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PH-EN01

Type 1 diabetes

How autoimmune destruction of the pancreatic beta cells removes insulin, why glucose then stays in the blood and spills into the urine, and why fat and muscle are broken down, which can lead to ketoacidosis.

By the end, you can

  • Describe where insulin is made and how it moves glucose into muscle and fat through GLUT4.
  • Explain how T-cell-mediated autoimmunity destroys beta cells gradually, and what islet autoantibodies show.
  • Relate insulin deficiency to hyperglycaemia, glycosuria, osmotic diuresis and thirst.
  • Explain why insulin deficiency causes weight loss and can progress to diabetic ketoacidosis.
  • Distinguish type 1 from type 2 diabetes by mechanism.
  • Recognise insulitis and the stages of type 1 diabetes, interpret glucose, autoantibody and C-peptide results, and explain how basal and mealtime insulin, closed-loop delivery, teplizumab and transplantation act on the mechanism.

What it is

Type 1 diabetes is diabetes mellitus caused by autoimmune destruction of the insulin-making beta cells of the pancreatic islets, which leads to absolute insulin deficiency. It most often begins in childhood or adolescence but can start at any age. A small minority of people with insulin-deficient diabetes have no sign of autoimmunity (idiopathic type 1 diabetes).

2 types to tell apart
Autoimmune type 1 diabetes
The usual form: islet autoantibodies are present and T cells destroy the beta cells over months to years.
Slowly progressive autoimmune diabetes in adults
Often called LADA. The same autoimmunity, but beta-cell loss is slower, so for a time some insulin is still made and it can be mistaken for type 2 diabetes.

Normal function

Islets, insulin and glucose uptake

The is mainly an exocrine gland that makes digestive enzymes. Scattered through it, a little more densely towards the , are about a million pancreatic islets (islets of Langerhans), clusters of endocrine cells making up only 1–2% of its mass. Most islet cells are beta cells, which make insulin; alpha cells make glucagon, which has the opposite effects.

When blood glucose rises after a meal, more glucose enters the beta cells and is metabolised. The rise in ATP closes ATP-sensitive potassium channels, the cell depolarises, calcium enters and insulin granules are released. Insulin reaches the liver first, through the portal vein, then the rest of the body.

Insulin binds its receptor, a tyrosine kinase, on target cells. In skeletal muscle and fat it moves the glucose transporter GLUT4 from vesicles inside the cell to the plasma membrane, so glucose can enter. In the liver it stops glucose release and promotes glycogen storage; in fat it stops the breakdown of stored triglyceride. Between meals, insulin falls and glucagon rises, releasing stored fuel. In health, fasting plasma glucose stays at about 4.0–5.5 mmol/L (72–99 mg/dL).

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