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Experimental Physiology 92.2 pp 311-319
DOI: 10.1113/expphysiol.2006.036004
© The Physiological Society 2007
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Glucose sensing by hypothalamic neurones and pancreatic islet cells: AMPle evidence for common mechanisms?

 Philip D. Mountjoy1 and Guy A. Rutter1

1 Department of Cell Biology, Division of Medicine, Faculty of Medicine, Sir Alexander Fleming Building, Exhibition Road, Imperial College London, London, UK

Abstract

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.

(Received 4 October 2006; accepted after revision 1 December 2006; first published online 7 December 2006)
Corresponding author G. A. Rutter: Department of Cell Biology, Division of Medicine, Faculty of Medicine, Sir Alexander Fleming Building, Exhibition Road, Imperial College London, London SW7 2AZ, UK. Email: g.rutter{at}imperial.ac.uk






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