Metabolic effects of high sucrose or fructose intake.
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Biomedical subjects
Publications and source records attributed to P Fábry.
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The authors studied the pathophysiological mechanisms the early stages of atherosclerosis induced by immunization in combination with short-term intake of dietary cholesterol. The mechanisms involved in the development of lesions comprised impaired endothelial integrity, increased permeability and transmural protein transport in the aorta. The changes were induced by the combined synergic action of immunization and cholesterol diet. Further, their study showed that progression of the thus induced atherosclerotic lesions can be inhibited by histamine and serotonin antagonists. The fact that the latter decreased the extent of endothelial injury, permeability and cholesterol accumulation in the aorta without changing the level of cholesterolaemia indicate that drugs are capable of controlling the pathophysiological processes in the artery participating in atherosclerotic lesions.
The study summarizes the metabolic effects of increased sucrose or fructose intake. Compared with the traditional carbohydrate source-starch, a high intake of the above two carbohydrates produces a number of metabolic and other changes that can have a pathological effect. A thus induced metabolic and other changes that can have hepatic lipid synthesis, hypertriglyceridaemia and increased tissue lipid utilization, while tissue glucose utilization decreases. Moreover, the increase of these carbohydrates can lead to some pathological organ changes and elevation of blood pressure.
Palmitate and glucose oxidation were investigated in isolated hemidiaphragm of rats in which hypertriglyceridemia was induced by dietary fructose. Palmitate oxidation was increased, and glucose oxidation was reduced, in fructose-fed rats, as compared with glucose-fed controls. Glucose incorporation into muscle glycogen was similar in both dietary groups.
Glucose tolerance and in vivo incorporation of glucose into liver glycogen were investigated in rats fed high carbohydrate diets containing glucose or fructose as the sole carbohydrate source. As compared with control glucose-adapted rats, a slight deterioration of the glucose tolerance was observed in fructose-adapted rats. The possivle cause of the deteriorated glucose tolerance in fructose-adapted rats seems to be among others reduced glucose incorporation into liver glycogen and a smaller depression of endogenous glucose production by exogenous glucose.
The effect of the type of dietary carbohydrate on oral glucose tolerance and on in vivo incorporation of labeled glucose or fructose into liver and muscle glycogen in the rat were investigated. The intake of fructose or sucrose reduced, as compared with starch or glucose, glucose incorporation into liver glycogen and caused a slight deterioration of the glucose tolerance. These effects were observed already when 50% of the total dietary carbohydrate was substituted by fructose or sucrose. The incorporation of labeled glucose into muscle glycogen was not affected by the type of dietary carbohydrate. Specific radioactivity of liver and muscle glycogen and the concentration of muscle glycogen after administration of labeled fructose were higher in fructose-adapted than in glucose-adapted rats.
The effect of dietary sucrose, fructose and glucose on the intestinal absorption of fructose and glucose was investigated in adult rats in vivo: Glucose absorption was not affected by the type of dietary carbohydrate, while the absorption of fructose was increased by the ingestion of the sucrose or fructose diet, as compared with the glucose diet. An almost maximal increase of fructose absorption was already observed when the quarter of the total dietary carbohydrates was replaced by fructose. Faecal fructose elimination declined during the feeding experiment. The enhanced intestinal absorption of the fructose load in rats fed the fructose diet was manifested by higher concentrations of fructose, but also of glucose and lactate in the hepatic portal blood.
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Administration of 20 mg/kg cyclophosphamide to unilaterally nephrectomized rats for a period of two weeks significantly increased the ratio of kidney weight to total body weight. This rise is, however, accountable more by the decrease of total body weight than by weight increase of the kidney. The RNA-DNA ratio in the hyperttrophic kidney after cyclophosphamide did not differ significantly from that found in the hyperttrophic kidneys of controls. The results obtained show that in our experimental lay-out cyclophosphamide did not inhibit significantly the compensatory renal hypettrophy. After cyclophosphamide, the hypertrophic kidney produced urine with lower concentrations of endogenous creatinine, all osmotically active substances and potassium than found in controls.
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