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Influence of D-Glucose upon the Respiratory and Secretory Response of Insulin-producing Tumor Cells to 2-Aminobicyclo[2,2,1]heptane-2-carboxylic Acid¹

Laboratory of Experimental Medicine, Brussels Free University, Brussels, Belgium [A. S., M-H. G., and W. J. M.], and Department of Medical Cell Biology, University of Uppsala, Uppsala, Sweden [C. H.]

In insulin-producing cells of the RINm5F line, the nonmetabolized analogue of L-leucine, 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid decreases O₂ consumption, lowers ATP content, and inhibits insulin release despite stimulation of both NH₄ production and ¹⁴CO₂ output from cells prelabeled with L-[U-¹⁴C]glutamine. The metabolic and secretory effects of 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid are opposed to those of D-glucose, which increases respiration, ATP content, and insulin release, while lowering NH⁺₄ production and ¹⁴CO₂ output from the prelabeled cells. D-Glucose also antagonizes the inhibitory action of 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid upon both respiration and secretion. These findings suggest that, in tumor as in normal islet cells, the regulation of insulin release by exogenous nutrients depends on the availability of endogenous ATP.

¹ This work was supported by grants from the Belgian Foundation for Scientific Medical Research and Swedish Medical Research Council.

² To whom requests for reprints should be addressed, at Laboratory of Experimental Medicine, 115 Boulevard de Waterloo, B-1000 Brussels, Belgium.

Received 4/ 6/87. Revised 7/29/87. Accepted 8/20/87.

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