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      肝組織 및 肺組織에서의 脂肪酸合成調節機轉에 대한 硏究 = Studies on the Regulating Mechanism of Liver and Lung Fatty Acid-Synthesizing System in Rats

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      https://www.riss.kr/link?id=A40004978

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      In starvation and streptozotocin-induced diabetes, the total activities of rat liver and lung acetyl co A carboxylase and fatty acid synthetase are reduced to one third on the normal values. Refeeding of the starved rats and administration of insulin to diabetic rats restores the levels to the original. values.
      A fat-free high-fructose diet which containing 60%w/w fructose enhances the activities of liver fatty acid-synthesizing enzymes 3 to 6 fold over the values of the control group on a laboratory diet, but has no effect on lung fatty acid-synthesizing enzymes. Longterm feeding of fructose diet also increases the activities of liver fatty acid-synthesizing enzymes from diabetic rats to twice the valus of the normal control group on a laboratory diet.
      Insulin administration to fructose-fed diabetic rats restores the enzyme activities to those obtained with the fructose-fed normal control group. But the stimulation of lung fatty acid-synthesizing enzymes of diabetic rats can be effected either by fructose or by insulin.
      In the above mentioned different conditions, plasma free fatty acid levels showed a similar pattern with liver and lung fatty acid-synthesizing enzyme activities.
      In conclusions, 1) A fat-free diet inhibits the synthesizing of liver fatty acid-synthesizing enzyme by one of the components of the fat-containing diet. 2) Liver and lung fatty acid-synthesizing enzyme activites were not under quantitatively identical controls, since the activities of lung enzymes are lowered to about a third in diabetes, whereas the actities of liver enzymes are decreased to about one-twentyfifth of the value for normal animals.
      3) The responses of the liver and lung fatty acid-synthesizing enzymes to insulin is greater and relatively faster than to the fructose diet, and the levels of stimulation of liver and lung fatty acid-synthesizing enzyme activities by the fructose diet and by insulin show very signifigant differences. 4) Fructose can be partially sbustituted for insulin in the restoration of activities of liver fatty acid-synthesizing enzymes could completely restore the Iung fatty acid-synthesizing- enzymes of diabetic rats. 5) These data suggest that the effects of insulin or fructose on fatty acid-synthesizing enzymes are mediated by intermediate. whose concentrations which affected the experimental diabetic rats, and all tissues may not have stringent insulin requirements since the lung enzymes can be stimulated by fructose alone.
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      In starvation and streptozotocin-induced diabetes, the total activities of rat liver and lung acetyl co A carboxylase and fatty acid synthetase are reduced to one third on the normal values. Refeeding of the starved rats and administration of insulin ...

      In starvation and streptozotocin-induced diabetes, the total activities of rat liver and lung acetyl co A carboxylase and fatty acid synthetase are reduced to one third on the normal values. Refeeding of the starved rats and administration of insulin to diabetic rats restores the levels to the original. values.
      A fat-free high-fructose diet which containing 60%w/w fructose enhances the activities of liver fatty acid-synthesizing enzymes 3 to 6 fold over the values of the control group on a laboratory diet, but has no effect on lung fatty acid-synthesizing enzymes. Longterm feeding of fructose diet also increases the activities of liver fatty acid-synthesizing enzymes from diabetic rats to twice the valus of the normal control group on a laboratory diet.
      Insulin administration to fructose-fed diabetic rats restores the enzyme activities to those obtained with the fructose-fed normal control group. But the stimulation of lung fatty acid-synthesizing enzymes of diabetic rats can be effected either by fructose or by insulin.
      In the above mentioned different conditions, plasma free fatty acid levels showed a similar pattern with liver and lung fatty acid-synthesizing enzyme activities.
      In conclusions, 1) A fat-free diet inhibits the synthesizing of liver fatty acid-synthesizing enzyme by one of the components of the fat-containing diet. 2) Liver and lung fatty acid-synthesizing enzyme activites were not under quantitatively identical controls, since the activities of lung enzymes are lowered to about a third in diabetes, whereas the actities of liver enzymes are decreased to about one-twentyfifth of the value for normal animals.
      3) The responses of the liver and lung fatty acid-synthesizing enzymes to insulin is greater and relatively faster than to the fructose diet, and the levels of stimulation of liver and lung fatty acid-synthesizing enzyme activities by the fructose diet and by insulin show very signifigant differences. 4) Fructose can be partially sbustituted for insulin in the restoration of activities of liver fatty acid-synthesizing enzymes could completely restore the Iung fatty acid-synthesizing- enzymes of diabetic rats. 5) These data suggest that the effects of insulin or fructose on fatty acid-synthesizing enzymes are mediated by intermediate. whose concentrations which affected the experimental diabetic rats, and all tissues may not have stringent insulin requirements since the lung enzymes can be stimulated by fructose alone.

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