1. Insulin release is triggered by the rise in glycemia level above 1.2 g/L. The graph shows that a rise in glycemia is followed by an increase in insulinemia which suggests a cause-effect relationship between the two.
2. Insulin is a protein that would be digested by digestive proteases if administered orally.
3. Experiment A: since the dog was starving before and after insulin injection, the change in glycemia is due to the liver. In fact, glycemia in the subhepatic vein was 0.9 g/L while it was 0.82 g/L before the injection of insulin. This shows that the liver was secreting glucose into the bloodstream to increase glycemia.
Following the injection of insulin, glycemia dropped in both the artery and the vein but, more importantly, the two values were now closer to each other which suggests that the liver is not secreting much glucose anymore. This shows that insulin inhibits the secretion of glucose by the liver thus contributing to lowering glycemia.
Experiment B: the ablation of the pancreas leads to a decrease in the hepatic glycogen level until it reaches a value that is less than 1 g/100g of liver. The subsequent injection of insulin increases this value. Hence insulin stimulates the synthesis of hepatic glycogen and its storage in the liver.
Experiment C: the amount of glucose absorbed by the muscle and that of glycogen present in the muscle both increase in presence of insulin. This shows that insulin acts upon muscle cells by increasing their absorption of glucose and the synthesis of muscular glycogen. Actually the absorbed glucose is stored in the form of glycogen.
Therefore insulin lowers glycemia by acting upon hepatic cells and inhibiting the release of glucose by these cells and promoting the storage of glucose in the form of hepatic glycogen. Insulin also acts upon muscle cells promoting their absorption of glucose and its storage as glycogen.
4. Review the course.
5. When beta cells of the islets of Langerhans secrete insulin into the bloodstream, insulin circulates and reaches its target cells. Insulin binds to specific membranous receptors of its target cells which triggers the formation of intracellular second messenger molecules. This leads to a series of modifications in the target cells that result in an increase of cellular permeability to glucose and promotes the storage of the absorbed glucose in the form of glycogen.