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Disruption of Acetyl-Lysine Turnover in Muscle Mitochondria Promotes Insulin
Resistance and Redox Stress without Overt Respiratory Dysfunction.
Authors Williams AS, Koves TR, Davidson MT, Crown SB, Fisher-Wellman KH, Torres MJ,
Draper JA, Narowski TM, Slentz DH, Lantier L, Wasserman DH, Grimsrud PA, Muoio
Submitted By Submitted Externally on 1/14/2020
Status Published
Journal Cell Metabolism
Year 2020
Date Published 1/1/2020
Volume : Pages 31 : 131 - 147.e11
PubMed Reference 31813822
Abstract This study sought to examine the functional significance of mitochondrial
protein acetylation using a double knockout (DKO) mouse model harboring
muscle-specific deficits in acetyl-CoA buffering and lysine deacetylation, due
to genetic ablation of carnitine acetyltransferase and Sirtuin 3, respectively.
DKO mice are highly susceptible to extreme hyperacetylation of the mitochondrial
proteome and develop a more severe form of diet-induced insulin resistance than
either single KO mouse line. However, the functional phenotype of
hyperacetylated DKO mitochondria is largely normal. Of the >120 measures of
respiratory function assayed, the most consistently observed traits of a
markedly heightened acetyl-lysine landscape are enhanced oxygen flux in the
context of fatty acid fuel and elevated rates of electron leak. In sum, the
findings challenge the notion that lysine acetylation causes broad-ranging
damage to mitochondrial quality and performance and raise the possibility that
acetyl-lysine turnover, rather than acetyl-lysine stoichiometry, modulates redox
balance and carbon flux.


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