TY - JOUR
T1 - Induction of TDO2 and IDO2 in liver by high-fat feeding in mice
T2 - Discrepancies with human obesity
AU - Poulain-Godefroy, Odile
AU - Eury, Elodie
AU - Leloire, Audrey
AU - Hennart, Benjamin
AU - Guillemin, Gilles J.
AU - Allorge, Delphine
AU - Froguel, Philippe
N1 - Copyright the Author(s) 2013. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.
PY - 2013
Y1 - 2013
N2 - Low-grade and chronic inflammation is elicited in white adipose tissue in human obesity. The presence of inflammatory molecules leads to an increased tryptophan catabolism through the induction of indoleamine-2,3-dioxygenase-1 (IDO1). In order to characterize the mechanisms underlying this dysregulation, we have studied 2 mouse models of obesity. Unexpectedly, we did not detect any IDO1 expression in obese or lean mice adipose tissue. In a previous study, we did not find any significant difference in the liver for IDO2 and tryptophan-2,3-dioxygenase (TDO2) gene expression between normal weight and obese patients. IDO2 and TDO2 expression was increased in the liver of high-fat fed mice, but not in ob/ob mice, and was strongly correlated with hydroxysteroid- (11-beta) dehydrogenase-1 (HSD11B1) expression, an enzyme that generates active cortisol within tissues. In conclusion, despite a dysregulation of tryptophan metabolism, obese mice display discrepancies with human obesity metabolism, rendering them inappropriate for further investigations in this animal model.
AB - Low-grade and chronic inflammation is elicited in white adipose tissue in human obesity. The presence of inflammatory molecules leads to an increased tryptophan catabolism through the induction of indoleamine-2,3-dioxygenase-1 (IDO1). In order to characterize the mechanisms underlying this dysregulation, we have studied 2 mouse models of obesity. Unexpectedly, we did not detect any IDO1 expression in obese or lean mice adipose tissue. In a previous study, we did not find any significant difference in the liver for IDO2 and tryptophan-2,3-dioxygenase (TDO2) gene expression between normal weight and obese patients. IDO2 and TDO2 expression was increased in the liver of high-fat fed mice, but not in ob/ob mice, and was strongly correlated with hydroxysteroid- (11-beta) dehydrogenase-1 (HSD11B1) expression, an enzyme that generates active cortisol within tissues. In conclusion, despite a dysregulation of tryptophan metabolism, obese mice display discrepancies with human obesity metabolism, rendering them inappropriate for further investigations in this animal model.
UR - http://www.scopus.com/inward/record.url?scp=84882719035&partnerID=8YFLogxK
U2 - 10.4137/IJTR.S11717
DO - 10.4137/IJTR.S11717
M3 - Article
C2 - 26882470
AN - SCOPUS:84882719035
SN - 1178-6469
VL - 6
SP - 29
EP - 37
JO - International Journal of Tryptophan Research
JF - International Journal of Tryptophan Research
IS - SUPPL.1
ER -