Evidence map›Paper›PMID 26625902›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2016

Rab GAPs AS160 and Tbc1d1 play nonredundant roles in the regulation of glucose and energy homeostasis in mice.

Stefan R Hargett, Natalie N Walker, Susanna R Keller

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  7. AKT ISOFORMS-AS160-GLUT4: The defining axis of insulin resistance.Reviews in endocrine & metabolic disorders · 2021
    Review
  8. Article
  9. Article
  10. Insulin-Stimulated Muscle Glucose Uptake and Insulin Signaling in Lean and Obese Humans.The Journal of clinical endocrinology and metabolism · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Thirty sweet years of GLUT4.The Journal of biological chemistry · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

3 authors at 1 institution in 1 country.

Stefan R HargettDepartment of Medicine-Division of Endocrinology, University of Virginia, Charlottesville Virginia.
Natalie N WalkerDepartment of Medicine-Division of Endocrinology, University of Virginia, Charlottesville Virginia.
Susanna R KellerDepartment of Medicine-Division of Endocrinology, University of Virginia, Charlottesville Virginia srk4b@virginia.edu.
University of Virginia · US

Funding

Role of Rab GAPs AS160 and Tbc1d1 in GLUT4 translocation and glucose homeostasisR01DK081471 · NIDDK · UNIVERSITY OF VIRGINIA · PI KELLER, SUSANNA R · 2011 to 2014
$1.4M
NIDDK NIH HHS R01 DK081471NIDDK NIH HHS R01-DK-81471
6 · The paper itself

Abstract

The related Rab GTPase-activating proteins (Rab GAPs) AS160 and Tbc1d1 regulate the trafficking of the glucose transporter GLUT4 that controls glucose uptake in muscle and fat cells and glucose homeostasis. AS160- and Tbc1d1-deficient mice exhibit different adipocyte- and skeletal muscle-specific defects in glucose uptake, GLUT4 expression and trafficking, and glucose homeostasis. A recent study analyzed male mice with simultaneous deletion of AS160 and Tbc1d1 (AS160(-/-)/Tbc1d1(-/-) mice). Herein, we describe abnormalities in male and female AS160(-/-)/Tbc1d1(-/-) mice on another strain background. We confirm the earlier observation that GLUT4 expression and glucose uptake defects of single-knockout mice join in AS160(-/-)/Tbc1d1(-/-) mice to affect all skeletal muscle and adipose tissues. In large mixed fiber-type skeletal muscles, changes in relative basal GLUT4 plasma membrane association in AS160(-/-) and Tbc1d1(-/-) mice also combine in AS160(-/-)/Tbc1d1(-/-) mice. However, we found different glucose uptake abnormalities in isolated skeletal muscles and adipocytes than reported previously, resulting in different interpretations of how AS160 and Tbc1d1 regulate GLUT4 translocation to the cell surface. In support of a larger role for AS160 in glucose homeostasis, in contrast with the previous study, we find similarly impaired glucose and insulin tolerance in AS160(-/-)/Tbc1d1(-/-) and AS160(-/-) mice. However, in vivo glucose uptake abnormalities in AS160(-/-)/Tbc1d1(-/-) skeletal muscles differ from those observed previously in AS160(-/-) mice, indicating additional defects due to Tbc1d1 deletion. Similar to AS160- and Tbc1d1-deficient mice, AS160(-/-)/Tbc1d1(-/-) mice show sex-specific abnormalities in glucose and energy homeostasis. In conclusion, our study supports nonredundant functions for AS160 and Tbc1d1.

Indexed as

AdipocytesAdipose TissueAnimalsBlood GlucoseEnergy MetabolismFemaleGlucoseGlucose Transporter Type 4GTPase-Activating ProteinsHomeostasisInsulinInsulin ResistanceMaleMiceMice, KnockoutMuscle Fibers, SkeletalBlood GlucoseGlucoseGlucose Transporter Type 4GTPase-Activating ProteinsInsulinProto-Oncogene Proteins c-aktSlc2a4 protein, mouseTbc1d1 protein, mouseTbc1d4 protein, mouseadipocytesAkt substrate of 160 kDaglucose transporter 4glucose uptakeRab GTPase-activating proteinsskeletal muscle

Identifiers

PMID26625902
PMCPMC4888528
OpenAlexW2181866290

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.