Evidence map›Paper›PMID 30875909›Full record

ReviewInternational journal of molecular sciences2019

Molecular Mechanisms of Hypothalamic Insulin Resistance.

Hiraku Ono

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Hypothalamus-liver talks: whispers in the language of metabolism.Reviews in endocrine & metabolic disorders · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Metabolic Status Modulates Global and Local Brain Age Estimates in Overweight and Obese Adults.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2025
    Article
  15. Review
  16. CORRELATION BETWEEN TRAUMATIC BRAIN INJURY, OBESITY AND INSULIN-RESISTANCE - A CASE REPORT.Journal of rehabilitation medicine. Clinical communications · 2025
    Article
  17. Review
  18. Differential Efficacy of Weight Loss Interventions in Patients with Versus Without Diabetes.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2024
    Review
  19. Review
  20. Review
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.

Hiraku OnoDepartment of Endocrinology, Hematology and Gerontology, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan. hono@chiba-u.jp.
Chiba University · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology 18K08502
6 · The paper itself

Abstract

Insulin exists in the central nervous system, where it executes two important functions in the hypothalamus: the suppression of food intake and the improvement of glucose metabolism. Recent studies have shown that both are exerted robustly in rodents and humans. If intact, these functions exert beneficial effects on obesity and diabetes, respectively. Disruption of both occurs due to a condition known as hypothalamic insulin resistance, which is caused by obesity and the overconsumption of saturated fat. An enormous volume of literature addresses the molecular mechanisms of hypothalamic insulin resistance. IKKβ and JNK are major players in the inflammation pathway, which is activated by saturated fatty acids that induce hypothalamic insulin resistance. Two major tyrosine phosphatases, PTP-1B and TCPTP, are upregulated in chronic overeating. They dephosphorylate the insulin receptor and insulin receptor substrate proteins, resulting in hypothalamic insulin resistance. Prolonged hyperinsulinemia with excessive nutrition activates the mTOR/S6 kinase pathway, thereby enhancing IRS-1 serine phosphorylation to induce hypothalamic insulin resistance. Other mechanisms associated with this condition include hypothalamic gliosis and disturbed insulin transport into the central nervous system. Unveiling the precise molecular mechanisms involved in hypothalamic insulin resistance is important for developing new ways of treating obesity and type 2 diabetes.

Indexed as

Insulin ResistanceSignal TransductionAnimalsDiabetes Mellitus, Type 2EatingHumansHypothalamusI-kappa B KinaseMAP Kinase Kinase 4ObesityPhosphorylationProtein Tyrosine Phosphatase, Non-Receptor Type 1Protein Tyrosine Phosphatase, Non-Receptor Type 2Receptor, InsulinUp-RegulationI-kappa B KinaseIKBKB protein, humanMAP Kinase Kinase 4Protein Tyrosine Phosphatase, Non-Receptor Type 1Protein Tyrosine Phosphatase, Non-Receptor Type 2PTPN1 protein, humanPTPN2 protein, humanReceptor, Insulinfood intakeglucose metabolismhypothalamusinflammationinsulin resistanceobesity

Identifiers

PMID30875909
PMCPMC6471380
OpenAlexW2921810509

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.