The translational regulator FMRP controls lipid and glucose metabolism in mice and humans.

ABSTRACT:

Objectives

The Fragile X Mental Retardation Protein (FMRP) is a widely expressed RNA-binding protein involved in translation regulation. Since the absence of FMRP leads to Fragile X Syndrome (FXS) and autism, FMRP has been extensively studied in brain. The functions of FMRP in peripheral organs and on metabolic homeostasis remain elusive; therefore, we sought to investigate the systemic consequences of its absence.

Methods

Using metabolomics, in vivo metabolic phenotyping of the Fmr1-KO FXS mouse model and in vitro approaches, we show that the absence of FMRP induced a metabolic shift towards enhanced glucose tolerance and insulin sensitivity, reduced adiposity, and increased β-adrenergic-driven lipolysis and lipid utilization.

Results

Combining proteomics and cellula

SUBMITTER: Leboucher A 

PROVIDER: S-EPMC6407369 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature