In order to elucidate the day-by-day development of
low T3 syndrome, we made rats diabetic by an injection of
streptozotocin. Untreated controls killed at day 0 and rats treated for 8 days with
insulin after they had received
streptozotocin served as controls. Sub-groups of animals were killed 1, 2, 3, 4 and 8 days after
streptozotocin. In serum, heart and liver, T3 was depressed to less than 50% of controls at day 4, whereas the
insulin-treated rats differed from controls only as to heart T3. Heart
iodothyronine 5'-deiodinase activity was depressed to a minimum at day 3 and depression was not prevented by
insulin. Liver
iodothyronine 5'-deiodinase activity had not reached a minimum at day 8, and again,
insulin treatment did not normalize this parameter. T3 contents and
iodothyronine 5'-deiodinase activity in brown adipose tissue did not differ from values in controls at any point of time. Thus, in the rats with
low T3 syndrome induced by
streptozotocin-diabetes, a lowered
iodothyronine 5'-deiodinase activity is not fully inhibited by
insulin treatment, whereas the T3 content in the liver is re-established during an observation period of 8 days. A direct toxic effect of
streptozotocin seems unlikely as an in vitro study showed no influence of
streptozotocin on
iodothyronine 5'-deiodinase activity in the liver. The study thus indicates that
iodothyronine 5'-deiodinase activity in the heart and liver is depressed in experimental diabetes, despite near optimal regulation of
blood glucose, and we suggest that lowered intracellular T3 production could, after some time, result in a hypothyroid state in different tissues.