What is Type 1 Diabetes Mellitus?

The pancreas has many functions. It produces digestive juices and releases them into the intestine, where they break down food so it can be absorbed through the intestinal lining. This part of the pancreas is called the exocrine gland (exocrine: secreting outward).

The pancreas produces insulin
Inside the pancreas are many small glands called the islets of Langerhans. These glands release their messenger substances (hormones) into the bloodstream (endocrine glands). The islets consist of different cells: alpha cells, beta cells, and others. These cells produce hormones. Alpha cells produce glucagon, beta cells produce insulin, and other cells produce hormones such as amylin, somatostatin, pancreatic polypeptide, and ghrelin.

The body’s cells need blood sugar (glucose) as fuel to maintain their energy balance. Glucose in the blood comes partly from food and partly from organs such as the liver and kidneys, which release it into the bloodstream.

Insulin is the cell’s energy supplier
Cells require insulin for glucose to enter. Glucose is the cell’s energy source. Without insulin, only a small amount of glucose can enter the cell — too little to meet its energy needs. Therefore, an active transport mechanism is needed to move glucose into the cell. Insulin binds to a specific structure (the insulin receptor) on the cell surface, triggering a transport system that moves glucose across the cell membrane.

Type 1 Diabetes: Pancreatic beta cells are destroyed
Type 1 diabetes mellitus is a disease in which beta cells are destroyed, meaning little or no insulin is produced. The body’s own immune system, which normally kills invading bacteria and viruses, destroys the beta cells. This malfunction of the immune system is called an autoimmune disease. When about 90% of the beta cells are destroyed, blood sugar levels rise. The disease progression varies: in children, beta cells are destroyed quickly; in adults and older people, the process can take years. The duration of this destruction also depends on genetic markers, such as the HLA system (Human Leukocyte Antigen system).

Inheritance plays only a minor role in Type 1 Diabetes
A genetic predisposition is required to develop type 1 diabetes, but it is less pronounced than in type 2 diabetes. If you have a first-degree relative with type 1 diabetes, the risk of developing it yourself is less than 5%. In addition to the genetic basis, a triggering factor is required — not yet precisely known. It is speculated that viruses may initiate the autoimmune process. In type 2 diabetes, this risk is much higher.

What are the external signs of Type 1 Diabetes Mellitus?
The disease often appears in children and young adults (<30 years), but older adults can also develop it. In children and young adults, insulin deficiency occurs suddenly, leading to a rapid and significant rise in blood sugar levels, causing increased urination, excessive thirst, weight loss, nausea, vomiting, and abdominal pain.

In acute, uncontrolled type 1 diabetes, the breath may smell of acetone (similar to nail polish remover), deep labored breathing (Kussmaul breathing) occurs due to blood acidification, muscles feel heavy, and coma can develop. This is a life-threatening emergency.

Why is artificial insulin supply necessary in Type 1 Diabetes Mellitus?
Currently, there is no way to stimulate beta cells in type 1 diabetes to produce insulin again. Therefore, insulin treatment is always necessary. It must be given in such a way that blood sugar levels normalize. With modern insulin therapy, this is usually achievable.

If blood sugar control is poor, long-term complications can occur after 5–10 years, affecting the eyes, kidneys, nerves, blood vessels, and the heart. These complications reduce quality of life and life expectancy. With good blood sugar control, they can be avoided.

LADA – Type 1 Diabetes Mellitus in late adulthood and older age
In adults and older people, an autoimmune process can also occur, slowly destroying the beta cells over years. The typical signs of type 1 diabetes are rare in LADA, so patients are often misclassified as type 2. If these patients are severely overweight, initial treatment may involve oral antidiabetics like in type 2 diabetes. However, as insulin production gradually decreases, insulin therapy becomes necessary over time.

Type 1 Diabetes Mellitus – Summary

Category

Key Points

Organ & Function

Pancreas: exocrine part → digestive enzymes; endocrine part (islets of Langerhans) → hormones (α-cells: glucagon, β-cells: insulin, others: amylin, somatostatin, PP, ghrelin).

Glucose Use

Glucose is main fuel; needs insulin to enter cells via insulin receptor → active transport mechanism.

Pathophysiology

Autoimmune destruction of β-cells → little/no insulin production. Trigger: immune system attacks own tissue.

Extent of Damage

Symptoms occur after ~90% β-cell destruction.

Onset Pattern

Children: rapid onset; Adults: gradual (months–years). Influenced by genetic markers (HLA).

Genetics

Risk if 1st-degree relative <5%; less genetic influence than type 2; triggering factor likely viral.

Typical Age & Presentation

Common in children/young adults (<30 y), but can occur at any age. Symptoms: polyuria, polydipsia, weight loss, nausea, vomiting, abdominal pain.

Acute Complications

Diabetic ketoacidosis: acetone breath, Kussmaul breathing, heavy muscles, risk of coma, life-threatening.

Treatment

Lifelong insulin therapy required; goal: normalize blood glucose.

Prognosis

Poor control → complications (eye, kidney, nerve, vascular, cardiac) in 5–10 years; good control prevents these.

Special Form – LADA

Late Autoimmune Diabetes in Adults: slow β-cell loss, often misdiagnosed as type 2; initial oral therapy possible, eventual insulin needed.