Evidence map›Paper›PMID 33758419›Full record

ArticleNature metabolism2021

Liver alanine catabolism promotes skeletal muscle atrophy and hyperglycaemia in type 2 diabetes.

Jürgen G Okun, Patricia M Rusu, Andrea Y Chan, Yuqin Wu, Yann W Yap, Thomas Sharkie, Jonas Schumacher, Kathrin V Schmidt, Katherine M Roberts-Thomson, Ryan D Russell and 11 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 126 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 8 institutions in 3 countries.

Jürgen G OkunDivision of Inherited Metabolic Diseases, University Children's Hospital, Heidelberg, Germany.
Patricia M RusuDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0001-7210-1976
Andrea Y ChanDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Melbourne, Victoria, Australia.
Yuqin WuDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Melbourne, Victoria, Australia.ORCID http://orcid.org/0000-0002-1762-1896
Yann W YapDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Melbourne, Victoria, Australia.
Thomas SharkieDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Melbourne, Victoria, Australia.
Jonas SchumacherDivision of Molecular Metabolic Control, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Kathrin V SchmidtDivision of Inherited Metabolic Diseases, University Children's Hospital, Heidelberg, Germany.
Katherine M Roberts-ThomsonInstitute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Geelong, Victoria, Australia.
Ryan D RussellDepartment of Health and Human Performance, College of Health Professions, University of Texas Rio Grande Valley, Brownsville, TX, USA.
Annika ZotaDivision of Molecular Metabolic Control, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Susanne HilleDepartment of Internal Medicine III, University of Kiel, Kiel, Germany.
Andreas JungmannGerman Center for Cardiovascular Research (DZHK), Heidelberg and Kiel sites, Germany.
Ludovico MaggiDivision of Molecular Metabolic Control, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0002-9543-7840
Young LeeTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Matthias BlüherHelmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG) of the Helmholtz Zentrum München at the University of Leipzig, Leipzig, Germany.ORCID http://orcid.org/0000-0003-0208-2065
Stephan HerzigDivision of Molecular Metabolic Control, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID http://orcid.org/0000-0003-3950-3652
Michelle A KeskeInstitute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Geelong, Victoria, Australia.
Mathias HeikenwalderDivision of Chronic Inflammation and Cancer, German Cancer Research Center, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-3135-2274
Oliver J MüllerDepartment of Internal Medicine III, University of Kiel, Kiel, Germany.ORCID http://orcid.org/0000-0001-8223-2638
Adam J RoseDepartment of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Melbourne, Victoria, Australia. adam.rose@monash.edu.ORCID http://orcid.org/0000-0001-9132-8244
German Cancer Research Center · DEAustralian Regenerative Medicine Institute · AUHeidelberg University · DEChristian-Albrechts-Universität zu Kiel · DEDeakin University · AUHelmholtz Zentrum München · DEThe University of Texas Rio Grande Valley · USThe University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both obesity and sarcopenia are frequently associated in ageing, and together may promote the progression of related conditions such as diabetes and frailty. However, little is known about the pathophysiological mechanisms underpinning this association. Here we show that systemic alanine metabolism is linked to glycaemic control. We find that expression of alanine aminotransferases is increased in the liver in mice with obesity and diabetes, as well as in humans with type 2 diabetes. Hepatocyte-selective silencing of both alanine aminotransferase enzymes in mice with obesity and diabetes retards hyperglycaemia and reverses skeletal muscle atrophy through restoration of skeletal muscle protein synthesis. Mechanistically, liver alanine catabolism driven by chronic glucocorticoid and glucagon signalling promotes hyperglycaemia and skeletal muscle wasting. We further provide evidence for amino acid-induced metabolic cross-talk between the liver and skeletal muscle in ex vivo experiments. Taken together, we reveal a metabolic inter-tissue cross-talk that links skeletal muscle atrophy and hyperglycaemia in type 2 diabetes.

Indexed as

AlanineAlanine TransaminaseAnimalsBlood GlucoseDiabetes Mellitus, Type 2Disease Models, AnimalHomeostasisHumansHyperglycemiaLiverMiceMice, Inbred C57BLMuscle, SkeletalMuscular AtrophyObesityAlanineAlanine TransaminaseBlood Glucose

Identifiers

PMID33758419
OpenAlexW3138014196

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.