Evidence map›Paper›PMID 31644699›Full record

ReviewArquivos brasileiros de cardiologia2019

Biochemical and Molecular Mechanisms of Glucose Uptake Stimulated by Physical Exercise in Insulin Resistance State: Role of Inflammation.

Filipe Ferrari, Patrícia Martins Bock, Marcelo Trotte Motta, Lucas Helal

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Arquivos brasileiros de cardiologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 5 pooled it
5.6field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 5 syntheses or guidelines pooled it, 58 citations in OpenAlex.

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  18. Breakfast Quality and Insulin Resistance in Spanish Schoolchildren: A Cross-Sectional Study.International journal of environmental research and public health · 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

4 authors at 4 institutions in 1 country.

Filipe FerrariPrograma de Pós-graduação em Cardiologia e Ciências Cardiovasculares - Faculdade de Medicina - Hospital de Clínicas de Porto Alegre (HCPA) - Universidade Federal do Rio Grande do Sul, Porto Alegre, RS - Brazil.ORCID 0000-0001-6929-8392
Patrícia Martins BockLaboratório de Fisiopatologia do Exercício (LaFiEx), (HCPA/UFRGS), Porto Alegre, RS - Brazil.ORCID 0000-0001-8572-3950
Marcelo Trotte MottaDepartamento de Ciências Biológicas, Universidade Estadual de Feira de Santana (UEFS), Feira de Santana, BA - Brazil.
Lucas HelalPrograma de Pós-graduação em Cardiologia e Ciências Cardiovasculares - Faculdade de Medicina - Hospital de Clínicas de Porto Alegre (HCPA) - Universidade Federal do Rio Grande do Sul, Porto Alegre, RS - Brazil.ORCID 0000-0002-6900-7185
Faculdades Integradas de Taquara · BRHospital de Clínicas de Porto Alegre · BRUniversidade Estadual de Feira de Santana · BRUniversidade Federal do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity associated with systemic inflammation induces insulin resistance (IR), with consequent chronic hyperglycemia. A series of reactions are involved in this process, including increased release of proinflammatory cytokines, and activation of c-Jun N-terminal kinase (JNK), nuclear factor-kappa B (NF-κB) and toll-like receptor 4 (TLR4) receptors. Among the therapeutic tools available nowadays, physical exercise (PE) has a known hypoglycemic effect explained by complex molecular mechanisms, including an increase in insulin receptor phosphorylation, in AMP-activated protein kinase (AMPK) activity, in the Ca2+/calmodulin-dependent protein kinase kinase (CaMKK) pathway, with subsequent activation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), Rac1, TBC1 domain family member 1 and 4 (TBC1D1 and TBC1D4), in addition to a variety of signaling molecules, such as GTPases, Rab and soluble N-ethylmaleimide-sensitive factor attached protein receptor (SNARE) proteins. These pathways promote greater translocation of GLUT4 and consequent glucose uptake by the skeletal muscle. Phosphoinositide-dependent kinase (PDK), atypical protein kinase C (aPKC) and some of its isoforms, such as PKC-iota/lambda also seem to play a fundamental role in the transport of glucose. In this sense, the association between autophagy and exercise has also demonstrated a relevant role in the uptake of muscle glucose. Insulin, in turn, uses a phosphoinositide 3-kinase (PI3K)-dependent mechanism, while exercise signal may be triggered by the release of calcium from the sarcoplasmic reticulum. The objective of this review is to describe the main molecular mechanisms of IR and the relationship between PE and glucose uptake.

Indexed as

ExerciseInsulin ResistanceGlucose Transporter Type 4HumansHyperglycemiaInflammationObesityPhosphorylationGlucose Transporter Type 4

Identifiers

PMID31644699
PMCPMC7021273
OpenAlexW2978545140

What Socratic holds

Textmetadata
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 Socratic graph.