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Microbiochemical studies on changes of phosphofructokinase and glucose-6-phosphate dehydrogenase activity in intima and media of aortic wall of rabbits in the course of cholesterol feeding.
Authors:F Numano  M Kobayashi  T Kuroiwa  T Takahashi  K Moriya
Affiliation:Institute for Cardiovascular Diseases, Tokyo Ika-Shika National University, Bunkyo-ku, Tokyo Japan
Abstract:The activities of phosphofructokinase (PFK), a key enzyme in the Embden-Meyerhof pathway, and glucose-6-phosphate dehydrogenase (G-6PDH), enzyme in the Warburg-Dickens pathway, were analyzed in the intima and media of aortic wall of rabbits by Lowry's quantitative histochemical method as modified by us. These rabbits were treated with a one-shot administration of cholesterol (1 g/kg PO) and epinephrine (1 μg/kg iv) or fed with 150 g pellets containing 1% of cholesterol for 1, 2, 5, and 15 wk.PFK in the intima exhibited a statistically significant decreased activity in one-shot treated rabbits, then restored to normal level in cholesterol-fed rabbits for 1 and 2 wk. A statistical significant decrease of this enzyme activity was observed in cholesterol-fed rabbits for more than 5 wk. The media showed the highest activity in the 1 wk cholesterol-fed rabbits (p < 0.05), then the gradual decrease towards cholesterol feeding. Decreased activity was also present in rabbits after 15 wk cholesterol feeding.On the other hand, G-6PDH showed an inclination toward the reverse change of PFK. One-shot treated rabbits showed an increased activity in both the media and intima of the aortic wall and rabbits fed with cholestrol for 1 and 2 wk revealed almost the same activity as those of rabbits fed with a regular diet. Gradual increase in this activity was observed in rabbits fed for more than 5 wk. However, there was not a statistically significant difference between the placebo control group and the treated group in the analysis of G-6PDH activity in both the intima and media of aortic wall.That change of these enzyme are possibly a protective reaction in the cells of the arterial wall against the atherogenic process.
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