Abstract
The metabolic fate of glucose in isolated muscle after addition of insulin was shown to be dependent upon the functional state of the tissue. While nonstimulated muscle responded primarily with an increased incorporation of glucose into glycogen, stimulated muscle showed predominantly an increased conversion of labeled glucose to CO2 following insulin addition. The oxidation of palmitic-I-C14 acid by muscle was not influenced by the presence of insulin. Ryanodine, used as a chemical agent for inducing contraction of diaphragm, resulted in stimulation of oxygen consumption, fatty acid oxidation and glucose oxidation to an extent comparable to that previously achieved with electrical stimulation of muscle. The conclusion was reached that insulin increased the oxidation of glucose but not of palmitate, and that the specific metabolic fate of intracellular glucose is not influenced by insulin. The data are discussed in relation to the prevailing theory that insulin acts by increasing permeability of muscle cell membranes to certain substrates.