
Loss of LAT1 sex-dependently delays recovery after caerulein-induced acute pancreatitis
Author(s) -
Cristina M Hagen,
Eva Roth,
Theresia Reding Graf,
François Verrey,
Rolf Graf,
Anurag Gupta,
Giovanni Pellegrini,
Nadège Poncet,
Simone M. R. Camargo
Publication year - 2022
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v28.i10.1024
Subject(s) - biology , knockout mouse , medicine , endocrinology , pancreatitis , pi3k/akt/mtor pathway , hereditary pancreatitis , ceruletide , pancreas , microbiology and biotechnology , trypsin , signal transduction , enzyme , gene , biochemistry , receptor , trypsinogen , cholecystokinin
The expression of amino acid transporters is known to vary during acute pancreatitis (AP) except for LAT1 ( slc7a5 ), the expression of which remains stable. LAT1 supports cell growth by importing leucine and thereby stimulates mammalian target of rapamycin (mTOR) activity, a phenomenon often observed in cancer cells. The mechanisms by which LAT1 influences physiological and pathophysiological processes and affects disease progression in the pancreas are not yet known.