SIRT5 deacylates metabolism-related proteins and attenuates hepatic steatosis in ob/ob mice.

ABSTRACT:

Background

Sirtuin 5 (SIRT5) is a NAD⁺-dependent lysine deacylase. The SIRT5 deficiency mouse model shows that it is dispensable for metabolic homeostasis under normal conditions. However, the biological role of SIRT5 and acylation in pathological states such as obesity and type 2 diabetes (T2D) remains elusive.

Methods

The hepatic SIRT5-overexpressing ob/ob mouse model (ob/ob-SIRT5 OE) was established by CRISPR/Cas9 gene editing tool Protein malonylation and succinylation lysine sites were identified by immunoprecipitation coupled lipid chromatography - tandem mass spectrometry (LC-MS/MS) methods.

Findings

The ob/ob-SIRT5 OE mice showed decreased malonylation and succinylation, improved cellular glycolysis, suppressed gluconeogenesis, enhanced fatty acid o

SUBMITTER: Du Y 

PROVIDER: S-EPMC6197389 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature