Evidence map›Paper›PMID 33184929›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021

Prokineticin receptor 1 ameliorates insulin resistance in skeletal muscle.

Jongsoo Mok, Tae Sub Park, Sunhong Kim, Daehoon Kim, Cheol Soo Choi, Joonghoon Park

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 pooled it
0.8field-weighted citation impact, top 28% 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

11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. PROKR1-CREB-NR4A2 axis for oxidative muscle fiber specification and improvement of metabolic function.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Pooled it
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  11. Prokineticin receptor 1 ameliorates insulin resistance in skeletal muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
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 1 country.

Jongsoo MokDepartment of International Agricultural Technology, Graduate School of International Agricultural Technology, Seoul National University, Seoul, Republic of Korea.ORCID https://orcid.org/0000-0003-0795-3608
Tae Sub ParkDepartment of International Agricultural Technology, Graduate School of International Agricultural Technology, Seoul National University, Seoul, Republic of Korea.ORCID https://orcid.org/0000-0002-0372-5467
Sunhong KimDisease Target Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Cheongwon-gun, Republic of Korea.
Daehoon KimPharmacology Research Division, New Drug Discovery Center, Hyundai Pharm Co, Cheonan-si, Republic of Korea.
Cheol Soo ChoiKorea Mouse Metabolic Phenotyping Center, Lee Gil Ya Cancer and Diabetes Institute, Gachon University School of Medicine, Seongnam-si, Republic of Korea.
Joonghoon ParkDepartment of International Agricultural Technology, Graduate School of International Agricultural Technology, Seoul National University, Seoul, Republic of Korea.ORCID https://orcid.org/0000-0002-3458-2913
Seoul National University of Science and Technology · KRGachon University · KRHyundai Pharm (South Korea) · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes mellitus may result from insulin resistance in skeletal muscle. Prokineticin receptor 1 (Prokr1) improves metabolic phenotype in adipose tissue and the cardiovascular system; however, its effects on skeletal muscle have not been investigated. We investigated the Prokr1 signaling pathways and its metabolic function in murine myoblast, satellite cells, and their differentiated myotubes. We measured the expression levels of Prokr1 in the skeletal muscle of mice as well as human skeletal muscle cell-derived myotubes. Prokineticin 2 (PROK2), a ligand of PROKR1, induced calcium mobilization in a dose-dependent manner and altered the mRNA levels of 578 genes in PROKR1-overexpressed HEK293T cells. Functional enrichment of differentially expressed genes revealed that PROKR1 activated Gq-mediated PI3K/AKT and MAPK/ERK signaling pathways in skeletal muscle cells. Prokr1 significantly activated the PI3K/AKT signaling pathway in myotubes derived from C2C12 and satellite cells, regardless of the presence or absence of insulin. Prokr1 also promoted the translocation of glucose transporter 4 (GLUT4) into the plasma membrane. In palmitate-induced insulin-resistant myotubes, Prokr1 enhanced insulin-stimulated AKT phosphorylation, GLUT4 translocation, and glucose uptake. mRNA and protein levels of Prokr1 were significantly decreased in skeletal muscle and white adipose tissue of diet-induced obese mice, and the amount of PROKR1 protein was significantly decreased in human skeletal muscle cell-derived myotubes under insulin resistance conditions. Taken together, these results demonstrate that Prokr1 plays an important role in insulin sensitivity and is a potential therapeutic target to ameliorate insulin resistance in skeletal muscle.

Indexed as

Insulin ResistanceAgedAnimalsDiabetes Mellitus, Type 2FemaleHEK293 CellsHumansMaleMiceMice, Inbred C57BLMice, ObeseMuscle DevelopmentMuscle Fibers, SkeletalReceptors, G-Protein-CoupledSatellite Cells, Skeletal MuscleSignal TransductionPKR1 protein, mousePROKR1 protein, humanReceptors, G-Protein-Coupled

Identifiers

PMID33184929
PMCPMC12315503
OpenAlexW3104692175

What OpenQuestion holds

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LicenceCC BY-NC
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.