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-cells and
their metabolic state
Diabetes Research Center, Vrije Universiteit Brussel, B-1090 Brussels, Belgium
Pancreatic 
-cells express glutamate
decarboxylase (GAD), which is responsible for the production and
release of 
-aminobutyric acid (GABA). Over a 24-h culture period,
total GABA release by purified rat -cells is eightfold higher than
the cellular GABA content and can thus be used as an index of cellular
GAD activity. GABA release is 40% reduced by glucose (58 pmol/103 cells at 10 mM glucose vs. 94 pmol at 3 mM
glucose, 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 -cell
activities were inhibited by addition of diazoxide, verapamil, or
cycloheximide or by reduction of extracellular calcium levels; it was
counteracted when -cell functions were activated by nonmetabolized
agents, such as glibenclamide, IBMX, glucagon, or glucacon-like
peptide-1 (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 -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 -cells, and hence GABA
production and release, is compatible with previous findings on ATP
suppression of brain GAD activity.
diabetes; glutamate decarboxylase; insulin
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