg cholesterol/kcal nutrient, ethanol (36% of calories); diet D, 1.0 mg cholesterol/ kcal nutrient, ethanol (36% of calories). Monkeys on the diets containing ethanol developed fatty liver. Mitochondria and microsomes isolated from these livers demonstrated ethanol-elicited alterations in metabolic functions as is described in the preceding paper.1 Accompanying these changes in metabolic activities were alterations in organelle phospholipids that were influenced by both dietary ethanol and cholesterol. The changes that could be attributed to ethanol were as follows. Phosphatidyl ethanolamine was decreased in microsomes and increased in mitochondria; the sphingomyelin content in microsomes was increased significantly. The levels of stearic and arachidonic acid were elevated, and palmitic and oleic acid decreased, in phospholipids from both mitochondria and microsomes. Cholesterol influenced the fatty acid composition of several phospholipids, usually in a direction opposite to those alterations attributed to ethanol. Cholesterol feeding increased levels of palmitic and oleic acid and decreased amounts of stearic, linoleic, and arachidonic acid in several phospholipids. The significant ethanol- and cholesterol-elicited alterations observed in this study suggest the possibility that the changes in metabolic functions in mitochondria and microsomes are controlled, at least in part, by alterations in the phospholipid compositions of these organmicrosomes are controlled, at least In part, by alterations in the phospholipid compositions of these organelles.  相似文献   
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