Glucose-induced B-cell recruitment and the expression of hexokinase isoenzymes.

Abstract

The balanced release of insulin and glucagon by the endocrine pancreas is an important feature of glucose homeostasis in mammals. Adaptation of hormonal output from the endocrine pancreas to physiological demands is thought to depend on a glucose sensor — also called glucostat — which not only measures the prevailing extracellular glucose concentration but also ensures the signal transduction mechanisms required for appropriate glucagon and insulin release by A-cells and B-cells respectively (1–4). The scope of this paper is restricted to review some recent research concerning glucose sensing in B-cells, neglecting the glucose sensor in glucagon-producing A-cells about which relatively little is known.