Evidence map›Paper›PMID 33672050›Full record

ArticleBiomolecules2021

Glucagon Prevents Cytotoxicity Induced by Methylglyoxal in a Rat Neuronal Cell Line Model.

Mohammad Sarif Mohiuddin, Tatsuhito Himeno, Yuichiro Yamada, Yoshiaki Morishita, Masaki Kondo, Shin Tsunekawa, Yoshiro Kato, Jiro Nakamura, Hideki Kamiya

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 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
3.0field-weighted citation impact, top 9% 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, 25 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Mohammad Sarif MohiuddinDepartment of Internal Medicine, Division of Diabetes, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan.ORCID 0000-0002-1885-646X
Tatsuhito HimenoDepartment of Internal Medicine, Division of Diabetes, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan.ORCID 0000-0002-5677-1125
Yuichiro YamadaDepartment of Internal Medicine, Division of Diabetes, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan.
Yoshiaki MorishitaDepartment of Internal Medicine, Division of Diabetes, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan.
Masaki KondoDepartment of Internal Medicine, Division of Diabetes, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan.
Shin TsunekawaDepartment of Internal Medicine, Division of Diabetes, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan.
Yoshiro KatoDepartment of Internal Medicine, Division of Diabetes, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan.
Jiro NakamuraDepartment of Internal Medicine, Division of Diabetes, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan.
Hideki KamiyaDepartment of Internal Medicine, Division of Diabetes, Aichi Medical University School of Medicine, Nagakute 480-1195, Japan.
Aichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although diabetic polyneuropathy (DPN) is a frequent diabetic complication, no effective therapeutic approach has been established. Glucagon is a crucial hormone for glucose homeostasis but has pleiotropic effects, including neuroprotective effects in the central nervous system. However, the importance of glucagon in the peripheral nervous system (PNS) has not been clarified. Here, we hypothesized that glucagon might have a neuroprotective function in the PNS. The immortalized rat dorsal root ganglion (DRG) neuronal cell line 50B11 was treated with methylglyoxal (MG) to mimic an in vitro DPN model. The cells were cultured with or without glucagon or MG. Neurotoxicity, survival, apoptosis, neurite projection, cyclic adenosine monophosphate (cAMP), and protein kinase A (PKA) were examined. Glucagon had no cytotoxicity and rescued the cells from neurotoxicity. Cell survival was increased by glucagon. The ratio of apoptotic cells, which was increased by MG, was reduced by glucagon. Neurite outgrowth was accelerated in glucagon-treated cells. Cyclic AMP and PKA accumulated in the cells after glucagon stimulation. In conclusion, glucagon protected the DRG neuronal cells from MG-induced cellular stress. The cAMP/PKA pathway may have significant roles in those protective effects of glucagon. Glucagon may be a potential target for the treatment of DPN.

Indexed as

AnimalsApoptosisCell LineCell SurvivalCyclic AMP-Dependent Protein KinasesDiabetic NeuropathiesGanglia, SpinalGlucagonMitochondriaNeuritesNeuronsPeripheral Nervous SystemPyruvaldehydeRatsReactive Oxygen SpeciesCyclic AMP-Dependent Protein KinasesGlucagonPyruvaldehydeReactive Oxygen Species50B11apoptosiscAMPdiabetic polyneuropathyglucagonmethylglyoxalperipheral neuronal cellPKA

Identifiers

PMID33672050
PMCPMC7919475
OpenAlexW3130824864

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.