Evidence map›Paper›PMID 39966707›Full record

ReviewMolecular medicine (Cambridge, Mass.)2025

Type 3 diabetes and metabolic reprogramming of brain neurons: causes and therapeutic strategies.

Xiangyuan Meng, Hui Zhang, Zhenhu Zhao, Siyao Li, Xin Zhang, Ruihan Guo, Huimin Liu, Yiling Yuan, Wanrui Li, Qi Song and 1 more

Abstract readReview
In one paragraph

Review in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Article
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  7. Tanycytes: bloodhounds of the metabolic brain.Trends in endocrinology and metabolism: TEM · 2026
    Review
  8. Review
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  10. Article
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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

11 authors.

Xiangyuan MengDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China.
Hui ZhangInstitute of Agricultural Quality Standard and Testing Technology, Jilin Academy of Agricultural Sciences, Changchun, 130021, China.
Zhenhu ZhaoDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China.
Siyao LiDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China.
Xin ZhangDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China.
Ruihan GuoDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China.
Huimin LiuDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China.
Yiling YuanDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China.
Wanrui LiDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China.
Qi SongDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China.
Jinyu LiuDepartment of Toxicology, School of Public Health, Jilin University, Changchun, 130021, China. jy_liu@jlu.edu.cn.

Funding

Medjaden Academy & Research Foundation for Young Scientists MJR202510105National Natural Science Foundation of China 82073581
6 · The paper itself

Abstract

Abnormal glucose metabolism inevitably disrupts normal neuronal function, a phenomenon widely observed in Alzheimer's disease (AD). Investigating the mechanisms of metabolic adaptation during disease progression has become a central focus of research. Considering that impaired glucose metabolism is closely related to decreased insulin signaling and insulin resistance, a new concept "type 3 diabetes mellitus (T3DM)" has been coined. T3DM specifically refers to the brain's neurons becoming unresponsive to insulin, underscoring the strong link between diabetes and AD. Recent studies reveal that during brain insulin resistance, neurons exhibit mitochondrial dysfunction, reduced glucose metabolism, and elevated lactate levels. These findings suggest that impaired insulin signaling caused by T3DM may lead to a compensatory metabolic shift in neurons toward glycolysis. Consequently, this review aims to explore the underlying causes of T3DM and elucidate how insulin resistance drives metabolic reprogramming in neurons during AD progression. Additionally, it highlights therapeutic strategies targeting insulin sensitivity and mitochondrial function as promising avenues for the successful development of AD treatments.

Indexed as

BrainNeuronsAlzheimer DiseaseAnimalsCellular ReprogrammingEnergy MetabolismGlucoseGlycolysisHumansInsulinInsulin ResistanceMetabolic ReprogrammingMitochondriaSignal TransductionGlucoseInsulinAlzheimer’s diseaseInsulin resistanceMetabolic reprogrammingType 3 diabetes mellitus

Identifiers

PMID39966707
PMCPMC11834690

What OpenQuestion holds

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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.