Insulin can be the only hormone in the body to lower the blood sugar level in the blood. Insulin synthesis is always necessary if carbohydrates are added during food intake. Insulin synthesis takes place in the Langerhans cells of the pancreas.
If too little insulin is produced, there is an increase in blood sugar because the glucose is no longer transported into the cells. An excessive insulin synthesis leads to low blood sugar (hypoglycaemia) with food cravings, restlessness and impending nerve damage.
The insulin synthesis takes place at intervals and is always stimulated by food intake. When the carbohydrate intake is lowered by starvation, for example, the blood sugar level drops. Glucagon increasingly forms as the antagonist of insulin. Glucagon raises blood sugar levels through gluconeogenesis. As a result, the secretion of insulin decreases and its synthesis is restricted.
Overall, insulin synthesis is part of a complicated regulatory mechanism for keeping blood sugar levels constant.
The supply of insulin ensures the supply of energy and bodybuilding to the body. Insulin has an anabolic effect on the metabolism. Insulin delivery involves both insulin synthesis and insulin secretion.
Insulin is produced and stored in the Langerhans islet cells of the pancreas. When the blood sugar level rises, glucose enters vesicles inside the beta cells of the islets of Langerhans, which release immediately stored insulin. At the same time the insulin synthesis is stimulated.
Initially, an inactive preproinsulin molecule with 110 amino acids is formed on the ribosomes. This preproinsulin consists of a signal sequence with 24 amino acids, the B chain with 30 amino acids, additionally two amino acids and a C chain with 31 amino acids, further two amino acids and an A chain with 21 amino acids.
After its formation, the stretched molecule is folded by forming three disulfide bridges. Two disulfide bridges connect the A and B chains, respectively. The third disulfide group is within the A chain. The preproinsulin is initially in the endoplasmic reticulum. From there it is transported through the membrane to enter the Golgi apparatus.
During the membrane passage of the ER, the signal peptide is split off, which then remains in the cisterns of the endoplasmic reticulum. After cleavage of the signal sequence forms proinsulin, which has 84 amino acids. After being admitted to the Golgi apparatus, it is stored there.
If there is a stimulus to release, the C chain is cleaved off by the action of specific peptidases. Now insulin forms, which consists of an A chain and a B chain. The two chains are interconnected only by two disulfide bridges. A third disulfide group is located within the A chain to stabilize the molecule.
Insulin is then stored in the vesicles of the Golgi apparatus in the form of zinc-insulin complexes. This forms hexamers that stabilize the structure of insulin. The release of insulin is triggered by certain stimuli. Increasing blood sugar levels is the most important triggering stimulus. But also the presence of various amino acids, fatty acids and hormones have a stimulating effect on insulin secretion.
Triggering hormones include secretin, gastrin, GLP-1 and GIP. These hormones always form when ingested. After ingestion, insulin secretion occurs in two phases. In the first phase, the stored insulin is released, while in the second phase of its resynthesis takes place. The second phase is completed only with the cessation of hyperglycemia.
If the insulin synthesis is disturbed, there is an increase in blood sugar levels. Chronic insulin deficiency is referred to as diabetes mellitus. There are two types of diabetes, type I diabetes and type II diabetes.
Type I diabetes is an absolute lack of insulin. Due to the absence or due to a disease of the islets Langerhansschen too little or no insulin is produced. The causes are severe inflammation of the pancreas or autoimmune diseases in question. The blood sugar level is extremely high in this form of diabetes. Without insulin substitution, the disease leads to death.
Type II diabetes is caused by a relative lack of insulin. This produces enough insulin, with even more insulin secretion. However, insulin resistance is increased because the effectiveness of insulin is reduced due to lack of receptors. The pancreas needs to produce more insulin to achieve the same effects. This increased insulin synthesis leads in the long run to the exhaustion of the islets of Langerhans. It develops a type II diabetes.
In the context of hormonal regulation disorders, it can also lead to increased blood sugar levels. Thus, increased cortisol activity leads to increased glucose from amino acids through gluconeogenesis. As a result, the insulin synthesis is permanently stimulated to lower the blood sugar level again. The excess glucose is transported into the fat cells, where increased fat accumulation takes place. It forms a Stammfettsucht. The disease is known as Cushings syndrome.
A permanently high insulin synthesis can also be triggered by a tumor in the islets of Langerhans. It is a hyperinsulinism that is often triggered by an insulinoma and leads to repeated hypoglycaemia.