Evidence map›Paper›PMID 25670827›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2015

Skeletal muscle insulin resistance in zebrafish induces alterations in β-cell number and glucose tolerance in an age- and diet-dependent manner.

Lisette A Maddison, Kaitlin E Joest, Ryan M Kammeyer, Wenbiao Chen

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.9field-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

35 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Ppid is necessary for overnutrition-induced β-cell loss.American journal of physiology. Endocrinology and metabolism · 2026
    Article
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  18. Review
  19. Which Hyperglycemic Model of Zebrafish (Frontiers in cell and developmental biology · 2021
    Review
  20. 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

4 authors at 2 institutions in 1 country.

Lisette A MaddisonDepartment of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee; and.
Kaitlin E JoestDepartment of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee; and.
Ryan M KammeyerIndiana University School of Medicine, Indianapolis, Indiana.
Wenbiao ChenDepartment of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee; and wenbiao.chen@vanderbilt.edu.
Vanderbilt University · USIndiana University – Purdue University Indianapolis · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
THREE-TIERED PREVENTION MODEL TO BETTER SERVE ALL STUDENP30HD015052 · NICHD · VANDERBILT UNIVERSITY · PI DYKENS, ELISABETH MAY · 1985 to 2014
$18.6M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
Vanderbilt Student Research Training ProgramT35DK007383 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI William Heerman · 1986 to 2026
$4.1M
A system for spatiotemporal gene inactivationR01DK088686 · NIDDK · VANDERBILT UNIVERSITY · PI CHEN, WENBIAO · 2010 to 2014
$1.7M
GENETIC ANALYSIS--DYSERYTHROPOIETIC ANEMIA IN ZEBRAFISHK08DK002593 · NIDDK · CHILDREN'S HOSPITAL BOSTON · PI PAW, BARRY H · 1998 to 2000
$120k
NCI NIH HHS CA-68485NEI NIH HHS EY-08126NICHD NIH HHS HD-15052NIDDK NIH HHS DK-02593NIDDK NIH HHS DK-088686NIDDK NIH HHS DK-20593NIDDK NIH HHS DK-58404NIDDK NIH HHS DK-59637NIDDK NIH HHS P30 DK020593NIDDK NIH HHS R01 DK088686NIDDK NIH HHS T35 DK007383
6 · The paper itself

Abstract

Insulin resistance creates an environment that promotes β-cell failure and development of diabetes. Understanding the events that lead from insulin resistance to diabetes is necessary for development of effective preventional and interventional strategies, and model systems that reflect the pathophysiology of disease progression are an important component toward this end. We have confirmed that insulin enhances glucose uptake in zebrafish skeletal muscle and have developed a zebrafish model of skeletal muscle insulin resistance using a dominant-negative IGF-IR. These zebrafish exhibit blunted insulin signaling and glucose uptake in the skeletal muscle, confirming insulin resistance. In young animals, we observed an increase in the number of β-cells and normal glucose tolerance that was indicative of compensation for insulin resistance. In older animals, the β-cell mass was reduced to that of control with the appearance of impaired glucose clearance but no elevation in fasting blood glucose. Combined with overnutrition, the insulin-resistant animals have an increased fasting blood glucose compared with the control animals, demonstrating that the β-cells in the insulin-resistant fish are in a vulnerable state. The relatively slow progression from insulin resistance to glucose intolerance in this model system has the potential in the future to test cooperating genes or metabolic conditions that may accelerate the development of diabetes and provide new therapeutic targets.

Indexed as

AgingInsulin ResistanceAnimalsAnimals, Genetically ModifiedBiological TransportCell CountDisease ProgressionGlucoseGlucose IntoleranceGreen Fluorescent ProteinsHyperglycemiaInsulinInsulin-Like Growth Factor IInsulin-Secreting CellsLuminescent ProteinsMuscle, Skeletalenhanced green fluorescent proteinGlucoseGreen Fluorescent ProteinsIGF1RA protein, zebrafishInsulinInsulin-Like Growth Factor ILuminescent ProteinsReceptor, IGF Type 1Recombinant Fusion ProteinsRed Fluorescent ProteinZebrafish Proteinsdiabetesglucose tolerancezebrafishβ-cell

Identifiers

PMID25670827
PMCPMC4398831
OpenAlexW2063036784

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.