Evidence map›Paper›PMID 27898058›Full record

ArticleScientific reports2016

CCL5/RANTES contributes to hypothalamic insulin signaling for systemic insulin responsiveness through CCR5.

Szu-Yi Chou, Reni Ajoy, Chun Austin Changou, Ya-Ting Hsieh, Yang-Kao Wang, Barry Hoffer

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
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

33 citing papers in PubMed, 49 citations in OpenAlex.

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  18. The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023
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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 4 institutions in 2 countries.

Szu-Yi ChouThe PhD Program for Neural Regenerative Medicine, College of Medicine, College of Medical Science and Technology, Taipei Medical University and National Health Research Institutes (NHRI), 250 Wuxing St. Taipei, Taiwan, 110.
Reni AjoyThe PhD Program for Neural Regenerative Medicine, College of Medicine, College of Medical Science and Technology, Taipei Medical University and National Health Research Institutes (NHRI), 250 Wuxing St. Taipei, Taiwan, 110.
Chun Austin ChangouThe Ph.D. Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Ya-Ting HsiehThe PhD Program for Neural Regenerative Medicine, College of Medicine, College of Medical Science and Technology, Taipei Medical University and National Health Research Institutes (NHRI), 250 Wuxing St. Taipei, Taiwan, 110.
Yang-Kao WangDepartment of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Barry HofferThe PhD Program for Neural Regenerative Medicine, College of Medicine, College of Medical Science and Technology, Taipei Medical University and National Health Research Institutes (NHRI), 250 Wuxing St. Taipei, Taiwan, 110.
National Health Research Institutes · TWTaipei Medical University · TWNational Cheng Kung University · TWUniversity School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many neurodegenerative diseases are accompanied by metabolic disorders. CCL5/RANTES, and its receptor CCR5 are known to contribute to neuronal function as well as to metabolic disorders such as type 2 diabetes mellitus, obesity, atherosclerosis and metabolic changes after HIV infection. Herein, we found that the lack of CCR5 or CCL5 in mice impaired regulation of energy metabolism in hypothalamus. Immunostaining and co-immunoprecipitation revealed the specific expression of CCR5, associated with insulin receptors, in the hypothalamic arcuate nucleus (ARC). Both ex vivo stimulation and in vitro tissue culture studies demonstrated that the activation of insulin, and PI3K-Akt pathways were impaired in CCR5 and CCL5 deficient hypothalamus. The inhibitory phosphorylation of insulin response substrate-1 at Ser302 (IRS-1

Indexed as

AnimalsArcuate Nucleus of HypothalamusChemokine CCL5Diabetes Mellitus, Type 2Disease Models, AnimalEnergy MetabolismGlucose Transporter Type 4HumansHypothalamusInsulinMiceNeuronsPhosphatidylinositol 3-KinasesPhosphorylationReceptor, InsulinSignal TransductionCcl5 protein, mouseChemokine CCL5Glucose Transporter Type 4InsulinPhosphatidylinositol 3-KinasesReceptor, InsulinSlc2a4 protein, mouse

Identifiers

PMID27898058
PMCPMC5127185
OpenAlexW2559717016

What OpenQuestion holds

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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.