In vivo control of insulin-sensitive phosphodiesterase in rat adipocytes by growth hormone and its parallelism to glucose transport.

As shown previously in adipocytes of hypophysectomized (hypox) rats, 3-O-methyl-glucose transport is already maximal in the basal state and insensitive to insulin. It is normalized by prolonged administration of GH to hypox rats. This study shows glucose transport in the presence and absence of phosphodiesterase (PDE) inhibitors in the fat cells of normal and hypox rats. Enhanced glucose transport in insulin-stimulated normal fat cells as well as enhanced glucose transport in adipocytes of hypox rats is inhibited by PDE inhibitors. The low Km phosphodiesterase activity, which is known to be acutely stimulated by insulin in normal adipocytes, is found to be increased in the fat cells of hypox rats, and further stimulation by insulin is not possible. Normalization occurs after GH administration for 4 days. Then, the low Km PDE activity is again low and stimulated in the presence of insulin. The similarity between the behavior of the activity of the glucose carrier system and that of the low Km PDE suggests that both may be dependent on a GH-induced membrane factor which would be acutely inhibited by insulin.