Evidence map›Paper›PMID 35204835›Full record

ReviewBiomolecules2022

Nutrient Regulation of Pancreatic Islet β-Cell Secretory Capacity and Insulin Production.

Kristen E Rohli, Cierra K Boyer, Sandra E Blom, Samuel B Stephens

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
7.2field-weighted citation impact, top 2% 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, 35 citations in OpenAlex.

  1. Atlas of lysine acetylation in the mouse.bioRxiv : the preprint server for biology · 2026
    Article
  2. Review
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  10. Effect of Resveratrol on the intestinal microbiota in Type2 diabetes Mellitus mice.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2025
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Supplementary Effects ofPharmaceuticals (Basel, Switzerland) · 2023
    Article
  17. Review
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Kristen E RohliFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA.ORCID 0000-0002-4805-111X
Cierra K BoyerFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA.ORCID 0000-0003-1195-7169
Sandra E BlomFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA.ORCID 0000-0002-7112-5404
Samuel B StephensFraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA.ORCID 0000-0003-1152-2691
University of Iowa · US

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM008629 · NIGMS · UNIVERSITY OF IOWA · PI EBERL, DANIEL F · 1997 to 2021
$4.1M
Predoctoral Training Program in GeneticsT32GM145441 · NIGMS · UNIVERSITY OF IOWA · PI Josep M Comeron, DANIEL F EBERL · 2022 to 2026
$1.5M
NIGMS NIH HHS T32 GM008629NIGMS NIH HHS T32 GM145441
6 · The paper itself

Abstract

Pancreatic islet β-cells exhibit tremendous plasticity for secretory adaptations that coordinate insulin production and release with nutritional demands. This essential feature of the β-cell can allow for compensatory changes that increase secretory output to overcome insulin resistance early in Type 2 diabetes (T2D). Nutrient-stimulated increases in proinsulin biosynthesis may initiate this β-cell adaptive compensation; however, the molecular regulators of secretory expansion that accommodate the increased biosynthetic burden of packaging and producing additional insulin granules, such as enhanced ER and Golgi functions, remain poorly defined. As these adaptive mechanisms fail and T2D progresses, the β-cell succumbs to metabolic defects resulting in alterations to glucose metabolism and a decline in nutrient-regulated secretory functions, including impaired proinsulin processing and a deficit in mature insulin-containing secretory granules. In this review, we will discuss how the adaptative plasticity of the pancreatic islet β-cell's secretory program allows insulin production to be carefully matched with nutrient availability and peripheral cues for insulin signaling. Furthermore, we will highlight potential defects in the secretory pathway that limit or delay insulin granule biosynthesis, which may contribute to the decline in β-cell function during the pathogenesis of T2D.

Indexed as

Diabetes Mellitus, Type 2Insulin-Secreting CellsHumansInsulinNutrientsProinsulinInsulinNutrientsProinsulinbeta-cell functionER functionglutathioneGolgigranule traffickinginsulin granuleinsulin secretionproinsulinsecretory granule biogenesis

Identifiers

PMID35204835
PMCPMC8869698
OpenAlexW4213344903

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.