Evidence map›Paper›PMID 34393754›Full record

ArticleFrontiers in aging neuroscience2021

α-Synuclein Regulates Peripheral Insulin Secretion and Glucose Transport.

Nadeeja Wijesekara, Rosemary Ahrens, Ling Wu, Tammy Langman, Anurag Tandon, Paul E Fraser

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

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  9. Potential mechanisms to modify impaired glucose metabolism in neurodegenerative disorders.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 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 2 institutions in 1 country.

Nadeeja WijesekaraTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada.
Rosemary AhrensTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada.
Ling WuTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada.
Tammy LangmanTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada.
Anurag TandonTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada.
Paul E FraserTanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada.
Occupational Cancer Research Centre · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimPopulation based studies indicate a positive association between type 2 diabetes (T2D) and Parkinson's disease (PD) where there is an increased risk of developing PD in patients with T2D. PD is characterized by the abnormal accumulation of intraneuronal aggregated α-synuclein (α-syn) in Lewy bodies, which negatively impact neuronal viability. α-syn is also expressed in both pancreatic islets and skeletal muscle, key players in glucose regulation. Therefore, we examined the functional role of α-syn in these tissues.

methodsUsing mice lacking, overexpressing or transiently injected with α-syn, effects on glucose and insulin tolerance and insulin secretion were determined, with further characterization of the effects on GLUT4 translocation using GLUT4

resultsMice genetically ablated for α-syn became glucose intolerant and insulin resistant with hyperinsulinemia and reduced glucose-stimulated insulin secretion (GSIS). Mice overexpressing human α-syn are more insulin senstive and glucose tolerant compared to controls with increased GSIS. Injection of purified α-syn monomers also led to improved glucose tolerance and insulin sensitivity with hightened GSIS. α-syn monomer treatments increased surface GLUT4 levels in myotubes but without any significant change in Akt phosphorylation. The increase in cell surface GLUT4 was largely due to a large reduction in GLUT4 endocytosis, however, with a compensatory reduction in GLUT4 exocytosis.

conclusionCumulatively, this data suggests that α-syn modulates both pancreatic beta cell function and glucose transport in peripheral tissues, thereby playing a pivitol role in the maintenance of normal glucose homeostasis.

Indexed as

diabetesGLUT4insulin secretionParkinson’s diseaseα-synuclein

Identifiers

PMID34393754
PMCPMC8361797
OpenAlexW3189917904

What OpenQuestion holds

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Registered trials

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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.