Evidence map›Paper›PMID 24281010›Full record

ReviewThe Journal of endocrinology2014

Insulin signaling, resistance, and the metabolic syndrome: insights from mouse models into disease mechanisms.

Shaodong Guo

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 352 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
352citing papers in PubMed, 3 pooled it
22.7field-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

352 citing papers in PubMed, 3 syntheses or guidelines pooled it, 613 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Review
  7. Diagnosis-dependent metabolic reprogramming of follicular fluid.Reproductive biology and endocrinology : RB&E · 2026
    Article
  8. Review
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  14. Disruption of Hepatic Insulin Signaling Causes Phospholipid Dysregulation in Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

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

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

1 author at 1 institution in 1 country.

Shaodong GuoDivision of Molecular Cardiology, Department of Medicine, College of Medicine, Texas A&M University Health Science Center, Scott & White, Central Texas Veterans Health Care System, 1901 South 1st Street, Bldg. 205, Temple, Texas 76504, USA.
Central Texas Veterans Health Care System · US

Funding

Transcriptional Regulation of Metabolic and Hepatic Homeostasis by FoxO SignalingR01DK095118 · NIDDK · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI GUO, SHAODONG · 2012 to 2016
$1.4M
NIDDK NIH HHS R01 DK095118
6 · The paper itself

Abstract

Insulin resistance is a major underlying mechanism responsible for the 'metabolic syndrome', which is also known as insulin resistance syndrome. The incidence of the metabolic syndrome is increasing at an alarming rate, becoming a major public and clinical problem worldwide. The metabolic syndrome is represented by a group of interrelated disorders, including obesity, hyperglycemia, hyperlipidemia, and hypertension. It is also a significant risk factor for cardiovascular disease and increased morbidity and mortality. Animal studies have demonstrated that insulin and its signaling cascade normally control cell growth, metabolism, and survival through the activation of MAPKs and activation of phosphatidylinositide-3-kinase (PI3K), in which the activation of PI3K associated with insulin receptor substrate 1 (IRS1) and IRS2 and subsequent Akt→Foxo1 phosphorylation cascade has a central role in the control of nutrient homeostasis and organ survival. The inactivation of Akt and activation of Foxo1, through the suppression IRS1 and IRS2 in different organs following hyperinsulinemia, metabolic inflammation, and overnutrition, may act as the underlying mechanisms for the metabolic syndrome in humans. Targeting the IRS→Akt→Foxo1 signaling cascade will probably provide a strategy for therapeutic intervention in the treatment of type 2 diabetes and its complications. This review discusses the basis of insulin signaling, insulin resistance in different mouse models, and how a deficiency of insulin signaling components in different organs contributes to the features of the metabolic syndrome. Emphasis is placed on the role of IRS1, IRS2, and associated signaling pathways that are coupled to Akt and the forkhead/winged helix transcription factor Foxo1.

Indexed as

AnimalsDisease Models, AnimalHumansInsulinInsulin Receptor Substrate ProteinsInsulin ResistanceMechanistic Target of Rapamycin Complex 1Metabolic SyndromeMiceMultiprotein ComplexesSignal TransductionTOR Serine-Threonine KinasesInsulinInsulin Receptor Substrate ProteinsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesTOR Serine-Threonine Kinases

Identifiers

PMID24281010
PMCPMC4087161
OpenAlexW2094166298

What OpenQuestion holds

Textmetadata
LicenceTDM
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.