Interference of a nonmetabolized analogue of l-leucine with lipid metabolism in tumoral pancreatic islet cells

Abstract

The nonmetabolized analogue of l-leucine, 2-aminobicyclo[2,2,]heptane-2-carboxylic acid (BCH), was recently found to inhibit O 2 uptake and insulin release from tumoral islet cells of the RINmSF line. BCH inhibited lipogenesis, stimulated lipolysis, and severely decreased the oxidation of endogenous [U- 14C]palmitate in prelabelled RINmSF cells. d-Glucose exerted metabolic effects which were sometimes opposite to those caused by BCH and, within limits, protected the islet cells against the inhibitor action of BCH. Since BCH augments NH 4 + production and facilitated the catabolism of 14C-labelled amino acids in the prelabelled cells, it is proposed that the unexpected inhibition of O 2 uptake by BCH is mainly attributable to a decrease in the oxidation of endogenous fatty acids.