Role of glucose on fatty liver formation in pyridoxine-deficient rats.

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Abstract
Studies were made on whether glucose starvation causes fatty liver in pyridoxine-deficient male Wistar rats. Pyridoxine deficiency resulted in significantly lower levels of liver glucose than in pair-fed controls but no significant change in the serum glucose concentration. In nonstarving animals, serum immunoreactive insulin (IRI) was significantly lower in pyridoxine-deficient rats than in pair- or ad lib-fed controls. Liver glucokinase activity in pyridoxine-deficient rats was also significantly lower than in ad lib-fed controls. The extent of insulin deficiency was evaluated by examining the effect of administration of insulin on pyridoxine-deficient rats. Administration of insulin had no effect on the activity of liver glucokinase in pyridoxine-deficient rats but induced the enzyme in ad lib-fed controls. In response to a decrease in the activity of liver glucokinase or hexokinase in the deficient group, glycolytic activity, estimated as lactate production from glucose in the liver supernatant spun at 100,000 .times. g, was reduced to half the control level in pyridoxine-deficient rats. The effects of glucose administration on the liver lipid content, serum insulin and serum glucose were investigated. The serum glucose concentration was not significantly different in pyridoxine-deficient and control rats at any time after the glucose load. The level of serum IRI after the load was similar in the 2 groups after 30 min but then gradually decreased in the deficient group. The liver lipid content of the deficient rats tended to decrease whereas that of the controls remained unchanged throughout the experiment. Glucose starvation in pyridoxine-deficient rats is 1 factor responsible for fatty liver formation. Possible mechanisms of this phenomenon are discussed.