Evidence map›Paper›PMID 22967500›Full record

Trial reportAmerican journal of physiology. Endocrinology and metabolism2012

Insulin fails to enhance mTOR phosphorylation, mitochondrial protein synthesis, and ATP production in human skeletal muscle without amino acid replacement.

Rocco Barazzoni, Kevin R Short, Yan Asmann, Jill M Coenen-Schimke, Matthew M Robinson, K Sreekumaran Nair

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in American journal of physiology. Endocrinology and metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  8. Review: Nutritional regulation of muscle growth in neonatal swine.Animal : an international journal of animal bioscience · 2023
    Review
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  13. Observational
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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

6 authors at 1 institution in 1 country.

Rocco BarazzoniEndocrine Research Unit, Mayo Clinic, Rochester, MN, USA.
Kevin R Short
Yan Asmann
Jill M Coenen-Schimke
Matthew M Robinson
K Sreekumaran Nair
Mayo Clinic in Florida · US

Funding

DIABETES AND METABOLISMT32DK007352 · NIDDK · MAYO CLINIC ROCHESTER · PI MICHAEL D. JENSEN · 1986 to 2026
$9.4M
IN VIVO REGULATION OF PROTEIN TURNOVER BY HORMONESR01DK041973 · NIDDK · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NAIR, K SREEKUMARAN · 1989 to 2014
$7.3M
In Vivo Regulation of Protein Turnover by HormonesR56DK041973 · NIDDK · MAYO CLINIC ROCHESTER · PI NAIR, K SREEKUMARAN · 2015 to 2015
$159k
NCATS NIH HHS UL1 TR-00135NIDDK NIH HHS R01 DK041973NIDDK NIH HHS R01 DK-41973NIDDK NIH HHS T32 DK007352NIDDK NIH HHS T32 DK-07352
6 · The paper itself

Abstract

Systemic insulin administration causes hypoaminoacidemia by inhibiting protein degradation, which may in turn inhibit muscle protein synthesis (PS). Insulin enhances muscle mitochondrial PS and ATP production when hypoaminoacidemia is prevented by exogenous amino acid (AA) replacement. We determined whether insulin would stimulate mitochondrial PS and ATP production in the absence of AA replacement. Using l-[1,2-¹³C]leucine as a tracer, we measured the fractional synthetic rate of mitochondrial as well as sarcoplasmic and mixed muscle proteins in 18 participants during sustained (7-h) insulin or saline infusion (n = 9 each). We also measured muscle ATP production, mitochondrial enzyme activities, mRNA levels of mitochondrial genes, and phosphorylation of signaling proteins regulating protein synthesis. The concentration of circulating essential AA decreased during insulin infusion. Mitochondrial, sarcoplasmic, and mixed muscle PS rates were also lower during insulin (2-7 h) than during saline infusions despite increased mRNA levels of selected mitochondrial genes. Under these conditions, insulin did not alter mitochondrial enzyme activities and ATP production. These effects were associated with enhanced phosphorylation of Akt but not of protein synthesis activators mTOR, p70(S6K), and 4EBP1. In conclusion, sustained physiological hyperinsulinemia without AA replacement did not stimulate PS of mixed muscle or protein subfractions and did not alter muscle mitochondrial ATP production in healthy humans. These results support that insulin and AA act in conjunction to stimulate muscle mitochondrial function and mitochondrial protein synthesis.

Indexed as

Adenosine TriphosphateAdultAmino AcidsCarbon IsotopesFemaleGene Expression RegulationHumansHyperinsulinismInfusions, IntravenousInsulinInsulin, Regular, HumanLeucineMaleMitochondrial ProteinsMitochondria, MuscleMuscle, SkeletalAdenosine TriphosphateAKT1 protein, humanAmino AcidsCarbon IsotopesInsulinInsulin, Regular, HumanLeucineMitochondrial ProteinsMTOR protein, humanProto-Oncogene Proteins c-aktRNA, MessengerTOR Serine-Threonine Kinases

Identifiers

PMID22967500
PMCPMC3492854
OpenAlexW2096749875

What OpenQuestion holds

Textmetadata
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.