Evidence map›Paper›PMID 25659350›Full record

ReviewMolecular aspects of medicine2015

Mitochondrial regulation of β-cell function: maintaining the momentum for insulin release.

Brett A Kaufman, Changhong Li, Scott A Soleimanpour

Abstract readReview
In one paragraph

Review in Molecular aspects of medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
–field-weighted citation impact
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

65 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Changes in Cells Associated with Insulin Resistance.International journal of molecular sciences · 2024
    Review
  18. Review
  19. CaFrontiers in endocrinology · 2024
    Review
  20. Review

5 more citing papers are in PubMed but not listed here.

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

3 authors.

Brett A Kaufman *Division of Cardiology, Vascular Medicine Institute, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Changhong Li *Division of Endocrinology and Diabetes, Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Scott A SoleimanpourDivision of Metabolism, Endocrinology & Diabetes and Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Scott Soleimanpour · 2013 to 2026
$24.3M
Insulin Secretion in Hyperinsulinism Human IsletsR01DK098517 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI DE LEON, DIVA D. · 2013 to 2023
$4.5M
The Role of Clec16a in the Pancreatic IsletK08DK089117 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI SOLEIMANPOUR, SCOTT · 2012 to 2016
$776k
NIDDK NIH HHS K08 DK089117NIDDK NIH HHS K08-DK089117NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK098517
6 · The paper itself

Abstract

All forms of diabetes share the common etiology of insufficient pancreatic β-cell function to meet peripheral insulin demand. In pancreatic β-cells, mitochondria serve to integrate the metabolism of exogenous nutrients into energy output, which ultimately leads to insulin release. As such, mitochondrial dysfunction underlies β-cell failure and the development of diabetes. Mitochondrial regulation of β-cell function occurs through many diverse pathways, including metabolic coupling, generation of reactive oxygen species, maintenance of mitochondrial mass, and through interaction with other cellular organelles. In this chapter, we will focus on the importance of enzymatic regulators of mitochondrial fuel metabolism and control of mitochondrial mass to pancreatic β-cell function, describing how defects in these pathways ultimately lead to diabetes. Furthermore, we will examine the factors responsible for mitochondrial biogenesis and degradation and their roles in the balance of mitochondrial mass in β-cells. Clarifying the causes of β-cell mitochondrial dysfunction may inform new approaches to treat the underlying etiologies of diabetes.

Indexed as

Amino AcidsDiabetes MellitusDNA, MitochondrialFatty AcidsGene ExpressionGlucoseGlutamineHomeodomain ProteinsHumansInsulinInsulin-Secreting CellsInsulin SecretionMitochondriaMitophagyMutationOxidative StressAmino AcidsDNA, MitochondrialFatty AcidsGlucoseGlutamineHomeodomain ProteinsInsulinpancreatic and duodenal homeobox 1 proteinPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanTrans-ActivatorsTranscription FactorsDiabetesIsletMetabolismMitochondriaMitophagymtDNA

Identifiers

PMID25659350
PMCPMC4404204

What Socratic holds

Textmetadata
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 Socratic graph.