Evidence that Insulin Deficiency in the Rat Has Disparate Effects on Fructose 2,6-Bisphosphate Levels in Muscle and Liver*

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Abstract
The level of fructose 2,6-bisphosphate (F2,6P2), a potent stimulator of 6-phosphofructo-1-kinase and inhibitor of fructose 1,6-bisphosphatase, was measured in three different muscle types (tensor fascia latae, biceps femoris, and soleus) and in the liver of normal and diabetic rats. The mean (.+-. SEM) content of F2,6P2 (nanomoles per g tissue) varied among the three types of skeletal muscle in normal rats, with the biceps femoris having the highest (0.97 .+-. 0.15) and the soleus the lowest (0.57 .+-. 0.03) levels. However, these differences were unrelated to simultaneous estimates of skeletal muscle activity of 6-phosphofructo-1-kinase activity. The total concentration of F2,6P2 was more than 8-fold higher (8.5 .+-. 0.9) in the liver, and this value fell to 5.3 .+-. 0.8 (P < 0.05) after the induction of diabetes with streptozotocin. In contrast, F2,6P2 levels did not fall in skeletal muscle of rats with streptozotocin-induced diabetes, and the concentration actually increased. Thus, the fall in hepatic F2,6P2 concentration associated with insulin deficiency was not observed in skeletal muscle.