Metabolism-secretion coupling and mitochondrial calcium activities in clonal pancreatic β-cells

Vitam Horm. 2014:95:63-86. doi: 10.1016/B978-0-12-800174-5.00003-X.

Abstract

Pancreatic β-cells are the only cells capable of lowering blood glucose by secreting insulin. The β-cell continuously adjusts its secretory activity to substrate availability in order to keep blood glucose levels within the physiological range--a process called metabolism-secretion coupling. Glucose is readily taken up by the β-cell and broken down into intermediates that fuel oxidative metabolism inside the mitochondria to generate ATP. The resulting increase in the ATP/ADP ratio causes closure of plasma membrane KATP channels, thereby depolarizing the cell and triggering the opening of voltage-gated Ca²⁺ channels. Consequential oscillations of cytosolic Ca²⁺ not only mediate the exocytosis of insulin granules but are also relayed to other subcellular compartments including the mitochondria, where Ca²⁺ is required to accelerate mitochondrial metabolism in response to nutrient stimulation. The mitochondrial Ca²⁺ uptake machinery plays a fundamental role in this feed-forward mechanism that guarantees sustained insulin secretion and, thus, represents a promising therapeutic target for type 2 diabetes.

Keywords: Diabetes mellitus; Energy metabolism; Insulin secretion; Mitochondrial Ca(2+); β-Cell.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Calcium Signaling*
  • Clone Cells
  • Diabetes Mellitus, Type 2 / metabolism
  • Diabetes Mellitus, Type 2 / pathology
  • Diabetes Mellitus, Type 2 / physiopathology
  • Energy Metabolism*
  • Humans
  • Insulin / metabolism*
  • Insulin Secretion
  • Insulin-Secreting Cells / cytology
  • Insulin-Secreting Cells / metabolism*
  • Insulin-Secreting Cells / pathology
  • Mitochondria / metabolism*
  • Models, Biological*
  • Pancreas / cytology
  • Pancreas / pathology
  • Pancreas / physiology
  • Pancreas / physiopathology
  • Up-Regulation*

Substances

  • Insulin