During and immediately after a meal, glucose is converted in the liver into the storage polysaccharide glycogen by a process known as glycogenesis.
Although the total quantity of glycogen in the human body is low, considerably less than one-tenth percent of the total body weight, its role is primarily that of a storage carbohydrate, similar to the role of starch in plants cells. It occurs predominantly in the liver where it is important in the homeostatic mechanism regulating glucose level of the blood.
Glycogen is a branched chain polymer of 6,000 to 30,000 glucose units, that contains two types of glycosidic linkages, extended chains of alpha1-- 4 linked glucose residues with alpha 1-- 6 branches spaced about every four to six residues along the alpha 1-- 4 chain. It is similar to amylopectin in structure but is more highly branched. The average chain length is only 10 to 24 glucose units with 3 to 4 glucose units between branching points.
The highly branched structure of glycogen makes it possible for several glucose residues to be released at once to meet energy needs.
Glycogen is stored in two tissues. In the liver, glycogen is stored for the short-termed maintenance of blood glucose. In muscle, glycogen is stored as a source of energy. Muscle glycogen is estimated to have a molecular weight of about 1000000 where as the liver of glycogen molecule is much larger, approximately 5 X 1000000. Both molecules, however, constantly change in size as glucose molecules are added or removed.
Glycogen plays an important role in the glucose cycle. The release of glycogen stored in the liver is triggered by low levels of glucose in blood. Liver glycogen breaks down to glucose-6-phosphate, which is hydrolyzed to give glucose.
The release of glucose from the liver by these breakdowns of glycogen replenishes the supply of glucose in the blood.
The most common disease in which glycogen metabolism becomes abnormal is diabetes, in which, because of abnormal amounts of insulin, liver glycogen can be abnormally accumulated or depleted.
Several hereditary defects have been identified in the synthesis and catabolism of glycogen including: Gierke’s disease, Type II glycogen disease, Type III glycogen, Type IV disease, and McArdle’s disease.
Glycogen in human nutrition
