Evidence map›Paper›PMID 28447730›Full record

ArticleMolecular medicine reports2017

Pioglitazone ameliorates Aβ42 deposition in rats with diet-induced insulin resistance associated with AKT/GSK3β activation.

Sisi Yang, Zhe Chen, Ming Cao, Renjie Li, Zhigang Wang, Muxun Zhang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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  10. Dietary supplements for prevention of Alzheimer's disease:Iranian journal of basic medical sciences · 2025
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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

6 authors at 3 institutions in 1 country.

Sisi YangDepartment of Geriatrics, Tongji Hospital Affiliated to The Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Zhe ChenDepartment of Integrated Chinese Traditional and Western Medicine, Tongji Hospital Affiliated to The Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Ming CaoDepartment of Geriatrics, Tongji Hospital Affiliated to The Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Renjie LiDepartment of Emergency, Tongji Hospital Affiliated to The Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Zhigang WangDepartment of Pathogen Biology, College of Basic Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei 430065, P.R. China.
Muxun ZhangDepartment of Endocrinology, Tongji Hospital Affiliated to The Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China.
Tongji Hospital · CNHuazhong University of Science and Technology · CNHubei University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pioglitazone may have potential benefits as an alternative therapeutic treatment for patients with Alzheimer's disease (AD), particularly in individuals that also have comorbid diabetes; however, the mechanisms of action remain unclear. The present study aimed to explore the effects of pioglitazone on amyloid β, isoform 42 (Aβ42) deposition in rats with diet‑induced insulin resistance (IR). Diet‑induced IR model rats were established in the presence or absence of pioglitazone. Plasma glucose and insulin levels, and cerebrospinal fluid insulin levels were measured; in addition, hippocampal tissues were collected for immunohistochemical analysis of Aβ42 expression. The levels of insulin‑degrading enzyme (IDE) and peroxisome proliferator‑activated receptor γ (PPARγ) mRNA and protein expression were analyzed by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. In addition, the activation of glycogen synthase kinase 3β (GSK3β) induced by phosphatidylinositol 3‑kinase (PI3K) /protein kinase B (AKT) signaling was detected by western blotting. Results from the present study demonstrated that pioglitazone may enhance peripheral and brain insulin sensitivity in diet‑induced IR model rats. Treatment with pioglitazone ameliorated Aβ42 deposition in the hippocampus by increasing IDE and PPARγ expression. Notably, activation of the PI3K/AKT/GSK3β pathway was also demonstrated to serve a role in pioglitazone‑induced Aβ42 degradation, which was abrogated by the PPARγ antagonist GW9662. Results from the present study indicated that pioglitazone may improve insulin sensitivity and ameliorate Aβ42 accumulation in rats with diet‑induced IR by regulating AKT/GSK3β activation, suggesting that pioglitazone may be a promising drug for AD treatment.

Indexed as

Insulin ResistanceSignal TransductionAlzheimer DiseaseAmyloid beta-PeptidesAnimalsDietGlycogen Synthase Kinase 3 betaMalePeptide FragmentsPioglitazoneProto-Oncogene Proteins c-aktRatsRats, WistarThiazolidinedionesAmyloid beta-Peptidesamyloid beta-protein (1-42)Glycogen Synthase Kinase 3 betaGsk3b protein, ratPeptide FragmentsPioglitazoneProto-Oncogene Proteins c-aktThiazolidinediones

Identifiers

PMID28447730
PMCPMC5428924
OpenAlexW2597327812

What Socratic 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 Socratic graph.