Glucose Oxidation in Isoproterenol-Stimulated Salivary Glands of the Rat 1

Summary

Administration of isoproterenol (IPR) to rats induced a 2.5-fold increase in submaxillary glands in 10 days, with no changes in the liver and kidney. This hypertrophy was completely prevented when methotrexate was administered concurrently with IPR. Salivary gland slices from fed or fasted animals, unlike diaphragm muscle, produced the same amount of ¹⁴CO₂ from labeled glucose when incubated in the presence, or absence, of insulin. This suggests that, in this tissue, glucose uptake is not dependent upon the presence of insulin. Salivary gland slices produced equal amounts of ¹⁴CO₂ when incubated with glucose-1-¹⁴C or glucose-6-¹⁴C. In contrast, liver slices produced twice as much ¹⁴CO₂ from glucose-l-¹⁴C than from glucose-6-¹⁴C. This suggests that, unlike liver tissue, glucose oxidation in salivary gland cells occurs via the Embden-Meyerhoff pathway plus TCA cycle with little or no pentose shunt activity. Although IPR had no demonstrable effect when added to in vitro, a single in vivo administration of the drug causes a 50% decrease in ¹⁴CO₂ production in salivary gland, but not in liver, slices at 10 hr. A return to normal was seen after 25 hr. Salivary glands that had undergone hypertrophy under the influence of 3 daily injections of IPR, showed no changes in salivary gland glucose oxidation, but an increase in liver activity was seen.