Effects of L-leucine, its 2-keto acid metabolite and its non-metabolized analogue on rat tumoral islet cell function.
J Mol Endocrinol
; 1(1): 69-76, 1988 Jul.
Article
em En
| MEDLINE
| ID: mdl-2855709
ABSTRACT
L-Leucine and 2-ketoisocaproate stimulated insulin release from perifused rat tumoral islet cells (RINm5F line). The secretory response coincided with an increase in the intracellular ATP/ADP ratio, a stimulation of 45Ca outflow from cells perifused in the presence of extracellular Ca2+, and an increase in 32P efflux from cells prelabelled with radioactive orthophosphate. In contrast to D-glucose, however, L-leucine or 2-ketoisocaproate failed to decrease 86Rb outflow, to inhibit 45Ca outflow from cells perifused in the absence of Ca2+ and to enhance the labelling of inositol-containing phospholipids in cells exposed to myo-[2-3H]inositol. These findings suggest that D-glucose, L-leucine and 2-ketoisocaproate exert dissimilar effects on the subcellular distribution of adenine nucleotides and/or 86Rb. The non-metabolized analogue of L-leucine, 2-aminobicyclo[2.2.1]heptane-2-carboxylic acid (BCH), also caused an initial stimulation of insulin release and 32P efflux, but this was soon followed by a severe and irreversible inhibition of insulin output, associated with a permanent enhancement of 86Rb outflow. The dual ionic and secretory response to BCH is interpreted in the light of its dual effect on the catabolism of endogenous amino and fatty acids, and raises the view that BCH could be used to interfere with the function of insulinoma cells.
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Base de dados:
MEDLINE
Assunto principal:
Adenoma de Células das Ilhotas Pancreáticas
/
Aminoácidos
/
Aminoácidos Cíclicos
/
Insulina
/
Insulinoma
/
Cetoácidos
/
Leucina
Limite:
Animals
Idioma:
En
Ano de publicação:
1988
Tipo de documento:
Article