Received October 4, 2006
Revised November 6, 2006
Accepted after revision December 4, 2006
Neuroendocrinology/Endocrinology [270]
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Glucose sensing by hypothalamic neurons and pancreatic
islet cells: AMPle evidence for common mechanisms?
Phillip D. Mountjoy 1
Guy A. Rutter 2*
1 University of Bristol
2 Imperial College London
* To whom correspondence should be addressed. E-mail: g.rutter{at}imperial.ac.uk.
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Abstract |
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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, specialised neurons respond to
both appetite-regulating hormones and to circulating
metabolites to regulate feeding behaviour accordingly.
Thus, the activity of hypothalamic glucose-excited (GE)
and glucose-inhibited (GI) neurons is increased or
decreased, respectively, by an increase in local glucose
concentration. These ‘glucose-sensing’ neurons therefore
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
neurons 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.
Key Words:
Glucose, Islet of Langerhans, Neuron
