RT Journal Article
T1 A Receptor of the Immunoglobulin Superfamily Regulates Adaptive Thermogenesis
A1 Hurtado del Pozo, Carmen
A1 Ruiz, Henry
A1 Arivazhagan, Lakshmi
A1 Aranda Gómez, Juan Francisco
A1 Shim, Cynthia
A1 Daya, Peter
A1 Derk, Julia
A1 MacLean, Michael
A1 He, Meilun
A1 Frye, Laura
A1 Randall, Friedline
A1 Hye, Lim Noh
A1 Kim, Jason
A1 Friedman, Richard
A1 Ramasamy, Ravichandran
A1 Schmidt, Ann Marie
AB Exquisite regulation of energy homeostasis protects from nutrient deprivation but causes metabolic dysfunction upon nutrient excess. In human and murine adipose tissue, the accumulation of ligands of the receptor for advanced glycation end products (RAGE) accompanies obesity, implicating this receptor in energy metabolism. Here, we demonstrate that mice bearing global- or adipocyte-specific deletion of Ager, the gene encoding RAGE, display superior metabolic recovery after fasting, a cold challenge, or high-fat feeding. The RAGE-dependent mechanisms were traced to suppression of protein kinase A (PKA)-mediated phosphorylation of its key targets, hormone-sensitive lipase and p38 mitogen-activated protein kinase, upon β-adrenergic receptor stimulation—processes that dampen the expression and activity of uncoupling protein 1 (UCP1) and thermogenic programs. This work identifies the innate role of RAGE as a key node in the immunometabolic networks that control responses to nutrient supply and cold challenges, and it unveils opportunities to harness energy expenditure in environmental and metabolic stress.
PB Cell Press
PB Elsevier
SN 2211-1247
YR 2019
FD 2019
LK https://hdl.handle.net/20.500.14352/95020
UL https://hdl.handle.net/20.500.14352/95020
LA eng
NO Hurtado Del Pozo, Carmen, et al. «A Receptor of the Immunoglobulin Superfamily Regulates Adaptive Thermogenesis». Cell Reports, vol. 28, n.o 3, julio de 2019, pp. 773-791.e7. https://doi.org/10.1016/j.celrep.2019.06.061.
NO This work was supported by grants from the United States Public Health Service (1R01DK109675 to A.M.S. and R.R.; 1PO1HL131481 to A.M.S.; 5T32HL098129-10 to H.H.R.; and 1F31AG054129-01 to J.D.); the American Diabetes Association (1-15-MI-14 to C.H.d.P.); and the American Heart Association (17SFRN33520045 to A.M.S. and H.H.R.). Part of this work was funded by Research Funds of the Diabetes Research Program at NYU (to A.M.S. and R.R.). The ExperimentalPathology Research Laboratory is partially funded by the Cancer Center Support grant P30CA016087 at NYU Langone’s Cancer Center. Part of this work was funded by the National Mouse Metabolic Phenotyping Center at UMassfunded by NIH grant 5U2C-DK093000 (to J.K.K.).
NO United States Public Health Service
NO American Diabetes Association
NO American Heart Association
NO New York University
DS Docta Complutense
RD 29 abr 2025