Glucose sensing by hypothalamic neurones and pancreatic islet cells: AMPle evidence for common mechanisms?

Exp Physiol. 2007 Mar;92(2):311-9. doi: 10.1113/expphysiol.2006.036004. Epub 2006 Dec 7.


A fuller understanding of the central mechanisms involved in controlling food intake and metabolism is likely to be crucial for developing treatments to combat the growing problem of obesity in Westernised societies. Within the hypothalamus, specialized neurones respond to both appetite-regulating hormones and circulating metabolites to regulate feeding behaviour accordingly. Thus, the activity of hypothalamic glucose-excited and glucose-inhibited neurones is increased or decreased, respectively, by an increase in local glucose concentration. These 'glucose-sensing' neurones may therefore play a key role in the central regulation of food intake and potentially in the regulation of blood glucose concentrations. Whilst the intracellular signalling mechanisms through which glucose-sensing neurones detect changes in the concentration of the sugar have been investigated quite extensively, many elements remain poorly understood. Furthermore, the similarities, or otherwise, with other nutrient-sensing cells, including pancreatic islet cells, are not completely resolved. In this review, we discuss recent advances in this field and explore the potential involvement of AMP-activated protein kinase and other nutrient-regulated protein kinases.

Publication types

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

MeSH terms

  • AMP-Activated Protein Kinases
  • Animals
  • Appetite Regulation
  • Energy Metabolism
  • Glucose / metabolism*
  • Homeostasis
  • Humans
  • Hypothalamus / metabolism*
  • Islets of Langerhans / metabolism*
  • Multienzyme Complexes / metabolism*
  • Neural Inhibition
  • Neurons / metabolism*
  • Obesity / metabolism
  • Obesity / physiopathology
  • Protein Serine-Threonine Kinases / metabolism*
  • Signal Transduction*
  • Synaptic Transmission


  • Multienzyme Complexes
  • Protein Serine-Threonine Kinases
  • AMP-Activated Protein Kinases
  • Glucose