Evidence map›Paper›PMID 25845663›Full record

ArticleDiabetes2015

Genetic Disruption of Protein Kinase STK25 Ameliorates Metabolic Defects in a Diet-Induced Type 2 Diabetes Model.

Manoj Amrutkar, Emmelie Cansby, Urszula Chursa, Esther Nuñez-Durán, Belén Chanclón, Marcus Ståhlman, Vincent Fridén, Louise Mannerås-Holm, Anna Wickman, Ulf Smith and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  10. Pathophysiological Mechanisms and Clinical Associations of Non-Alcoholic Fatty Pancreas Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
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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

14 authors at 3 institutions in 3 countries.

Manoj AmrutkarLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Emmelie CansbyLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Urszula ChursaLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Esther Nuñez-DuránLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Belén ChanclónLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Marcus StåhlmanWallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Vincent FridénCenter for Physiology and Bio-Imaging, Core Facilities, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Louise Mannerås-HolmWallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Anna WickmanCenter for Physiology and Bio-Imaging, Core Facilities, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Ulf SmithLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Fredrik BäckhedWallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden The Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark.
Jan BorénWallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden.
Brian W HowellDepartment of Neuroscience and Physiology, State University of New York Upstate Medical University, Syracuse, NY.
Margit MahlapuuLundberg Laboratory for Diabetes Research, Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg, Sweden margit.mahlapuu@gu.se.
University of Gothenburg · SENovo Nordisk Foundation · DKSUNY Upstate Medical University · US

Funding

Regulation of Neuronal Lamination and Dendritogenesis by Reelin-Dab1 SignalingR01NS073662 · NINDS · UPSTATE MEDICAL UNIVERSITY · PI HOWELL, BRIAN W. · 2011 to 2015
$1.7M
NINDS NIH HHS NS-073662NINDS NIH HHS R01 NS073662
6 · The paper itself

Abstract

Understanding the molecular networks controlling ectopic lipid deposition, glucose tolerance, and insulin sensitivity is essential to identifying new pharmacological approaches to treat type 2 diabetes. We recently identified serine/threonine protein kinase 25 (STK25) as a negative regulator of glucose and insulin homeostasis based on observations in myoblasts with acute depletion of STK25 and in STK25-overexpressing transgenic mice. Here, we challenged Stk25 knockout mice and wild-type littermates with a high-fat diet and showed that STK25 deficiency suppressed development of hyperglycemia and hyperinsulinemia, improved systemic glucose tolerance, reduced hepatic gluconeogenesis, and increased insulin sensitivity. Stk25(-/-) mice were protected from diet-induced liver steatosis accompanied by decreased protein levels of acetyl-CoA carboxylase, a key regulator of both lipid oxidation and synthesis. Lipid accumulation in Stk25(-/-) skeletal muscle was reduced, and expression of enzymes controlling the muscle oxidative capacity (Cpt1, Acox1, Cs, Cycs, Ucp3) and glucose metabolism (Glut1, Glut4, Hk2) was increased. These data are consistent with our previous study of STK25 knockdown in myoblasts and reciprocal to the metabolic phenotype of Stk25 transgenic mice, reinforcing the validity of the results. The findings suggest that STK25 deficiency protects against the metabolic consequences of chronic exposure to dietary lipids and highlight the potential of STK25 antagonists for the treatment of type 2 diabetes.

Indexed as

Diet, High-FatAcetyl-CoA CarboxylaseAnimalsBlood GlucoseBody CompositionBody WeightDiabetes Mellitus, Type 2Fatty LiverGluconeogenesisGlucose Tolerance TestHippo KinasesHyperglycemiaHyperinsulinismInsulinInsulin ResistanceIntracellular Signaling Peptides and ProteinsAcetyl-CoA CarboxylaseBlood GlucoseHippo KinasesInsulinIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesStk25 protein, mouse

Identifiers

PMID25845663
PMCPMC4876789
OpenAlexW2125372126

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.