Evidence map›Paper›PMID 31428057›Full record

ReviewFrontiers in endocrinology2019

Anabolic and Pro-metabolic Functions of CREB-CRTC in Skeletal Muscle: Advantages and Obstacles for Type 2 Diabetes and Cancer Cachexia.

Rebecca Berdeaux, Chase Hutchins

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  6. Review
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  9. Review
  10. Article
  11. Article
  12. Nutrients · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Activation of Crtc2/Creb1 in skeletal muscle enhances weight loss during intermittent fasting.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Rebecca BerdeauxDepartment of Integrative Biology and Pharmacology, Center for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center Houston, Houston, TX, United States.
Chase HutchinsDepartment of Integrative Biology and Pharmacology, Center for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center Houston, Houston, TX, United States.
Brown Foundation · USThe University of Texas MD Anderson Cancer Center · US

Funding

Regulation of glucose utilization by skeletal muscle SIK1R01DK092590 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BERDEAUX, REBECCA L · 2011 to 2021
$3.3M
Promotion of satellite cell proliferation by cAMP signalingR01AR072368 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BERDEAUX, REBECCA L · 2019 to 2023
$1.9M
NIAMS NIH HHS R01 AR072368NIDDK NIH HHS R01 DK092590
6 · The paper itself

Abstract

cAMP is one of the earliest described mediators of hormone action in response to physiologic stress that allows acute stress responses and adaptation in every tissue. The classic role of cAMP signaling in metabolic tissues is to regulate nutrient partitioning. In response to acute stress, such as epinephrine released during strenuous exercise or fasting, intramuscular cAMP liberates glucose from glycogen and fatty acids from triglycerides. In the long-term, activation of Gs-coupled GPCRs stimulates muscle growth (hypertrophy) and metabolic adaptation through multiple pathways that culminate in a net increase of protein synthesis, mitochondrial biogenesis, and improved metabolic efficiency. This review focuses on regulation, function, and transcriptional targets of CREB (cAMP response element binding protein) and CRTCs (CREB regulated transcriptional coactivators) in skeletal muscle and the potential for targeting this pathway to sustain muscle mass and metabolic function in type 2 diabetes and cancer. Although the muscle-autonomous roles of these proteins might render them excellent targets for both conditions, pharmacologic targeting must be approached with caution. Gain of CREB-CRTC function is associated with excess liver glucose output in type 2 diabetes, and growing evidence implicates CREB-CRTC activation in proliferation and invasion of different types of cancer cells. We conclude that deeper investigation to identify skeletal muscle specific regulatory mechanisms that govern CREB-CRTC transcriptional activity is needed to safely take advantage of their potent effects to invigorate skeletal muscle to potentially improve health in people with type 2 diabetes and cancer.

Indexed as

cAMPcancer cachexiaCREBCRTCmuscle atrophymuscle hypertrophySIKtype 2 diabetes

Identifiers

PMID31428057
PMCPMC6688074
OpenAlexW2963836170

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.