PuSH - Publikationsserver des Helmholtz Zentrums München

Di Francesco, A.* ; Choi, Y.* ; Bernier, M.* ; Zhang, Y.* ; Diaz-Ruiz, A.* ; Aon, M.A.* ; Kalafut, K.* ; Ehrlich, M.R.* ; Murt, K.* ; Ali, A.* ; Pearson, K.J.* ; Levan, S.* ; Preston, J.D.* ; Martin-Montalvo, A.* ; Martindale, J.L.* ; Abdelmohsen, K.* ; Michel, C.R.* ; Willmes, D.M. ; Henke, C. ; Navas, P.* ; Villalba, J.M.* ; Siegel, D.* ; Gorospe, M.* ; Fritz, K.* ; Biswal, S.* ; Ross, D.* ; de Cabo, R.*

NQO1 protects obese mice through improvements in glucose and lipid metabolism.

npj Aging Mech. Dis. 6:13 (2020)
Verlagsversion DOI
Open Access Gold
Creative Commons Lizenzvertrag
This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply. Chronic nutrient excess leads to metabolic disorders and insulin resistance. Activation of stress-responsive pathways via Nrf2 activation contributes to energy metabolism regulation. Here, inducible activation of Nrf2 in mice and transgenesis of the Nrf2 target, NQO1, conferred protection from diet-induced metabolic defects through preservation of glucose homeostasis, insulin sensitivity, and lipid handling with improved physiological outcomes. NQO1-RNA interaction mediated the association with and inhibition of the translational machinery in skeletal muscle of NQO1 transgenic mice. NQO1-Tg mice on high-fat diet had lower adipose tissue macrophages and enhanced expression of lipogenic enzymes coincident with reduction in circulating and hepatic lipids. Metabolomics data revealed a systemic metabolic signature of improved glucose handling, cellular redox, and NAD+ metabolism while label-free quantitative mass spectrometry in skeletal muscle uncovered a distinct diet- and genotype-dependent acetylation pattern of SIRT3 targets across the core of intermediary metabolism. Thus, under nutritional excess, NQO1 transgenesis preserves healthful benefits.
Weitere Metriken?
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
ISSN (print) / ISBN 2056-3973
e-ISSN 2056-3973
Quellenangaben Band: 6, Heft: 1, Seiten: , Artikelnummer: 13 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London [u.a.]
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Pancreatic Beta Cell Research (IPI)