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Articles in PresS, published online ahead of print February 5, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00460.2001
Submitted on October 15, 2001
Accepted on January 30, 2002
1 Physiology and Pharmacology, SUNY Downsate Medical Center, Brooklyn, NY, USA
* To whom correspondence should be addressed. E-mail: kirch{at}ix.netcom.com.
In this study we determined whether islets express functional group III metabotropic glutamate (mGlu) receptors. RT-PCR analysis showed that rat islets express the mGlu8 receptor subtype. mGlu8 receptor immunoreactivity was primarily displayed by glucagon-secreting 
-cells and intrapancreatic neurons. We established that -cells express a glutamatergic phenotype by demonstrating the immunoreactivities of both glutamate and the vesicular glutamate transporter 2 (VGLUT2) in these cells. VGLUT2 was concentrated in the secretory granules of islet cells, suggesting that glutamate might play a role in the regulation of glucagon processing. The expression of mGlu8 by glutamatergic cells also suggests that mGlu8 may function as an autoreceptor to regulate glutamate release. Pancreatic group III mGlu receptors are functional because group III mGlu receptor agonists inhibited glucagon release and forskolin-stimulated cAMP formation in isolated islets, and (RS)-cyclopropyl-4-phosphonophenylglycine, a group III mGlu receptor antagonist, reduced these effects. Since excess glucagon secretion causes postprandial hyperglycemia in patients with type 2 diabetes, group III mGlu receptor agonists could be of value in the treatment of these patients.
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