Evidence map›Paper›PMID 23523565›Full record

ReviewMolecular and cellular endocrinology2013

Metabolic functions of glucocorticoid receptor in skeletal muscle.

Taiyi Kuo, Charles A Harris, Jen-Chywan Wang

Abstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

117 citing papers in PubMed, 1 synthesis or guideline pooled it, 233 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Puerarin-RichPreventive nutrition and food science · 2026
    Article
  7. Article
  8. Article
  9. Article
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  13. Effects and Molecular Mechanisms of Heat-Killed PostbioticInternational journal of molecular sciences · 2026
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

57 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Taiyi KuoDepartment of Nutritional Science & Toxicology, University of California at Berkeley, Berkeley, CA 94720, United States; Graduate Program of Endocrinology, University of California at Berkeley, Berkeley, CA 94720, United States.
Charles A Harris
Jen-Chywan Wang
University of California, Berkeley · USUniversity of California, San Francisco · US

Funding

Glucocorticoid Receptor and Lipid HomeostasisR01DK083591 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI WANG, JEN-CHYWAN · 2009 to 2013
$1.5M
Functional Dissection of Glucocorticoid Action in Metabolic DiseaseK08DK081680 · NIDDK · WASHINGTON UNIVERSITY · PI HARRIS, CHARLES A · 2008 to 2012
$773k
NIDDK NIH HHS K08 DK081680NIDDK NIH HHS R01 DK083591NIDDK NIH HHS R01DK083591
6 · The paper itself

Abstract

Glucocorticoids (GCs) exert key metabolic influences on skeletal muscle. GCs increase protein degradation and decrease protein synthesis. The released amino acids are mobilized from skeletal muscle to liver, where they serve as substrates for hepatic gluconeogenesis. This metabolic response is critical for mammals' survival under stressful conditions, such as fasting and starvation. GCs suppress insulin-stimulated glucose uptake and utilization and glycogen synthesis, and play a permissive role for catecholamine-induced glycogenolysis, thus preserving the level of circulating glucose, the major energy source for the brain. However, chronic or excess exposure of GCs can induce muscle atrophy and insulin resistance. GCs convey their signal mainly through the intracellular glucocorticoid receptor (GR). While GR can act through different mechanisms, one of its major actions is to regulate the transcription of its primary target genes through genomic glucocorticoid response elements (GREs) by directly binding to DNA or tethering onto other DNA-binding transcription factors. These GR primary targets trigger physiological and pathological responses of GCs. Much progress has been made to understand how GCs regulate protein and glucose metabolism. In this review, we will discuss how GR primary target genes confer metabolic functions of GCs, and the mechanisms governing the transcriptional regulation of these targets. Comprehending these processes not only contributes to the fundamental understanding of mammalian physiology, but also will provide invaluable insight for improved GC therapeutics.

Indexed as

AnimalsCarbohydrate MetabolismGene Expression RegulationGlucocorticoidsHumansInsulinMuscle ProteinsMuscle, SkeletalProtein BiosynthesisReceptors, GlucocorticoidResponse ElementsGlucocorticoidsInsulinMuscle ProteinsReceptors, GlucocorticoidGlucocorticoid receptorGlucocorticoidsGlucose metabolismInsulinProtein metabolismSkeletal muscle

Identifiers

PMID23523565
PMCPMC4893778
OpenAlexW2026424902

What OpenQuestion holds

Textmetadata
LicenceTDM
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.