Is REDD1 a Metabolic Éminence Grise?

Christopher Lipina; Harinder Hundal

doi:10.1016/j.tem.2016.08.005

Is REDD1 a Metabolic Éminence Grise?

Christopher Lipina
, Harinder Hundal (Lead / Corresponding author)

Cell Signalling and Immunology

Research output: Contribution to journal › Review article › peer-review

55 Citations (Scopus)

249 Downloads (Pure)

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 mTORC1, a key protein complex controlled by hormonal and nutrient cues. Notably, emerging evidence suggests that REDD1 may also regulate a number of 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 may play a more prominent role in energy homeostasis than previously thought, and implicates REDD1 as a potential therapeutic target for treatment of metabolic disorders.

Original language	English
Pages (from-to)	868-880
Number of pages	13
Journal	Trends in Endocrinology and Metabolism
Volume	27
Issue number	12
Early online date	6 Sept 2016
DOIs	https://doi.org/10.1016/j.tem.2016.08.005
Publication status	Published - Dec 2016

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

REDD1
skeletal muscle
insulin
protein kinase B
Akt
mTOR
obesity

Access to Document

10.1016/j.tem.2016.08.005Licence: CC BY

Final Published Version
© 2016 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
Final published version, 2.53 MBLicence: CC BY

Defining the Molecular Roles of Peripheral CB1 and CB2 Cannabinoid Receptors in Age-Induced Changes in Energy and Metabolic Homeostasis (Joint with University of Aberdeen)
Hundal, H. (Investigator) & Lipina, C. (Investigator)
Biotechnology and Biological Sciences Research Council
1/01/16 → 28/02/19
Project: Research
Wellcome Trust PhD Studentship
Cowling, V. (Investigator), Owen-Hughes, T. (Investigator) & Ryan, R. (Investigator)
1/09/15 → 5/09/19
Project: Research
Non-Genomic Mechanisms Stabilizing the Abundance of SNAT2, a Nutrient Transceptor Protein, in Response to Diverse Catabotic Signals
Hundal, H. (Investigator) & Taylor, P. (Investigator)
3/10/11 → 2/07/15
Project: Research

Cite this

@article{dcf37e4f9d45462da1c045bf2443832c,

title = "Is REDD1 a Metabolic {\'E}minence Grise?",

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 mTORC1, a key protein complex controlled by hormonal and nutrient cues. Notably, emerging evidence suggests that REDD1 may also regulate a number of 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 may play a more prominent role in energy homeostasis than previously thought, and implicates REDD1 as a potential therapeutic target for treatment of metabolic disorders.",

keywords = "REDD1, skeletal muscle, insulin, protein kinase B, Akt, mTOR, obesity",

author = "Christopher Lipina and Harinder Hundal",

note = "Funding: BBSRC and Diabetes UK.",

year = "2016",

month = dec,

doi = "10.1016/j.tem.2016.08.005",

language = "English",

volume = "27",

pages = "868--880",

journal = "Trends in Endocrinology and Metabolism",

issn = "1043-2760",