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. / Land and Food Systems, Faculty of / Graduate
| Identifer | oai:union.ndltd.org:UBC/oai:circle.library.ubc.ca:2429/32932 |
| Date | January 1973 |
| Creators | Mellor, Ruth Marie |
| Publisher | University of British Columbia |
| Source Sets | University of British Columbia |
| Language | English |
| Detected Language | English |
| Type | Text, Thesis/Dissertation |
| Rights | For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use. |
Page generated in 0.014 seconds