Diabetes Mellitus: Introduction

Diabetes mellitus is a chronic metabolic disorder characterized by persistently high blood glucose levels, called hyperglycemia. It occurs due to impaired insulin secretion, reduced insulin sensitivity, or both. Insulin, produced by pancreatic β-cells, normally regulates glucose metabolism by allowing cells to absorb glucose from the bloodstream for energy or storage. When insulin production or function is disrupted, glucose accumulates in the bloodstream.

Type 1 diabetes results from autoimmune destruction of insulin-producing β-cells in the pancreas. The immune system mistakenly attacks these cells, leading to absolute insulin deficiency. 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 1 diabetes involves autoimmune destruction of β-cells causing absolute insulin deficiency, while type 2 diabetes develops when the body resists insulin and the pancreas gradually produces insufficient insulin. Type 2 is often linked to obesity, physical inactivity, and genetic factors. Type 1 typically appears in childhood, whereas type 2 usually develops later in life and represents the more common form of 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.

Insulin, produced by specialized β-cells in the pancreas, regulates glucose metabolism by facilitating cellular glucose uptake from the bloodstream. It allows cells to absorb glucose for immediate energy or storage as glycogen and fat. This process maintains glucose homeostasis by preventing excessive blood glucose accumulation. When insulin production or action is impaired, cells cannot efficiently absorb glucose, leading to hyperglycemia.

Pancreatic β-cells produce insulin, which is essential for maintaining glucose homeostasis. In type 1 diabetes, autoreactive T lymphocytes progressively destroy these cells, eliminating insulin-secreting capacity. In type 2 diabetes, β-cells gradually fail to produce enough insulin despite initial compensation. Dysfunction or destruction of β-cells is central to both major forms of diabetes mellitus.

Persistent hyperglycemia in diabetes leads to glucose accumulation in the bloodstream, causing clinical features and long-term complications of diabetes mellitus. Chronic high blood glucose damages blood vessels and nerves, potentially resulting in complications affecting the kidneys, eyes, feet, and cardiovascular system. Understanding these complications helps guide prevention and management strategies for diabetic patients.