Metabolic Effects of Insulin

Insulin's major targets are muscle (both cardiac and skeletal), adipose tissue, and liver, the most important responses of these targets, and liver, and the most important responses of these targets are summarized in Figure 1. Compare Figure 1 to Figure 3 and you will see that these responses to insulin are the same as the events of the absorptive-state pattern. Conversely, the effects of a reducing in plasma insulin are the same as the events of the postabsorptive pattern in Figure 4.

The first step in the biochemical sequence of events that lead to the responses summarized in Figure 1 is the binding of insulin to specific receptor on the outer surface of the plasma membrane of its target cells. The insulin activated receptor is a tyrosin kinase enzyme, which catalyzes its own phosphorylation using ATP. This autophosphorylation is necessary for the insulin receptor to trigger the next steps in the sequence to the cell's responses, that is, to initiate the signal transduction mechanism. In some case, the insulin receptor inhibits adenylyl cyclase, thereby reducing the intracellular cyclic AMP concentration, but in most cases the signal transduction mechanisms remain unclear, involving as yet unidentified second messengers.

Whatever the signal mechanisms are, the final steps of the sequences leading to the cell's responses are changes in the target-cell's membrane transport and/or enzymes. Figure 2 shows some of the specific biochemical reactions that underlie these ultimate responses.