Novel aspects on signal-transduction in the pancreatic beta-cell.

Per-Olof Berggren, Ingo B Leibiger
Author Information
  1. Per-Olof Berggren: The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska University Hospital Solna L3, Karolinska Institutet, SE-171 76 Stockholm, Sweden. per-olof.berggren@ki.se

Abstract

The glucose-stimulus/insulin-secretion-coupling by the pancreatic beta-cell, which guarantees the maintenance of glucose homeostasis in man, is regulated by a sophisticated interplay between glucose and a plethora of additional factors. Besides other nutrients, incretins, nerval innervation, systemic growth factors as well as autocrine and paracrine regulatory loops within the islet of Langerhans modulate the function of the insulin-producing beta-cell. Although the modulatory role of these factors is well appreciated, the underlying molecular mechanisms involved remain poorly understood. However, in most cases beta-cell membrane receptors coupled primarily to either G-proteins or tyrosine kinases, which subsequently activate respective second messenger cascades, are involved. In the present mini-review we will discuss the role of signaling through some of these receptor-operated effector systems in the light of pancreatic beta-cell signal-transduction.

Grants

  1. DK58508/NIDDK NIH HHS

MeSH Term

Diabetes Mellitus
GTP-Binding Proteins
Glucose
Humans
Inositol Phosphates
Insulin
Insulin Secretion
Insulin-Secreting Cells
Islets of Langerhans
Protein-Tyrosine Kinases
Receptor, Insulin
Receptors, Cell Surface
Signal Transduction

Chemicals

Inositol Phosphates
Insulin
Receptors, Cell Surface
Protein-Tyrosine Kinases
Receptor, Insulin
GTP-Binding Proteins
Glucose