Betaceller

Betaceller are endocrine cells located in the islets of Langerhans in the pancreas. They are the most abundant cell type within an islet and are specialized for the production and secretion of insulin, the hormone that lowers blood glucose. Betaceller also release C-peptide in equimolar amounts with insulin and, together with amylin, participate in metabolic regulation.

Function and mechanism: Betaceller sense changes in blood glucose and release insulin in response to elevated levels. Glucose enters the cells via GLUT2 transporters and is metabolized by glucokinase, raising ATP levels. This closes ATP-sensitive potassium channels, depolarizes the cell membrane, and triggers calcium influx that stimulates exocytosis of insulin-containing granules. Insulin promotes glucose uptake in muscle and adipose tissue and suppresses hepatic glucose production. C-peptide is a byproduct of insulin production and serves as a marker of endogenous insulin secretion.

Development and regulation: Betaceller develop from progenitor cells during embryogenesis, and the adult beta-cell mass can expand through replication and, to a lesser extent, neogenesis. Key transcription factors involved in beta-cell identity and function include PDX1, NKX6.1, MAFA, and NEUROD1. Beta-cell function is influenced by metabolic stress, inflammatory signals, and endoplasmic reticulum stress, all of which can contribute to impaired insulin secretion.

Clinical significance: In type 1 diabetes, autoimmune destruction of betaceller leads to insulin deficiency. In type 2 diabetes, beta-cell dysfunction progresses alongside insulin resistance, contributing to hyperglycemia. Rare genetic forms, such as MODY, involve beta-cell development or function defects. Beta-cell loss and dysfunction are central targets in diabetes research and therapy.

Research and therapy: Efforts include developing stem-cell–derived beta-like cells, beta-cell replacement strategies, and interventions to protect beta-cells from autoimmune attack or metabolic stress, aiming to restore or preserve endogenous insulin secretion.