Diabetes

Disease / Phenomenon

Diabetes mellitus is a group of metabolic disorders defined by chronically elevated blood glucose arising from insufficient insulin, impaired insulin action, or both. Type 1 diabetes results from autoimmune destruction of pancreatic beta cells and requires insulin replacement. Type 2 diabetes, which accounts for the large majority of cases, develops when tissues become resistant to insulin and beta cells eventually fail to compensate. Gestational diabetes appears during pregnancy and raises later risk. Persistent hyperglycemia damages small and large vessels over time, producing retinopathy, nephropathy, neuropathy, and greatly increased cardiovascular risk, while acute decompensation can cause ketoacidosis or hyperosmolar states.

Mechanistically, type 2 diabetes involves impaired insulin receptor signaling through IRS-1, PI3K, and Akt, reduced GLUT4 translocation in muscle and fat, and unrestrained hepatic gluconeogenesis. Ectopic lipid accumulation in liver and muscle, adipose tissue inflammation with elevated TNF-alpha and IL-6, endoplasmic reticulum stress, mitochondrial dysfunction, and oxidative injury all contribute to resistance, while glucotoxicity, lipotoxicity, and amyloid deposition progressively exhaust beta cells. Advanced glycation end products and polyol flux drive downstream complications. This page separates diabetes into these biological processes, follows the molecular pathways within each, and identifies the biomarkers that track them.