During the Absorptive Phase, the Liver Takes up Glucose and Converts It into Glycogen and Triglyceride
When a meal is ingested, insulin secretion begins even before maximal absorption of glucose is achieved. This secretion is stimulated by the action of gastric inhibitory peptide (see Chapter 27) and perhaps other enteric hormones.
Early insulin secretion ensures that the liver and other tissues will be"primed'' and ready for the arrival of glucose from the gut. A large portion of the glucose absorbed postprandially is taken up by the liver as portal blood traverses the hepatic sinusoids. Under the influence of insulin, glucose in the liver is directed into glycogen synthesis. The net effect is that glucose from the digestion and absorption of carbohydrate is stored in the liver during absorptive periods. This process moderates the flow of glucose from the gut to the general circulation and keeps blood glucose concentrations from becoming excessively high during the digestion of a carbohydrate meal. Insulin exerts its stimulatory effect on hepatic glycogen synthesis by stimulating intracellular metabolic pathways that lead to the formation of glycogen. These effects are discussed further in reference to the counterbalancing effects of glucagon.The amount of glycogen that can be stored in the liver is limited and, under normal conditions, probably never exceeds 10% of the total weight of the liver. In humans, this represents about IOO g of glycogen, and a proportionately similar limit likely exists for the storage of glycogen in the livers of other species. This amount of glycogen does not account for all the glucose taken up by the liver during the digestion and absorption of a large carbohydrate meal; therefore, some additional mechanism must exist for the disposal of excess glucose. If there were no such alternatives for glucose disposal, blood glucose concentrations could rise out of control after glycogen stores had reached their maximum. Fatty-acid synthesis offers an alternative mechanism for glucose removal.