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Lipogenesis in pyridoxine deficient rats Song, Gil-Won


The purpose of this study was to evaluate the effect of pyridoxine deficiency on lipogenesis in the rat. It is important in studies of this type to standardize not only the food intake but also the feeding pattern of the experimental and control animals. Pair-feeding of the control rats with the deficient ones imposes on the former animals a feeding pattern similar to meal-feeding. The latter pattern elicits several adaptive changes related to energy utilization by the rat. Therefore, an attempt was made to minimize the difference in the feeding frequency between the deprived and control groups by meal-feeding of the former group. The data were compared with those obtained when only food intake was controlled. Male weanling Wistar rats were used in the present studies. The deprived rats were allowed food either ad libitum (nibbling) or for 2 hours each day (meal-feeding). The appropriate controls were given a complete diet in quantities isocaloric with the consumption of the deprived groups. Decreased fat storage as well as feed efficiency in pyridoxine deficient rats were obvious at that time, regardless of the mode of feeding employed. The fatty acid content of the epididymal adipose tissue was affected in the same manner as body fat. Pyridoxine deprivation also suppressed total body fatty acid synthesis in vivo from glucose-U-¹⁴ C, whether the animals were meal-fed or nibbling. However, the rates of fatty acid synthesis in the epididymal adipose tissue of the meal-fed deprived rats tended to exceed those observed in the control. The lipogenic capacity of liver slices from fed nibbling deprived rats exceeded that of the controls, as evidenced by increased fatty acid labelling in the presence of glucose-U-¹⁴C or acetate-1-¹⁴ C. However, when the nibbling deprived rats were fasted and refed prior to sacrifice, the incorporation of acetate-1-¹⁴ C into fatty acids was lower than in the controls. No differences in the labelling of liver fatty acids and glyceride glycerol were observed when the meal-fed deprived rats were compared with their controls. However, pyridoxine deficiency in meal-fed rats was associated with a decrease in the capacity of the liver to oxidize glucose, as comparison with the controls revealed. Epididymal adipose tissue segments from nibbling deprived rats showed less incorporation of ¹⁴C from labelled glucose into CO₂, fatty acids and glyceride glycerol than those from the corresponding controls (expressed on the basis of the deoxyribonucleic acid content of the tissue). In contrast, increased lipogenic potential of adipose tissue preparation from the deprived meal-fed rats in the presence of insulin was observed. In these rats, a decrease in adipocyte size was suggested by lipid/DNA ratio lower than that of the controls. Thus, the increased lipogenic capacity observed was possibly due to a decrease in adipocyte size, itself associated with increased sensitivity to insulin. The activities of glucose-6-phosphate dehydrogenase and malic enzyme were depressed in both the liver and the adipose tissue of the pyridoxine-deprived rats. Since these enzymes are concerned with the production of the NADPH needed for reductive fatty acid synthesis, the results were consistent with the in vivo finding. However, the activities of these enzymes did not appear to limit the in vitro lipogenic potential of the tissues investigated, since NADPH produced from glucose-6-phosphate dehydrogenase and malic enzyme alone seemed to be sufficient to support the rates of lipogenesis seen. The alterations in lipogenesis in pyridoxine deprivation observed in the present and other investigation could not be explained on the basis of the known functions of the pyridoxine-dependent enzymes.

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