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 non-starving animals, serum immuno-reactive
insulin (IRI) was significantly lower in
pyridoxine-deficient rats than in pair- or ad libitum-fed controls. Liver
glucokinase activity in
pyridoxine-deficient rats was also significantly lower than in ad libitum-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 libitum-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 X 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 two 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. Thus
glucose starvation in
pyridoxine-deficient rats is one factor responsible for
fatty liver formation. Possible mechanisms of this phenomenon are discussed.