Deletion of translin (Tsn) induces robust adiposity and hepatic steatosis without impairing glucose tolerance.

ABSTRACT:

Objective

Translin knockout (KO) mice display robust adiposity. Recent studies indicate that translin and its partner protein, trax, regulate the microRNA and ATM kinase signaling pathways, both of which have been implicated in regulating metabolism. In the course of characterizing the metabolic profile of these mice, we found that they display normal glucose tolerance despite their elevated adiposity. Accordingly, we investigated why translin KO mice display this paradoxical phenotype.

Methods

To help distinguish between the metabolic effects of increased adiposity and those of translin deletion per se, we compared three groups: (1) wild-type (WT), (2) translin KO mice on a standard chow diet, and (3) adiposity-matched WT mice that were placed on a high-fat diet until they

SUBMITTER: Shah AP 

PROVIDER: S-EPMC6629527 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature