M. Munoz et al., INSULIN STIMULATES CATIONIC AMINO-ACID-TRANSPORT ACTIVITY IN THE ISOLATED-PERFUSED RAT PANCREAS, Experimental physiology, 80(5), 1995, pp. 745-753
The effects of exogenous insulin, glucagon and streptozotocin-diabetes
on influx (15 s) of L-lysine via a cationic amino acid transporter re
sembling system yi were investigated in the isolated perfused rat panc
reas. In non-diabetic pancreata, transport of L-lysine was saturable w
ith an apparent K-m of 2 . 11 +/- 0 . 29 mM and V-max of 2 . 21 +/- 0
. 20 mu mol min(-1) g(-1) (n = 6). Bovine insulin (100 mu u ml(-1)) in
creased the maximal transport rate (V-max = 3 . 49 +/- 0 . 30 mu mol m
in(-1) g(-1), n = 4, P < 0 . 05) for L-lysine 1 . 6-fold without alter
ing the K-m. L-Lysine transport was not elevated significantly in diab
etic pancreata, although insulin (100 mu u ml(-1)) enhanced transport
to values measured in non-diabetic preparations. Human glucagon (1 . 5
x 10(-9) M) had no stimulatory effect on L-lysine transport. These fi
ndings provide the first evidence that exogenous insulin stimulates ca
tionic amino acid transport activity in the exocrine pancreatic epithe
lium. Activation of the cationic pancreatic amino acid transporter may
provide a mechanism to enhance the supply of L-arginine and thus sust
ain nitric oxide-mediated pancreatic secretion in response to islet ho
rmones and secretagogues.