1. The metabolism of [U-14C]glucose in perfused resting and contracting diaphragm muscle from normal rats and rats made diabetic with streptozotocin was studied in the presence and absence of insulin. 2. The incorporation of [U-14C]-glucose into glycogen and oligosaccharides was stimulated by insulin under all experimental conditions studied. 3. In the normal perfused resting diaphragm muscle the incorporation of radioactivity from [14C]glucose into lactate and CO2 was not affected by insulin. 4. Periodic contractions, induced by electrical stimulation of the perfused diaphragm muscle in the absence of insulin, caused an increased incorporation of 14C into glycogen and hexose phosphate esters, whereas incorporation of 14C into lactate was greatly decreased. Production of 14CO2 in the contracting muscle was not significantly different from that in resting muscle. Addition of insulin to the perfusion liquid caused a further increase in formation of [14C]-glycogen in contracting muscle to values reached in the resting muscle in the presence of insulin. Formation of [14C]lactate was also stimulated by insulin, to values close to those found in the resting muscle in the presence of insulin. 5. In the diabetic resting muscle the rate of glucose metabolism was very low in the absence of insulin. Insulin increased formation of [14C]glycogen to the value found in normal muscle in the absence of insulin. Production of 14CO2 and formation of [14C]hexose phosphate remained unchanged. 6. In the diabetic contracting muscle production of 14CO2 was increased to values approaching those found in normal contracting muscle. Formation of [14C]lactate and [14C]glycogen was also increased by contraction, to normal values. Only traces of [14C]hexose phosphate were detectable. Addition of insulin to the perfusion medium stimulated formation of [14C]glycogen, to values found in normal contracting muscle. Production of [14C]hexose phosphate was stimulated by insulin, to approximately the values found in the normal contracting muscle. Production of 14CO2 and [14C]lactate, however, was not significantly affected by insulin. 7. These results indicate that the defects of glucose metabolism observed in perfused resting diabetic diaphragm muscle can be partially corrected by contraction, and in the presence of insulin the contracting diabetic muscle has a completely normal pattern of glycogen synthesis and lactate production, but CO2 production remains impaired.

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