How do adipose and liver respond to insulin during the absorptive phase?

In response to elevated glucose levels, insulin is released from the pancreatic islets. Insulin interacts with plasmalemmal receptors of a number of different cell types. Most important are the actions of insulin and hepatic cells, muscle cells and adipose tissue cells. In each case, the effect of insulin is to enhance the uptake of glucose into the cells, where it is metabolized and stored as glycogen or used as an energy substrate in synthesis of protein or fats.
Within the liver, insulin activates glycogen synthase, which produces a direct flow of glucose towards glycogen formation. Glucokinase activity is enhanced, which provides a pool of glucose-6-phosphate that is then converted to glucose 1 phosphate and to uridine diphosphoglucose. Conversion of intracellular glucose to glucose-6-phosphate prevents glucose release from hepatocytes.
In fat cells, insulin-stimulated glucose uptake results in enhanced catabolism of the sugar to glycerol. Insulin activation of endothelial cell lipoprotein lipase results in the release of Free fatty acids from chylomicrons. These fatty acids are then transported into fat cells where they combine with glycerol to form triglycerides and are added to the lipid droplets within the fat cells. Lipid synthesis is stimulated by insulin via an activation of citrate lipase, acetyl- CoA carboxylase, fatty acid synthase and glycerol-3-phosphate dehydrogenase.