Effects of physical training on fatty acid metabolism in liver and skeletal muscle of rats fed four different high-carbohydrate diets
1996
Garrido, G. | Guzmán, M. | Odriozola, J.M.
The adaptation of regulatory enzymes of fatty acid metabolism to endurance training and to the administration of four different diets containing fructose, sucrose, maltodextrins, or starch as carbohydrate (CH) was studied in rat liver and skeletal muscle (soleus). (i) In the soleus, physical training induced carnitine palmitoyltransferase I (CPT-I) activity upon complex (but not simple) CH feeding, whereas citrate synthase activity was enhanced by endurance exercise in the four different diets. No effect of diet or training was evident on glycerol 3-phosphate acyltransferase (G3PAT) activity or intramuscular triacylglycerol content. Glycogen levels were notably diminished in the soleus of trained rats fed simple-CH diets compared with their corresponding sedentary controls. (ii) In liver, CPT-I activity was depressed in trained animals fed the fructose diet, whereas citrate synthase was induced by endurance exercise in the four different diets. The activity of key lipogenic enzymes (acetyl-CoA carboxylase, fatty acid synthase, G3PAT) was induced by simple-CH feeding, and this increase was blunted by physical exercise. However, triacylglycerol accumulation and glycogen depletion ensued in liver of trained rats fed simple-CH diets. In these animals this was accompanied by a remarkable decrease of serum triacylglycerol levels and a strong increase of circulating non-esterified fatty acids (NEFA) and glycerol. Results thus suggest that in trained rats fed simple-CH diets (i) the preferential mobilization of adipose tissue triacylglycerols, by increasing the availability of circulating NEFA, may be responsible for liver triacylglycerol accumulation as well as for liver and muscle glycogen depletion, and (ii) decreased triacylglycerol secretion by the liver--but not changes in the activity of regulatory lipogenic enzymes--may be involved in hepatic triacylglycerol accumulation.
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