TY - JOUR
T1 - eIF6 coordinates insulin sensitivity and lipid metabolism by coupling translation to transcription
AU - Brina, Daniela
AU - Miluzio, Annarita
AU - Ricciardi, Sara
AU - Clarke, Kim
AU - Davidsen, Peter K.
AU - Viero, Gabriella
AU - Tebaldi, Toma
AU - Offenhäuser, Nina
AU - Rozman, Jan
AU - Rathkolb, Birgit
AU - Neschen, Susanne
AU - Klingenspor, Martin
AU - Wolf, Eckhard
AU - Gailus-Durner, Valerie
AU - Fuchs, Helmut
AU - Hrabe De Angelis, Martin
AU - Quattrone, Alessandro
AU - Falciani, Francesco
AU - Biffo, Stefano
N1 - Publisher Copyright:
© 2015 Macmillan Publishers Limited. All rights reserved.
PY - 2015/9/18
Y1 - 2015/9/18
N2 - Insulin regulates glycaemia, lipogenesis and increases mRNA translation. Cells with reduced eukaryotic initiation factor 6 (eIF6) do not increase translation in response to insulin. The role of insulin-regulated translation is unknown. Here we show that reduction of insulin-regulated translation in mice heterozygous for eIF6 results in normal glycaemia, but less blood cholesterol and triglycerides. eIF6 controls fatty acid synthesis and glycolysis in a cell autonomous fashion. eIF6 acts by exerting translational control of adipogenic transcription factors like C/EBPβ, C/EBPδ and ATF4 that have G/C rich or uORF sequences in their 5′ UTR. The outcome of the translational activation by eIF6 is a reshaping of gene expression with increased levels of lipogenic and glycolytic enzymes. Finally, eIF6 levels modulate histone acetylation and amounts of rate-limiting fatty acid synthase (Fasn) mRNA. Since obesity, type 2 diabetes, and cancer require a Fasn-driven lipogenic state, we propose that eIF6 could be a therapeutic target for these diseases.
AB - Insulin regulates glycaemia, lipogenesis and increases mRNA translation. Cells with reduced eukaryotic initiation factor 6 (eIF6) do not increase translation in response to insulin. The role of insulin-regulated translation is unknown. Here we show that reduction of insulin-regulated translation in mice heterozygous for eIF6 results in normal glycaemia, but less blood cholesterol and triglycerides. eIF6 controls fatty acid synthesis and glycolysis in a cell autonomous fashion. eIF6 acts by exerting translational control of adipogenic transcription factors like C/EBPβ, C/EBPδ and ATF4 that have G/C rich or uORF sequences in their 5′ UTR. The outcome of the translational activation by eIF6 is a reshaping of gene expression with increased levels of lipogenic and glycolytic enzymes. Finally, eIF6 levels modulate histone acetylation and amounts of rate-limiting fatty acid synthase (Fasn) mRNA. Since obesity, type 2 diabetes, and cancer require a Fasn-driven lipogenic state, we propose that eIF6 could be a therapeutic target for these diseases.
UR - http://www.scopus.com/inward/record.url?scp=84942011622&partnerID=8YFLogxK
U2 - 10.1038/ncomms9261
DO - 10.1038/ncomms9261
M3 - Article
C2 - 26383020
AN - SCOPUS:84942011622
SN - 2041-1723
VL - 6
JO - Nature Communications
JF - Nature Communications
M1 - 8261
ER -