Evidence map›Paper›PMID 23990361›Full record

ArticleDiabetes2013

TRIB3 mediates glucose-induced insulin resistance via a mechanism that requires the hexosamine biosynthetic pathway.

Wei Zhang, Jiarong Liu, Ling Tian, Qinglan Liu, Yuchang Fu, W Timothy Garvey

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Tribbles 3 blunts exercise-induced skeletal muscle adaptation.bioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Cells · 2022
    Review
  13. Article
  14. Frontiers in genetics · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. TRB3 regulates skeletal muscle mass in food deprivation-induced atrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    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

6 authors at 2 institutions in 1 country.

Wei ZhangDepartment of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, Alabama.
Jiarong Liu
Ling Tian
Qinglan Liu
Yuchang Fu
W Timothy Garvey
University of Alabama at Birmingham · USBirmingham VA Medical Center · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
UAB Diabetes Research and Training CenterP60DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GARVEY, W TIMOTHY · 2008 to 2012
$8.4M
MECHANISMS OF HUMAN INSULIN RESISTANCER01DK038765 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GARVEY, W TIMOTHY · 1993 to 2010
$4.0M
NR4A Orphan Receptors And Insulin ResistanceR01DK083562 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GARVEY, W TIMOTHY · 2009 to 2012
$2.1M
ROLE OF GLUCOSE TRANSPORT PROTEINS IN DIABETES MELLITUSR29DK038765 · NIDDK · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI GARVEY, W TIMOTHY · 1988 to 1992
–
CSRD VA I01 CX000432NIDDK NIH HHS DK-038765NIDDK NIH HHS DK-083562NIDDK NIH HHS P30 DK079626NIDDK NIH HHS P60 DK-079626NIDDK NIH HHS P60 DK079626NIDDK NIH HHS R01 DK038765NIDDK NIH HHS R01 DK083562
6 · The paper itself

Abstract

In the current study, we investigated the role of tribbles homolog 3 (TRIB3) in glucose-induced insulin resistance and whether the induction of TRIB3 by glucose is dependent on the nutrient-sensing hexosamine biosynthetic pathway (HBP) known to mediate glucose toxicity in diabetes. In diabetic rats, TRIB3 expression in skeletal muscle was increased after 10 days of hyperglycemia, and glycemia and muscle TRIB3 were both restored toward normal by insulin therapy. In L6 myocytes, the induction of TRIB3 by high glucose or glucosamine was reversible upon removal of these substrates. To assess the role of HBP in the induction of TRIB3, we demonstrated that the ability of high glucose to augment TRIB3 expression was prevented by azaserine, an inhibitor of glutamine: fructose-6-phosphate amidotransferase (GFAT), which is the rate-limiting enzyme in the HBP pathway. TRIB3 expression was also substantially stimulated by glucosamine, which bypasses GFAT, accompanied by a decrease in the insulin-stimulated glucose transport rate, and neither response was affected by azaserine. Further, knockdown of TRIB3 inhibited, and TRIB3 overexpression enhanced, the ability of both high glucose and glucosamine to induce insulin resistance. These data provide the mechanistic link between the HBP flux and insulin resistance and point to TRIB3 as a novel target for treatment of glucose-induced insulin resistance.

Indexed as

AnimalsBiosynthetic PathwaysDiabetes Mellitus, ExperimentalGlucoseHexosaminesHyperglycemiaInsulinInsulin ResistanceMaleMuscle, SkeletalProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyUp-RegulationGlucoseHexosaminesInsulinProtein Serine-Threonine KinasesTrib3 protein, rat

Identifiers

PMID23990361
PMCPMC3837074
OpenAlexW2100466447

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.