Evidence map›Paper›PMID 23011063›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2012

Deletion of Rab GAP AS160 modifies glucose uptake and GLUT4 translocation in primary skeletal muscles and adipocytes and impairs glucose homeostasis.

Melissa N Lansey, Natalie N Walker, Stefan R Hargett, Joseph R Stevens, Susanna R Keller

Abstract read
In one paragraph

Article 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 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 107 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Sex Differences in Glucose Homeostasis.Handbook of experimental pharmacology · 2023
    Article
  11. Article
  12. Normalization of maternal adiponectin in obese pregnant mice prevents programming of impaired glucose metabolism in adult offspring.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. AKT ISOFORMS-AS160-GLUT4: The defining axis of insulin resistance.Reviews in endocrine & metabolic disorders · 2021
    Review
  17. Role of Akt isoforms in neuronal insulin signaling and resistance.Cellular and molecular life sciences : CMLS · 2021
    Article
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

Melissa N LanseyDept. of Medicine/Division of Endocrinology, Univ. of Virginia, Charlottesville, VA 22908, USA. srk4b@virginia.edu
Natalie N Walker
Stefan R Hargett
Joseph R Stevens
Susanna R Keller
University of Virginia · US

Funding

THE MONOSACCHARIDE TRANSPORT SYSTEM OF THE ADIPOCYTER01DK025336 · NIDDK · DARTMOUTH COLLEGE · PI LIENHARD, GUSTAV E. · 1986 to 2008
$2.6M
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
Role of Rab GAPs AS160 and Tbc1d1 in GLUT4 translocation and glucose homeostasisR56DK081471 · NIDDK · UNIVERSITY OF VIRGINIA · PI KELLER, SUSANNA R · 2008 to 2009
$379k
The Role of the Rab GAP AS 160 in adipocyte MetabolismF31DK084767 · NIDDK · UNIVERSITY OF VIRGINIA · PI LANSEY, MELISSA N · 2009 to 2010
$56k
NIDDK NIH HHS F31 DK-084767NIDDK NIH HHS R01 DK025336NIDDK NIH HHS R01 DK081471NIDDK NIH HHS R01 DK-81471NIDDK NIH HHS R56 DK-081471
6 · The paper itself

Abstract

Tight control of glucose uptake in skeletal muscles and adipocytes is crucial to glucose homeostasis and is mediated by regulating glucose transporter GLUT4 subcellular distribution. In cultured cells, Rab GAP AS160 controls GLUT4 intracellular retention and release to the cell surface and consequently regulates glucose uptake into cells. To determine AS160 function in GLUT4 trafficking in primary skeletal muscles and adipocytes and investigate its role in glucose homeostasis, we characterized AS160 knockout (AS160(-/-)) mice. We observed increased and normal basal glucose uptake in isolated AS160(-/-) adipocytes and soleus, respectively, while insulin-stimulated glucose uptake was impaired and GLUT4 expression decreased in both. No such abnormalities were found in isolated AS160(-/-) extensor digitorum longus muscles. In plasma membranes isolated from AS160(-/-) adipose tissue and gastrocnemius/quadriceps, relative GLUT4 levels were increased under basal conditions and remained the same after insulin treatment. Concomitantly, relative levels of cell surface-exposed GLUT4, determined with a glucose transporter photoaffinity label, were increased in AS160(-/-) adipocytes and normal in AS160(-/-) soleus under basal conditions. Insulin augmented cell surface-exposed GLUT4 in both. These observations suggest that AS160 is essential for GLUT4 intracellular retention and regulation of glucose uptake in adipocytes and skeletal muscles in which it is normally expressed. In vivo studies revealed impaired insulin tolerance in the presence of normal (male) and impaired (female) glucose tolerance. Concurrently, insulin-elicited increases in glucose disposal were abolished in all AS160(-/-) skeletal muscles and liver but not in AS160(-/-) adipose tissues. This suggests AS160 as a target for differential manipulation of glucose homeostasis.

Indexed as

AdipocytesAnimalsFemaleGlucoseGlucose Tolerance TestGlucose Transporter Type 4GTPase-Activating ProteinsHomeostasisImmunoblottingInsulinMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMuscle, SkeletalGlucoseGlucose Transporter Type 4GTPase-Activating ProteinsInsulinRNA, MessengerSlc2a4 protein, mouseTbc1d4 protein, mouse

Identifiers

PMID23011063
PMCPMC3517634
OpenAlexW2045271318

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.