Evidence map›Paper›PMID 27615135›Full record

ReviewDiabetes, obesity & metabolism2016

Mechanisms of β-cell functional adaptation to changes in workload.

M Wortham, M Sander

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, obesity & metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Pan-hypoileism: an endocrine disease.Einstein (Sao Paulo, Brazil) · 2026
    Review
  5. Article
  6. β-Cells: So Sensitive.Diabetes · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Observational
  14. Article
  15. Article
  16. How Can Insulin Resistance Cause Alzheimer's Disease?International journal of molecular sciences · 2023
    Review
  17. Article
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

M WorthamDepartments of Pediatrics and Cellular and Molecular Medicine, Pediatric Diabetes Research Center, University of California San Diego, La Jolla.
M SanderDepartments of Pediatrics and Cellular and Molecular Medicine, Pediatric Diabetes Research Center, University of California San Diego, La Jolla. masander@ucsd.edu.
University of California, San Diego · US

Funding

Nkx6 gene function in pancreas developmentR01DK068471 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI WORTHAM, MATTHEW · 2004 to 2024
$6.6M
TRAINING PROGRAM IN DIABETES RESEARCHT32DK007494 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SALTIEL, ALAN R. · 1986 to 2021
$4.7M
Novel insights into nutrient-dependent regulation of beta cell proliferationR01DK078803 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SANDER, MAIKE · 2007 to 2022
$4.4M
NIDDK NIH HHS R01 DK068471NIDDK NIH HHS R01 DK078803NIDDK NIH HHS T32 DK007494
6 · The paper itself

Abstract

Insulin secretion must be tightly coupled to nutritional state to maintain blood glucose homeostasis. To this end, pancreatic β-cells sense and respond to changes in metabolic conditions, thereby anticipating insulin demands for a given physiological context. This is achieved in part through adjustments of nutrient metabolism, which is controlled at several levels including allosteric regulation, post-translational modifications, and altered expression of metabolic enzymes. In this review, we discuss mechanisms of β-cell metabolic and functional adaptation in the context of two physiological states that alter glucose-stimulated insulin secretion: fasting and insulin resistance. We review current knowledge of metabolic changes that occur in the β-cell during adaptation and specifically discuss transcriptional mechanisms that underlie β-cell adaptation. A more comprehensive understanding of how β-cells adapt to changes in nutrient state could identify mechanisms to be co-opted for therapeutically modulating insulin secretion in metabolic disease.

Indexed as

Adaptation, PhysiologicalGene Expression RegulationProtein Processing, Post-TranslationalAllosteric RegulationAnimalsBlood GlucoseFastingHomeostasisHumansInsulinInsulin ResistanceInsulin-Secreting CellsInsulin SecretionBlood GlucoseInsulinadaptationfastinginsulin resistanceinsulin secretionmetabolismtranscriptionβ-cell

Identifiers

PMID27615135
PMCPMC5021190
OpenAlexW2519537568

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.