Is REDD1 a Metabolic Éminence Grise?

Trends Endocrinol Metab. 2016 Dec;27(12):868-880. doi: 10.1016/j.tem.2016.08.005. Epub 2016 Sep 6.

Abstract

Regulated in development and DNA damage response 1 (REDD1) has been functionally linked to the control of diverse cellular processes due, at least in part, to its ability to repress mammalian or mechanistic Target of Rapamycin (mTOR) Complex-1 (mTORC1), a key protein complex controlled by hormonal and nutrient cues. Notably, emerging evidence suggests that REDD1 also regulates several pathways involved in modulating energy balance and metabolism. Herein, we discuss evidence implicating REDD1 as a key modulator of insulin action and metabolic function, including its potential contribution to mitochondrial biology and pancreatic islet function. Collectively, the available evidence suggests that REDD1 has a more prominent role in energy homeostasis than was previously thought, and implicates REDD1 as a potential therapeutic target for treatment of metabolic disorders.

Keywords: Akt; REDD1; insulin; mTOR; obesity; protein kinase B; skeletal muscle.

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • Muscle, Skeletal / metabolism
  • Obesity / genetics
  • Obesity / metabolism
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / genetics
  • Signal Transduction / physiology
  • TOR Serine-Threonine Kinases / genetics
  • TOR Serine-Threonine Kinases / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*

Substances

  • DDIT4 protein, human
  • Transcription Factors
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases