Evidence map›Paper›PMID 33327428›Full record

ArticleLife (Basel, Switzerland)2020

Mitochondrial Dysfunction in Pancreatic Alpha and Beta Cells Associated with Type 2 Diabetes Mellitus.

Vladimir Grubelnik, Jan Zmazek, Rene Markovič, Marko Gosak, Marko Marhl

Open access · goldAbstract read
In one paragraph

Article in Life (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview.International journal of molecular sciences · 2022
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Hepatic-Metabolite-Based Intermittent Fasting Enables a Sustained Reduction in Insulin Resistance in Type 2 Diabetes and Metabolic Syndrome.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2021
    Article
  16. Article
  17. Article
  18. 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

5 authors at 1 institution in 1 country.

Vladimir GrubelnikFaculty of Electrical Engineering and Computer Science, University of Maribor, SI-2000 Maribor, Slovenia.
Jan ZmazekFaculty of Natural Sciences and Mathematics, University of Maribor, SI-2000 Maribor, Slovenia.
Rene MarkovičFaculty of Electrical Engineering and Computer Science, University of Maribor, SI-2000 Maribor, Slovenia.ORCID 0000-0001-9068-6373
Marko GosakFaculty of Natural Sciences and Mathematics, University of Maribor, SI-2000 Maribor, Slovenia.ORCID 0000-0001-9735-0485
Marko MarhlFaculty of Natural Sciences and Mathematics, University of Maribor, SI-2000 Maribor, Slovenia.ORCID 0000-0003-0387-1162
University of Maribor · SI

Funding

Javna Agencija za Raziskovalno Dejavnost RS P1-0055, P3-0396, N3-0133, J3-9289
6 · The paper itself

Abstract

Type 2 diabetes mellitus is a complex multifactorial disease of epidemic proportions. It involves genetic and lifestyle factors that lead to dysregulations in hormone secretion and metabolic homeostasis. Accumulating evidence indicates that altered mitochondrial structure, function, and particularly bioenergetics of cells in different tissues have a central role in the pathogenesis of type 2 diabetes mellitus. In the present study, we explore how mitochondrial dysfunction impairs the coupling between metabolism and exocytosis in the pancreatic alpha and beta cells. We demonstrate that reduced mitochondrial ATP production is linked with the observed defects in insulin and glucagon secretion by utilizing computational modeling approach. Specifically, a 30-40% reduction in alpha cells' mitochondrial function leads to a pathological shift of glucagon secretion, characterized by oversecretion at high glucose concentrations and insufficient secretion in hypoglycemia. In beta cells, the impaired mitochondrial energy metabolism is accompanied by reduced insulin secretion at all glucose levels, but the differences, compared to a normal beta cell, are the most pronounced in hyperglycemia. These findings improve our understanding of metabolic pathways and mitochondrial bioenergetics in the pathology of type 2 diabetes mellitus and might help drive the development of innovative therapies to treat various metabolic diseases.

Indexed as

cellular bioenergeticsdiabetesglucagoninsulinmathematical modelmitochondrial dysfunctionpancreatic endocrine cells

Identifiers

PMID33327428
PMCPMC7764865
OpenAlexW3111637597

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.