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Glycogen metabolism in meal-fed pyridoxine-deficient rats Mellor, Ruth Marie


Pyridoxine-deficient rats are known to exhibit little, if any, weight gain; they also have decreased fat stores in comparison with their pair-fed controls. The defect in energy metabolism responsible for this phenomenon is not well understood at present. This study was undertaken to investigate some aspects of glycogenesis and glycogenolysis in order to add to the present information on energy metabolism in the pyridoxine deficiency state. Meal-fed animals were used, in order to eliminate differences due to the mode of feeding between the experimental and the pair-fed control animals. Male weanling rats were fed a pyridoxine-deficient diet in one 2-hour daily meal, while the controls were pair-fed. This eliminated differences due to feeding frequency when these groups were compared with each other. Aspartate amino-transferase and alanine aminotransferase activities were assayed in liver and erythrocytes in order to verify the presence of a pyridoxine deficiency state under the conditions used in this laboratory. The activities of glycogen phosphorylase, the rate-limiting enxyme in glycogenolysis, and glycogen UDP-glucosyltransferase were assayed in liver and muscle. Glycogen storage in these tissues was also measured. Finally, the incorporation of labelled carbon atoms into blood glucose and liver glycogen following intraperitoneal injection of L-alanine-¹⁴C was assayed. Glycogen phosphorylase activity was reduced in pyridoxine-deficient animals. This defect was not accompanied by a concomitant increase in the deposition of glycogen. There was, therefore, the possibility of a decreased ability to form glycogen. Glycogen UDP-glucosyltransferase activity was normal in muscle and elevated in liver indicating, if anything, an unimpaired ability to synethesize glycogen from UDPG. A trend towards a lesser incorporation of labelled carbon atoms into the blood glucose by the pyridoxine-deficient group appeared when the results were expressed as a percent of administered dose per ml. This became statistically significant when the data was expressed in terms of the circulating glucose pool. Although not at a statistically significant level, there was a greater incorporation of labelled carbon atoms into the liver glycogen of the pyridoxine-deficient group. It appeared from these findings that the defect in energy metabolism in pyridoxine deficiency may be the result of a reduced availability of carbon skeletons and occurred prior to the formation of glycogen. Further study in this area is necessary to reveal the exact point at which energy loss occurred.

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