Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Impact of alcohol cessation on hepatic metabolic signaling during cancer cachexia.

Biochemical and biophysical research communications·2026
Same author

GSK3β promotes p53/Nrf2-dependent expression of the stress response protein REDD2 in retinal Müller glia exposed to hyperlipidemic conditions.

Experimental eye research·2026
Same author

Response of male and female mice to chronic alcohol use before and during cancer.

Alcohol (Fayetteville, N.Y.)·2026
Same author

Adaptation to cystine limitation stress confers a targetable lipid metabolism vulnerability in pancreatic ductal adenocarcinoma.

Nature communications·2025
Same author

Androgen deprivation induces distinct muscle-specific transcriptional changes to genes regulating glucose, lipid, and amino acid metabolism.

Molecular and cellular endocrinology·2025
Same author

Acute binge alcohol increases risk of arrhythmias and myocardial fibrosis in a mouse model of arrhythmogenic cardiomyopathy.

American journal of physiology. Heart and circulatory physiology·2025

Related Experiment Video

Updated: Apr 3, 2026

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
06:26

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis

Published on: July 18, 2025

1.1K

Acute Alcohol-Induced Decrease in Muscle Protein Synthesis in Female Mice Is REDD-1 and mTOR-Independent.

Jennifer L Steiner1, Scot R Kimball1, Charles H Lang2

  • 1Department of Cellular and Molecular Physiology, Penn State College of Medicine, 500 University Drive, Hershey, PA 17033, USA.

Alcohol and Alcoholism (Oxford, Oxfordshire)
|September 24, 2015
PubMed
Summary

Regulated in development and DNA damage-1 (REDD1) protein does not affect alcohol-induced muscle protein synthesis changes. However, REDD1 may play a role in alcohol-induced ubiquitin-proteasome mediated protein breakdown.

More Related Videos

Author Spotlight: Advanced Integrated Model for Sepsis-Induced Myopathy and Single-Cell Metabolic Analysis
04:01

Author Spotlight: Advanced Integrated Model for Sepsis-Induced Myopathy and Single-Cell Metabolic Analysis

Published on: June 14, 2024

1.7K
Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice
09:50

Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice

Published on: April 24, 2013

12.2K

Related Experiment Videos

Last Updated: Apr 3, 2026

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
06:26

Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis

Published on: July 18, 2025

1.1K
Author Spotlight: Advanced Integrated Model for Sepsis-Induced Myopathy and Single-Cell Metabolic Analysis
04:01

Author Spotlight: Advanced Integrated Model for Sepsis-Induced Myopathy and Single-Cell Metabolic Analysis

Published on: June 14, 2024

1.7K
Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice
09:50

Experimental Methods for Testing the Effects of Neurotrophic Peptide, ADNF-9, Against Alcohol-induced Apoptosis during Pregnancy in C57BL/6 Mice

Published on: April 24, 2013

12.2K

Area of Science:

  • Muscle physiology and molecular biology
  • Alcohol metabolism and its effects on cellular processes
  • Protein synthesis and degradation pathways

Background:

  • Acute alcohol consumption can impair muscle protein synthesis.
  • The protein regulated in development and DNA damage-1 (REDD1) is a known negative regulator of mTOR kinase.
  • The role of REDD1 in alcohol-induced muscle protein synthesis changes is not well understood.

Purpose of the Study:

  • To investigate the role of REDD1 in alcohol-induced changes in muscle protein synthesis.
  • To determine if REDD1 influences mTOR kinase activity following acute alcohol exposure.
  • To examine the impact of REDD1 on protein degradation pathways after alcohol administration.

Main Methods:

  • Adult female REDD1 knockout (REDD1-/-) and wild-type (WT) mice were administered ethanol (alcohol) or saline via intraperitoneal injection.
  • Skeletal muscle was collected 1 hour post-injection for analysis.
  • In vivo protein synthesis, mTORC1 signaling activation, and protein degradation markers were assessed.

Main Results:

  • Acute alcohol administration decreased muscle protein synthesis similarly in both WT and REDD1-/- mice.
  • Ethanol and genotype did not significantly alter mTORC1 signaling, as indicated by downstream target phosphorylation.
  • While alcohol decreased certain autophagy-related proteins, markers of autophagy initiation and completion remained unchanged.
  • Alcohol increased MuRF1 and atrogin-1 mRNA levels in REDD1-/- mice, suggesting increased ubiquitin-proteasome activity.
  • REDD1-/- mice did not exhibit alcohol-induced hyperinsulinemia observed in WT mice.

Conclusions:

  • REDD1 does not appear to mediate the acute alcohol-induced reduction in muscle protein synthesis or affect mTOR activity.
  • REDD1 may contribute to the regulation of ubiquitin-proteasome-mediated protein breakdown in response to alcohol.
  • The findings suggest a potential role for REDD1 in modulating protein degradation pathways rather than synthesis inhibition following acute alcohol exposure.