Diabetes

A chronic metabolic disease characterised by elevated blood glucose levels (hyperglycaemia) due to defects in insulin secretion, insulin action, or both.

An autoimmune condition in which the immune system destroys pancreatic beta cells in the islets of Langerhans, resulting in absolute insulin deficiency.

Inflammation of the pancreatic islets, often caused by immune cell infiltration, and associated with the development of type 1 diabetes.

A combination of genetic susceptibility and environmental factors triggers an autoimmune response against pancreatic beta cells, progressively reducing insulin production.

Genetic susceptibility, particularly variants in HLA class II genes (especially HLA-DR and HLA-DQ), which influence antigen presentation and autoimmune responses. Other associated genes include INS, PTPN22 and CTLA4.

Viral infections, particularly enteroviruses, may contribute to triggering autoimmunity in genetically susceptible individuals. Other potential factors include early-life environmental exposures. No single environmental trigger has been definitively established.

Stage 1: Multiple islet autoantibodies are present, but blood glucose levels are normal and there are no symptoms. Stage 2: Multiple islet autoantibodies and dysglycaemia are present, but there are no symptoms. Stage 3: Clinical diabetes develops, with significant beta-cell loss, hyperglycaemia and possible symptoms such as polyuria, polydipsia and weight loss.

A chronic metabolic disease characterised by insulin resistance and progressive pancreatic beta-cell dysfunction, resulting in insufficient insulin action and persistent hyperglycaemia.

Genetic variants can affect insulin secretion, beta-cell function, insulin sensitivity and glucose metabolism, increasing susceptibility to type 2 diabetes.

Physical inactivity, excess energy intake, an unhealthy diet, obesity and ageing can increase insulin resistance and contribute to beta-cell dysfunction.

Insulin resistance, progressive beta-cell dysfunction, relative insulin deficiency and increased hepatic glucose production, resulting in chronic hyperglycaemia.

Excess adipose tissue releases increased free fatty acids and inflammatory mediators, which disrupt insulin signalling. Ectopic fat accumulation in the liver and skeletal muscle also contributes to insulin resistance.

Impaired insulin receptor signalling, reduced GLUT4-mediated glucose uptake, increased free fatty acids, chronic inflammation, ectopic lipid accumulation and mitochondrial dysfunction.

Impaired insulin signalling reduces GLUT4 translocation to the cell membrane, decreasing glucose uptake. Reduced glycogen synthesis, intramuscular lipid accumulation and impaired mitochondrial function can also contribute to insulin resistance.

Genetic predisposition, ageing, physical inactivity, hormonal disorders such as Cushing's syndrome and acromegaly, certain medications such as glucocorticoids, and lipodystrophy.

No. Insulin resistance can occur without diabetes because pancreatic beta cells may compensate by secreting more insulin. Type 2 diabetes develops when insulin secretion is no longer sufficient to overcome insulin resistance and maintain normal blood glucose levels.

Pancreatic beta cells initially increase insulin secretion to compensate for insulin resistance, maintaining near-normal blood glucose levels. This can cause compensatory hyperinsulinaemia.

Persistent metabolic stress, increased insulin demand, glucotoxicity, lipotoxicity and genetic susceptibility contribute to beta-cell dysfunction. Insulin secretion progressively becomes inadequate, and beta-cell mass may decrease, resulting in worsening hyperglycaemia.

An abnormally elevated concentration of glucagon in the blood, which increases hepatic glucose production and contributes to hyperglycaemia in diabetes.

A form of diabetes caused by a mutation in a single gene affecting insulin production or secretion. Examples include maturity-onset diabetes of the young (MODY) and neonatal diabetes.

A slowly progressive form of autoimmune diabetes that develops in adulthood. Patients have diabetes-associated autoantibodies and may initially not require insulin, but many eventually need insulin as beta-cell function declines.

Diabetes first diagnosed during pregnancy, usually caused by pregnancy-related insulin resistance that exceeds the pancreas's ability to increase insulin secretion. It increases the risk of pregnancy complications and future type 2 diabetes.