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Articles in PresS, published online ahead of print December 4, 2001
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00071.2001
Submitted on March 2, 2001
Accepted on November 29, 2001
1 Diabetes Research Center, VUB, Brussels, Belgium
* To whom correspondence should be addressed. E-mail: Daniel.Pipeleers{at}vub.ac.be.
Pancreatic ß cells express glutamate decarboxylase (GAD) which is responsible for the production and release of gamma-aminobutyric acid (GABA). Over a 24 hour culture period, total GABA release by purified rat ß cells is 8 fold higher than the cellular GABA content, and can thus be used as an index of cellular GAD activity. GABA release is 40 percent reduced by glucose (58 pmol per 103 cells at 10 mM glucose versus 94 pmol at 3 mM, p< 0.05). This suppressive effect of glucose was not observed when glucose metabolism was blocked by mannoheptulose or 2,4 dinitrophenol; it was amplified when ATP-dependent ß cell activities were inhibited by diazoxide, verapamil or cycloheximide, or by reducing extracellular calcium levels; it was counteracted when ß cell functions were activated by non-metabolized agents such as glibenclamide, isobutylmethylxanthine, glucagon or GLP-1 which are known to stimulate calcium-dependent activities, such as hormone release and calcium dependent ATPases. These observations suggest that GABA release from ß cells varies with the balance between ATP producing and ATP consuming activities in the cells. Less GABA is released in conditions of elevated glucose metabolism - and hence ATP production -, but this effect is counteracted by ATP-dependent activities. The notion that increased cytoplasmic ATP levels can suppress GAD activity in ß cells, and hence GABA production and release, is compatible with previous findings on ATP suppression of brain GAD activity.
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