Glucagon does not modulate the alterations in T3 metabolism consequent to dietary manipulation and diabetes.

Abstract

Low serum T3 levels and hyperglucagonemia are characteristic features of a number of catabolic states such as fasting and uncontrolled diabetes. The present study was performed to elucidate the relationship between this hyperglucagonemia and T3 metabolism. Serum glucagon and T3 and hepatic T4-5'-deiodinase activity (T4 leads to T3) were examined in groups of rats (T4-treated) fed (chow versus carbohydrate), fasted, or diabetic (streptozotocin 100 mg/kg i.p.) for 48-72 h. In the carbohydrate-fed (20% glucose in H2O ad libitum) group the mean serum T3 concentration and mean hepatic T4-5'-deiodinase activity were significantly higher (P less than 0.01) and the mean serum glucagon level significantly lower (P less than 0.05) than the respective means in the chow-fed control group. The mean serum T3 concentration was significantly less (P less than 0.05) in both the fasted (72 h) and diabetic (72 h) groups compared with the control mean, whereas the mean serum glucagon values were similar to the chow-fed group. The mean hepatic T4-5'-deiodinase activity was low in the diabetic group (P less than 0.05) but similar in the fasted group compared with the chow-fed control. A significant inverse correlation (r = -0.9; P less than 0.001) was noted between these alterations in serum T3, hepatic T4-5'-deiodinase activity, and serum glucagon, suggesting that glucagon could be a modulator of T3 metabolism. Hyperglucagonemia was induced in the glucose-fed group with a continuous glucagon infusion for 48 h (0.15 micrograms/kg/min s.c.).(ABSTRACT TRUNCATED AT 250 WORDS)