Insulin Production: Function, Role & Diseases

Insulin production occurs in the islets of Langerhans in the pancreas. Lack or absence of insulin production leads to type 1 diabetes mellitus

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What is insulin production?

Insulin production takes place in the islets of Langerhans in the pancreas. A lack or absence of insulin production leads to type 1 diabetes mellitus. Insulin is a vital hormone that, along with glucagon, regulates blood glucose levels. It is produced in the ß-cells (beta cells) of the pancreas. The ß-cells are found only in the islets of Langerhans. Derived from the Latin word insula, the islets of Langerhans gave the hormone its name. Insulin has the task of regulating blood glucose levels. To do this, it transports glucose from the blood into the body’s cells. If insulin production is deficient or absent, diabetes mellitus type 1 develops, which is an autoimmune disease. While in diabetes mellitus type 1 there is an absolute insulin deficiency, in diabetes mellitus type 2 there is a relative insulin deficiency. There is plenty of insulin in the blood, but it is not sufficient to transport the glucose into the cells due to insulin resistance of the cells. In the long term, however, type 2 diabetes mellitus can also lead to an insulin deficiency. Insulin synthesis takes place in the islets of Langerhans. In a first step, the messenger RNA is translated into preproinsulin at the ribosomes. This is a protein consisting of 110 amino acids. In the next step, the molecule is folded. This results in two chains that are connected by disulfide bridges. The signal peptide is required for this connection. It is cleaved off after the connection has been made. The actual insulin molecule is formed by a further cleavage of the C-peptide after it has passed through the Golgi apparatus. The insulin molecule then consists of two peptide chains. After production, the individual insulin molecules are stored in the vesicles of the Golgi apparatus. These are located directly on the cell membrane of the insulin-producing ß cells.

Function and purpose

The stimulus for the release of insulin molecules is a blood glucose level of 5 mmol glucose or more per liter of blood. Various amino acids and free fatty acids can also cause secretion and stimulate production. The hormones secretin, GLP-1, GIP and gastrin also stimulate secretion. In particular, glucose-dependent insulinotropic peptide (GIP) plays an important role. It stimulates insulin production and insulin secretion after food intake. Insulin secretion occurs intermittently. Thus, insulin molecules are released into the blood every three to five minutes. A biphasic course can be seen. The first major insulin release occurs three to five minutes after food intake. This first peak lasts for around ten minutes. Here, the insulin molecules come largely from storage. The second phase then lasts as long as there is hyperglycemia in the blood. This phase is mainly determined by newly formed insulin. The insulin-producing cells are very active during this second phase after food intake and produce abundant insulin. In the blood, insulin ensures that glucose is transported from the blood to the target cells. To do this, the hormone binds to special insulin receptors and thus enables the glucose molecules to enter the target cells. Muscle and liver cells have a particularly large number of insulin receptors. They can therefore absorb large amounts of glucose within a very short time and store it in the form of glycogen or convert it to energy.

Diseases and complaints

In type 1 diabetes mellitus, the cells of the immune system target the ß-cells of the islets of Langerhans. Type 1 diabetes mellitus is therefore one of the autoimmune diseases. Why these autoimmune processes occur is still unclear. A genetic predisposition seems to play a decisive role. The autoimmune processes in the pancreas usually proceed insidiously and remain unnoticed for a long time. Only when 80 percent of the ß-cells have been destroyed is insulin production no longer sufficient to lower blood glucose levels. The first symptoms then appear within a few days or weeks. Typical of type 1 diabetes mellitus are increased thirst and a strong urge to urinate. Those affected are tired and fatigued due to the lack of energy. They suffer from dry skin and scaly scalp.An acetone-like odor of the breath is an indication of ketoacidosis and thus also a sign of metabolic derailment. If the cells no longer receive sufficient glucose for energy production, they generate energy from fats. This produces ketone bodies. In large quantities, these cause hyperacidity of the body. A so-called metabolic acidosis develops. Characteristic of this hyperacidity is an obstinate odor in the air we breathe and kissing-mouth breathing. In diabetes mellitus, the ß-cells of the pancreas initially function normally. They produce sufficient insulin, but the cells are insulin resistant. Increasing amounts of insulin are needed to get glucose from the blood into the cells. Despite the increased insulin levels in the blood, hyperglycemia occurs. In this case, therefore, there is not an absolute insulin deficiency, as in type 1 diabetes mellitus, but a relative insulin deficiency. If this condition persists, a vicious circle develops. The ß-cells produce more and more insulin, and at the same time the body’s cells become increasingly insensitive to the hormone. As a result, insulin production increases again. Finally, the cells of the pancreas can become exhausted, so that insulin production is completely or partially stopped. Then, similar to type 1 diabetes mellitus, there is an absolute insulin deficiency.