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Diabetes mellitus consists of chronic metabolic disorders characterized by persistent hyperglycemia. This elevated blood glucose results from defects in insulin secretion, impaired insulin action, or both. Insulin, produced by pancreatic β-cells, is essential for maintaining glucose homeostasis by facilitating cellular glucose uptake for energy or storage. Disruptions in insulin production or function lead to glucose accumulation in the bloodstream, causing the clinical features and long-term complications associated with diabetes.
Type 1 Diabetes
Type 1 diabetes results from autoimmune destruction of β cells, leading to an absolute insulin deficiency. Autoreactive T lymphocytes target pancreatic islet tissue, progressively eliminating insulin-secreting capacity. Without endogenous insulin, glucose cannot enter peripheral tissues effectively, and exogenous insulin becomes essential for survival. Although type 1 diabetes can appear at any age, it most often presents in childhood or adolescence.
Type 2 Diabetes
Diabetes mellitus consists of chronic metabolic disorders characterized by persistent hyperglycemia. This elevated blood glucose results from defects in insulin secretion, impaired insulin action, or both. Insulin, produced by pancreatic β-cells, is essential for maintaining glucose homeostasis by facilitating cellular glucose uptake for energy or storage. Disruptions in insulin production or function lead to glucose accumulation in the bloodstream, causing the clinical features and long-term complications associated with diabetes.
Gestational Diabetes
Gestational diabetes emerges during pregnancy when placental hormones—such as human placental lactogen—induce insulin resistance. Most individuals compensate by increasing insulin production, but those with limited β-cell reserve develop hyperglycemia. Although glucose levels usually normalize postpartum, gestational diabetes increases the lifetime risk of developing type 2 diabetes and may affect fetal growth and perinatal outcomes.
These major categories illustrate how distinct mechanisms of insulin impairment produce the shared metabolic hallmark of diabetes mellitus.
