Evidence map›Paper›PMID 32945450›Full record

ArticleMolecular medicine reports2020

Fluoxetine regulates glucose and lipid metabolism via the PI3K‑AKT signaling pathway in diabetic rats.

Hailong Yang, Qiuyun Cao, Xiaolu Xiong, Peng Zhao, Diwen Shen, Yuzhe Zhang, Ning Zhang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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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

7 authors at 2 institutions in 1 country.

Hailong YangDepartment of Clinical Psychology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Qiuyun CaoDepartment of Clinical Psychology, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical College, Nanjing, Jiangsu 210000, P.R. China.
Xiaolu XiongDepartment of Endocrinology, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical College, Nanjing, Jiangsu 210000, P.R. China.
Peng ZhaoDepartment of Clinical Psychology, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical College, Nanjing, Jiangsu 210000, P.R. China.
Diwen ShenDepartment of Clinical Psychology, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical College, Nanjing, Jiangsu 210000, P.R. China.
Yuzhe ZhangDepartment of Clinical Psychology, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical College, Nanjing, Jiangsu 210000, P.R. China.
Ning ZhangDepartment of Clinical Psychology, Nanjing Brain Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu 210000, P.R. China.
Nanjing Drum Tower Hospital · CNNanjing Brain Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus poses a major threat towards global heath due to a lack of effective treatment. Fluoxetine hydrochloride, a selective 5‑hydroxytryptamine reuptake inhibitor, is the most commonly used antidepressant in clinical therapy; however, the potential molecular mechanisms of fluoxetine in diabetes remain unknown. In the present study, reduced glucose, total cholesterol and triglyceride levels and lipid metabolism, as well as upregulated proliferator‑activated receptor γ, fatty acid synthase and lipoprotein lipase, and downregulated sterol regulatory element‑binding protein 1‑c were detected in rats with streptozotocin (STZ)‑induced diabetes following treatment with fluoxetine. Furthermore, fluoxetine significantly inhibited the expression levels of glucose metabolism‑associated proteins in liver tissues, including glycogen synthase kinase 3β (GSK‑3β), glucose‑6 phosphatase catalytic subunit (G6PC), phosphoenolpyruvate carboxykinase (PEPCK) and forkhead box protein O1 (FOXO1). In addition, fluoxetine treatment notably attenuated morphological liver damage in rats with STZ‑induced diabetes. Additionally, fluoxetine could inhibit the phosphatidylinositol 3‑kinase‑protein kinase B (PI3K‑AKT) signaling pathway, whereas LY294002, a specific inhibitor of PI3K, suppressed the function of PI3K‑AKT signaling and suppressed the expression levels of glucose metabolism‑associated proteins, including GSK‑3β, G6PC, PEPCK and FOXO1 in BRL‑3A cells. The results of the present study revealed that fluoxetine may regulate glucose and lipid metabolism via the PI3K‑AKT signaling pathway in diabetic rats.

Indexed as

AnimalsCell LineChromonesDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2FluoxetineGene Expression RegulationLipid MetabolismMaleMorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsSignal TransductionStreptozocin2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesFluoxetineMorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktStreptozocin

Identifiers

PMID32945450
PMCPMC7453494
OpenAlexW3047598395

What OpenQuestion 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 OpenQuestion graph.