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GEOFFREY BURNSTOCK AN. R. ACAD. NAC. FARM.

ATP, released as a cotransmitter from sympathetic nerves, has
been shown to stimulate brown adipocytes. Deficits in receptor
regulation, transporter mobilization and adipocyte hormone
secretion are all thought to contribute to the pathology of obesity. A
recent paper described stimulation of lipogenesis in rat adipocytes
by ATP, which regulates fat stores independently from established
hormones.

GASTROENTEROLOGY

Purinergic signalling plays a major role in different activities of
the gut (9). ATP is a cotransmitter in NANC nerves responsible for
the inhibitory phase in peristalsis; it participates in synaptic
transmission in the myenteric and submucosal ganglia; it is involved
in vascular control of the gastrointestinal tract and in the control of
mucosal secretion. Both glial cells and interstitial cells of Cajal
express P2 receptors, although their roles have yet to be clarified.

A limited number of studies have been conducted to date
on changes in purinergic signalling in the diseased gut. ATP and
adenosine have been implicated in the development of gastric
ulcers, Hirschsprung’s and Chagas’ diseases, ischaemia and colonic
tumours (9). Extracellular nucleotides and their receptors have been
implicated in the pathogenesis of inflammatory bowel disease (IBD).
T cells are thought to play a primary role in the induction of
epithelial cell damage in IBD and the P2Y6 receptor was found to be
highly expressed on the T cells infiltrating IBD, but absent in T cells
of unaffected bowel. This suggests that P2Y6 receptor and its selective
agonists, may play a role in the pathogenesis of IBD. Later papers
have shown that P2Y6 receptors are involved in monocytic release
of IL-8 and stimulation of NaCl secretion. P2X3 receptor expression
is increased in the enteric plexuses in human IBD, suggesting a
potential role in dysmotility and pain. During inflammation of
the gastrointestinal tract, glial cells proliferate and produce
cytokines; thus, P2X7 receptors may play a role in the response of
enteric glia to inflammation. P2X3 purinergic signalling enhancement
in an animal model of colitis has been described (10). A recent paper
has raised the possibility that P2X receptors are potential targets

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