SUMMARY1. The hypothesis that part of the insulin transduction system consists of a co-ordinated stimulation of the Na pump and of Na-H exchange by the hormone (Moore, 1981) requires that insulin plays a physiological role in the regulation of intracellular Na+. Moreover, this model predicts that in hypoinsulinaemic states, such as diabetes and fasting, intracellular pH and intracellular ATP levels would be depressed. The present study tests the hypothesis that in hypoinsulinaemic states intracellular Na+ is increased and intracellular ATP is decreased by measuring these parameters in soleus muscles removed from both diabetic and fasted rats.2. When rats were made diabetic by injection of streptozotocin (SZ) plasma insulin significantly decreased by 24 hr and plasma glucose and triglyceride levels increased.3. Intracellular Na+ was significantly elevated by 48 hr after injection of SZ. The elevation ranged from 18 to 48 % and persisted for the duration of the experimental observation (up to 28 days).4. Intracellular ATP decreased significantly by the seventh day after SZ injection and remained depressed by about 24 % for the duration (35 days) of the observation.5. In one series, a significant negative correlation was seen between plasma insulin levels and intracellular Na+ of both SZ-diabetic animals and their controls.6. Intracellular Na+ also significantly increased when hypoinsulinaemia was induced by fasting.7. Again, intracellular ATP did not decrease until after the elevation ofintracellular Na+. After 72 hr of fasting, intracellular ATP was still decreased in spite of normal plasma glucose levels. 8. Insulin therapy of SZ diabetic rats restored intracellular ATP and plasma glucose to normal, but did not restore intracellular Na+ to normal levels.9. The results confirm two predictions of the 'insulin transduction system model (Moore, 1981). Most strongly supported is that part of the model which indicates that the Na pump is regulated by physiological levels of insulin. This is especially convincing since hypoinsulinaemia produced by a non-pharmacological procedure, fasting, was associated with an increase in intracellular Na+.

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Previous reports of "insulin shock" induced in fish (and frogs) by externally applied insulin have been confirmed. The insulin induced coma can be reversed by either external glucose, sucrose, or epinephrine. Experiments on rainbow trout have shown that the externally applied insulin acts as though it enters the fish in that a typical hypoglycemia is caused. The action of insulin is via the gills and does not require participation of the digestive tract.It has been occasionally reported in physiology laboratory manuals (Zarrow et al., '64; Kalbus and Neal, '69; and Haupt et al., '72) and it seems to be well-known among fish endocrinologists that when insulin is added to the water in which a fish is swimming, a condition termed "insulin shock can be induced in the fish. It is at least implicit in the descriptions of this phenomenon that the externally applied insulin somehow crosses the fish gill and enters the circulation of the fish where the insulin then has its usual physiological effect of lowering the blood glucose concentration to an extent which induces a hypoglycemic coma. Associated with these descriptions and explanations is the concomitant observation that the comatose fish can be revived by placing them in a 2% glucose solution. Again, it is at least suggested in explaining this phenomenon that the external glucose diffuses into the fish, across its gills, and then increases the plasma glucose level to a degree which will support normal neural function.The notions that either glucose or insulin can enter a fish's circulation from the external solution have been supported by various other studies. When goldfish (Carassius auratus) are maintained in glucose solutions, both chronic hyperglycemia and hepatic fat deposition are found to result (Schuster-Woldan, '36; and Sterne, '67). Also, Kohler ('63) reported that the hepatic fat deposition associated with keep ing fish in glucose solutions can be reversed by adding insulin to that glucose solution.

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