Evidence map›Paper›PMID 11489937›Full record

ArticleThe Journal of clinical investigation2001

Prevention of fat-induced insulin resistance by salicylate.

J K Kim, Y J Kim, J J Fillmore, Y Chen, I Moore, J Lee, M Yuan, Z W Li, M Karin, P Perret and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers.

0numbers the graph read from it
0cells of the map it votes in
229citing papers in PubMed
14.7field-weighted citation impact, top 1% 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

229 citing papers in PubMed, 715 citations in OpenAlex.

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  16. The Emerging Role of p21 in Diabetes and Related Metabolic Disorders.International journal of molecular sciences · 2024
    Review
  17. Endoplasmic Reticulum Stress and Obesity.Advances in experimental medicine and biology · 2024
    Review
  18. Review
  19. Article
  20. Article

169 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

J K KimHoward Hughes Medical Institute, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06536-8012, USA.
Y J Kim
J J Fillmore
Y Chen
I Moore
J Lee
M Yuan
Z W Li
M Karin
P Perret
S E Shoelson
G I Shulman
Yale University · USHoward Hughes Medical Institute · USJoslin Diabetes Center · USUniversity of California San Diego · US

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
Yale Mouse Metabolic Phenotyping CenterU24DK059635 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2001 to 2015
$8.9M
Mechanisms of Lipid-Induced Hepatic Insulin ResistanceR01DK040936 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 1989 to 2015
$5.1M
MEDIATORS AND MODIFIERS OF NF-kB IN INSULIN RESISTANCER37DK051729 · NIDDK · JOSLIN DIABETES CENTER · PI SHOELSON, STEVEN E · 2005 to 2010
$2.7M
RECEPTOR/SUBSTRATE COMPLEXES IN TRANSMEMBRANE SIGNALINGR01DK051729 · NIDDK · JOSLIN DIABETES CENTER · PI SHOELSON, STEVEN E · 1996 to 2004
$2.1M
NIDDK NIH HHS DK-51729NIDDK NIH HHS P30 DK045735NIDDK NIH HHS P30 DK-45735NIDDK NIH HHS R01 DK040936NIDDK NIH HHS R01 DK051729NIDDK NIH HHS R01 DK-45493NIDDK NIH HHS R01 DK-59635NIDDK NIH HHS U24 DK059635NIDDK NIH HHS U24 DK-59635
6 · The paper itself

Abstract

Insulin resistance is a major factor in the pathogenesis of type 2 diabetes and may involve fat-induced activation of a serine kinase cascade involving IKK-beta. To test this hypothesis, we first examined insulin action and signaling in awake rats during hyperinsulinemic-euglycemic clamps after a lipid infusion with or without pretreatment with salicylate, a known inhibitor of IKK-beta. Whole-body glucose uptake and metabolism were estimated using [3-(3)H]glucose infusion, and glucose uptake in individual tissues was estimated using [1-(14)C]2-deoxyglucose injection during the clamp. Here we show that lipid infusion decreased insulin-stimulated glucose uptake and activation of IRS-1-associated PI 3-kinase in skeletal muscle but that salicylate pretreatment prevented these lipid-induced effects. To examine the mechanism of salicylate action, we studied the effects of lipid infusion on insulin action and signaling during the clamp in awake mice lacking IKK-beta. Unlike the response in wild-type mice, IKK-beta knockout mice did not exhibit altered skeletal muscle insulin signaling and action following lipid infusion. In summary, high-dose salicylate and inactivation of IKK-beta prevent fat-induced insulin resistance in skeletal muscle by blocking fat-induced defects in insulin signaling and action and represent a potentially novel class of therapeutic agents for type 2 diabetes.

Indexed as

Insulin ResistanceAnimalsDiabetes Mellitus, Type 2Dietary FatsEnzyme InhibitorsGlucoseGlucose Clamp TechniqueI-kappa B KinaseInfusions, IntravenousLipidsMaleMuscle, SkeletalProtein Serine-Threonine KinasesRatsRats, WistarSalicylic AcidDietary FatsEnzyme InhibitorsGlucoseI-kappa B KinaseLipidsProtein Serine-Threonine KinasesSalicylic Acid

Identifiers

PMID11489937
PMCPMC209353
OpenAlexW2097838137

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.