Evidence map›Paper›PMID 28870245›Full record

ArticleSkeletal muscle2017

Mice overexpressing growth hormone exhibit increased skeletal muscle myostatin and MuRF1 with attenuation of muscle mass.

Leslie A Consitt, Alicson Saneda, Gunjan Saxena, Edward O List, John J Kopchick

Open access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Taurine drives body protein renewal and accretion in beef steers.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024
    Article
  4. Article
  5. Article
  6. Review
  7. Musculoskeletal Effects of Altered GH Action.Frontiers in physiology · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
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

5 authors at 2 institutions in 1 country.

Leslie A ConsittDepartment of Biomedical Sciences, Ohio University, 228 Irvine Hall, Athens, Ohio, 45701, USA. consitt@ohio.edu.
Alicson SanedaDepartment of Biological Sciences, Ohio University, Athens, Ohio, 45701, USA.
Gunjan SaxenaDepartment of Biomedical Sciences, Ohio University, 228 Irvine Hall, Athens, Ohio, 45701, USA.
Edward O ListDiabetes Institute, Ohio University, Athens, Ohio, 45701, USA.
John J KopchickDepartment of Biomedical Sciences, Ohio University, 228 Irvine Hall, Athens, Ohio, 45701, USA.
Ohio University · USBiotechnology Institute · US

Funding

Mechanisms regulating myostatin-induced insulin resistance in skeletal muscleR15DK102115 · NIDDK · OHIO UNIVERSITY ATHENS · PI CONSITT, LESLIE · 2014 to 2014
$371k
NIDDK NIH HHS R15 DK102115
6 · The paper itself

Abstract

backgroundIn contrast to the acute effects of growth hormone (GH) on skeletal muscle protein synthesis, long-term GH treatment appears to have negligible effects on muscle mass. Despite this knowledge, little is known regarding the chronic effects of GH on skeletal muscle protein synthesis and atrophy signaling pathways. The purpose of this study was to determine if protein synthesis pathways are attenuated and/or muscle atrophy intracellular signaling pathways are altered in the skeletal muscle of transgenic bovine GH (bGH) mice.

methodsThe gastrocnemius and soleus from 5-month-old male bGH mice (n = 9) and wild type (WT) controls (n = 9) were harvested and analyzed for proteins involved in the protein synthesis (Akt/mTOR), growth and proliferation (MAPK), and muscle atrophy (MuRF1 and myostatin) pathways.

resultsTotal body mass was significantly increased in bGH mice compared to WT controls (49%, P < 0.0001). When expressed relative to total body mass, the gastrocnemius (- 28%, P < 0.0001), but not the soleus, was significantly lower in mice overexpressing GH, compared to controls. Transgenic bGH mice had elevated phosphorylation levels of protein kinase b (Akt1), 4E-binding protein 1 (4E-BP1), p70 S6 kinase, p42/44, and p38 (P < 0.05) compared to WT littermates. Mature myostatin (26 kDa), premature myostatin (52 kDa), and activin receptor type IIB (AcvR2B) protein levels were increased in bGH mice (P < 0.05), along with elevated phosphorylation levels of mothers against decapentaplegic homolog (Smad2) (59%, P < 0.0001). Mice overexpressing GH had increased MuRF1 expression (30%, P < 0.05) and insulin receptor substrate 1 (IRS1) serine phosphorylation (44%, P < 0.05) in the gastrocnemius, but not the soleus, when compared to controls.

conclusionsThese findings demonstrate that chronic elevations in circulating GH have a critical impact on signaling pathways involved in skeletal muscle protein synthesis and atrophy, and suggest that MuRF1, myostatin, and IRS1 serine phosphorylation may act to inhibit exaggerated glycolytic muscle growth, in environments of chronic GH/IGF-1 excess.

Indexed as

Muscle DevelopmentActivin Receptors, Type IIAdaptor Proteins, Signal TransducingAnimalsCarrier ProteinsCell Cycle ProteinsEukaryotic Initiation FactorsGrowth HormoneInsulin Receptor Substrate ProteinsMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMuscle ProteinsMuscle, SkeletalMyostatinActivin Receptors, Type IIactivin receptor type II-BAdaptor Proteins, Signal TransducingAkt1 protein, mouseCarrier ProteinsCell Cycle ProteinsEif4ebp1 protein, mouseEukaryotic Initiation FactorsGrowth HormoneInsulin Receptor Substrate ProteinsIrs1 protein, mouseMstn protein, mouseMuscle ProteinsMyostatinPhosphoproteinsProto-Oncogene Proteins c-aktSmad2 ProteinSmad2 protein, mouseTrim63 protein, mouseTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID28870245
PMCPMC5583757
OpenAlexW2753339372

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.