Actual Glucose Concentration Research Articles

Ketogluconate formation by Gluconobacter species

When G. oxydans ATCC 621-H was grown in batch culture in a complex medium with glucose, ketogluconates were produced when the pH in the culture was maintained at 5.5. Without pH control gluconate was the only product of glucose oxidation, but at pH 5.5 the gluconate so produced was further oxidized to ketogluconates. Production of ketogluconates started when glucose was almost completely exhausted. It was shown that the actual glucose and gluconate concentrations in the culture do not determine the onset of ketogluconate formation during growth. Both 2 and 5 ketogluconate were produced. Addition of CaCO3 to the medium favored the production of 5 ketogluconate. However, under these conditions minor quantities of 2 ketogluconate were also formed. The sequential production of gluconate and ketogluconates from glucose was not only restricted to G. oxydans ATCC 621-H. A number of G. oxydans strains when grown under standard conditions in a pH controlled batch culture, all produced ketogluconates from glucose via an intermediate accumulation of gluconate. Although the ratios of the ketogluconates produced varied from strain to strain, all strains produced both 2 and 5 ketogluconate.

Pathophysiological aspects of glucose uptake by the tumor tissue under various conditions of oxygen and glucose supply.

Earlier examinations of the glucose uptake in neoplastic tissue by isolated DS- Carcinosarcoma implanted into the rat kidney had the results as follows (VAUPEL, 1974): 1. An increase of the tumor mass from 3 to 13 g wet weight caused an exponential decrease of the glucose consumption by the tumor tissue from 44.4 to 6.7/umoles per 100 g/min; very young tumors of 3 – 4 g bad uptake rates from 27.8 to 44.4/umoles/100 g/min. 2. Simultaneous measurements of the mean actual glucose concentrations in the tumor tissue showed that in the very young tumors the concentration still ranged from 1.75 to 2.25/umoles/g wet weight, whereas those in old tumors drop as low as 0 to 0.17/umoles/g.

Correlation between the effects of several substances on food intake and on the hepatic concentration of reducing sugars

Food intake, and concentration of reducing sugars in blood, liver, muscle and adipose tissue were determined after intraperitoneal injections of: adrenaline, noradrenaline, glucose, insulin and amphetamine. Excluding amphetamine, the changes in liver sugar concentration, measured in 23 hr fasted or non-fasted rats, showed a significant inverse correlation with the changes in food intake of rats eating for 1 hr daily ( r=−0.98; p<0.01 and r=−0.94; p<0.001 respectively), while those of muscle and adipose tissue did not. The blood glucose of fasted rats did not show any correlation with food-intake. On the other hand, amphetamine produced a smaller increase in liver reducing sugars than that expected from the above correlation and no increase in blood sugar, but elicited a reduction of liver glycogen similar to that produced by the isoanorexigenic dose of adrenaline. Moreover, the anorexigenic effects of both adrenaline and amphetamine decreased significantly in rats with reduced liver glycogen. These observations appear to support the hypothesis that liver glucoreceptors play an important role in the control of food-intake. The results of amphetamine suggest that stimulus for these receptors may not be the actual glucose concentration, but the rate of glucose change (−dGl/dt). A decreasing glucose concentration in the liver cells would produce hunger signals, while an increasing concentration would stop these signals.