Evidence map›Paper›PMID 28712011›Full record

ArticleMolecular neurobiology2018

FGF21 Attenuates High-Fat Diet-Induced Cognitive Impairment via Metabolic Regulation and Anti-inflammation of Obese Mice.

Qingzhi Wang, Jing Yuan, Zhanyang Yu, Li Lin, Yinghua Jiang, Zeyuan Cao, Pengwei Zhuang, Michael J Whalen, Bo Song, Xiao-Jie Wang and 4 more

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

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
4.8field-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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.

  1. Pooled it
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26 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

14 authors at 3 institutions in 2 countries.

Qingzhi WangDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450007, China.
Jing YuanDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450007, China.
Zhanyang YuNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02129, USA.
Li LinKey Laboratory of Biotechnology and Pharmaceutical Engineering, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Yinghua JiangNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02129, USA.
Zeyuan CaoNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02129, USA.
Pengwei ZhuangNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02129, USA.
Michael J WhalenNeurobehavioral Core Facility, Department of Pediatrics, Pediatric Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02129, USA.
Bo SongDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450007, China.
Xiao-Jie WangKey Laboratory of Biotechnology and Pharmaceutical Engineering, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Xiaokun LiKey Laboratory of Biotechnology and Pharmaceutical Engineering, School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China.
Eng H LoNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02129, USA.
Yuming XuDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450007, China. xuyuming@zzu.edu.cn.
Xiaoying WangNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02129, USA. wangxi@helix.mgh.harvard.edu.ORCID http://orcid.org/0000-0003-3636-7931
Harvard University · USWenzhou Medical University · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

Recombinant FGF21 as a novel approach for treating ischemic stroke in type 2 diabetesR01NS099539 · NINDS · TULANE UNIVERSITY OF LOUISIANA · PI WANG, XIAOYING · 2016 to 2020
$1.8M
Department of S and T for Social Development 2011ZX09102-004National Institute of Neurological Disorders and Stroke RO1 NS099539National Natural Science Foundation of China 52111000National Natural Science Foundation of China 81470999NINDS NIH HHS R01 NS099539
6 · The paper itself

Abstract

Accumulating studies suggest that overnutrition-associated obesity may lead to development of type 2 diabetes mellitus and metabolic syndromes (MetS). MetS and its components are important risk factors of mild cognitive impairment, age-related cognitive decline, vascular dementia, and Alzheimer's disease. It has been recently proposed that development of a disease-course modification strategy toward early and effective risk factor management would be clinically significant in reducing the risk of metabolic disorder-initiated cognitive decline. In the present study, we propose that fibroblast growth factor 21 (FGF21) is a novel candidate for the disease-course modification approach. Using a high-fat diet (HFD) consumption-induced obese mouse model, we tested our hypothesis that recombinant human FGF21 (rFGF21) administration is effective for improving obesity-induced cognitive dysfunction and anxiety-like behavior, by its multiple metabolic modulation and anti-pro-inflammation actions. Our experimental findings support our hypothesis that rFGF21 is protective to HFD-induced cognitive impairment, at least in part by metabolic regulation in glucose tolerance impairment, insulin resistance, and hyperlipidemia; potent systemic pro-inflammation inhibition; and improvement of hippocampal dysfunction, particularly by inhibiting pro-neuroinflammation and neurogenesis deficit. This study suggests that FGF21 might be a novel molecular target of the disease-course-modifying strategy for early intervention of MstS-associated cognitive decline.

Indexed as

AnimalsAnti-Inflammatory AgentsAnxietyBehavior, AnimalBlood-Brain BarrierCognitive DysfunctionCytokinesDiet, High-FatFibroblast Growth FactorsGlucoseHippocampusHumansHyperlipidemiasInflammationInsulin ResistanceMaleAnti-Inflammatory AgentsCytokinesfibroblast growth factor 21Fibroblast Growth FactorsGlucoseReceptors, Fibroblast Growth FactorRecombinant ProteinsCognitive impairmentFibroblast growth factor 21High-fat dietInflammationMetabolic disordersObese mice

Identifiers

PMID28712011
PMCPMC5971086
OpenAlexW2735844318

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.