Evidence map›Paper›PMID 41543436›Full record

ReviewPhysiology (Bethesda, Md.)2026

Metabolic Programming of β-Cell Fate, State, and Function through Time and Space.

Tara L MacDonald, Susan Bonner-Weir

Abstract readReview
In one paragraph

Review in Physiology (Bethesda, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Tara L MacDonaldDepartment of Physiology, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada.ORCID 0000-0001-7986-5223
Susan Bonner-WeirSection for Islet Cell and Regenerative Biology, Joslin Diabetes Center, Boston, Massachusetts, United States.ORCID 0000-0003-4682-0656

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
Breakthrough T1D (JDF) 4-COE-2025-1751-A-NNIDDK NIH HHS P30 DK036836Stem Cell Network (SCN) ECR-C5R1-11
6 · The paper itself

Abstract

β-cells maintain glucose homeostasis by adjusting insulin secretion to meet the demands of (patho)physiological triggers; yet, they also undergo energy-dependent transitions between proliferation, differentiation, and maturation that underlie function across the lifespan. There are energy costs to prioritizing distinct cell states within β-cells. As such, specific metabolic programming is likely essential for distinct β-cell states as they toggle between immaturity and maturity. Transcriptional, nutritional, hormonal, and stress-based cues coordinately regulate the development of native β-cells in vivo. These steps are mirrored in protocols to differentiate human pluripotent stem cells (hPSCs) into β-like cells, but these cells remain functionally immature. Understanding how metabolic programs drive β-cell state transitions may reveal strategies to accelerate stem cell-derived (sc)-islet maturation, restore β-cell function in diabetes, and improve cell-based therapies. Here, we outline the known and unknown metabolic physiology of β-cells throughout development in vivo and in vitro.

Indexed as

Cell DifferentiationEnergy MetabolismInsulin-Secreting CellsAnimalsHumansInsulinMetabolic ReprogrammingPluripotent Stem CellsInsulindevelopmentdiabetesmetabolismstem cellsβ-cell

Identifiers

PMID41543436
PMCPMC12931737

What Socratic 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 Socratic graph.