Evidence mapPaperPMID 38775784Full record

ArticleDiabetes2024

Glucose Transporters Are Key Components of the Human Glucostat.

Inbal Caspi, Daniel M Tremmel, Julian Pulecio, Dapeng Yang, Dingyu Liu, Jielin Yan, Jon S Odorico, Danwei Huangfu

Abstract read
In one paragraph

Article in Diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
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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

8 authors.

Inbal CaspiWeill Cornell Graduate School of Medical Sciences, Weill Cornell Medicine, New York, NY.
Daniel M TremmelTransplantation Division, Department of Surgery, University of Wisconsin-Madison, Madison, WI.
Julian PulecioDevelopmental Biology Program, Sloan Kettering Institute, New York, NY.
Dapeng YangDevelopmental Biology Program, Sloan Kettering Institute, New York, NY.
Dingyu LiuDevelopmental Biology Program, Sloan Kettering Institute, New York, NY.
Jielin YanDevelopmental Biology Program, Sloan Kettering Institute, New York, NY.
Jon S OdoricoTransplantation Division, Department of Surgery, University of Wisconsin-Madison, Madison, WI.
Danwei HuangfuDevelopmental Biology Program, Sloan Kettering Institute, New York, NY.ORCID 0000-0002-1145-6199

Funding

The Patient-Reported Outcomes, Community-Engagement and Language (PRO-CEL) CoreP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · 1985 to 2025
$88.4M
American Diabetes Association 1-19-IBS-125Breakthrough T1D 3-SRA-2021-1060-S-BCenter for Stem Cell Biology of the Sloan Kettering Institute DOH01-TRAIN3-2015-2016-00006DoDNCI NIH HHS P30 CA008748NIDDK NIH HHS R01 DK096239NIH HHS P30CA008748PRMRP W81XWH-20-1-0670the University of Wisconsin-Madison, Office of the Vice Chancellor for ResearchWisconsin Alumni Research Foundation
6 · The paper itself

Abstract

Mouse models are extensively used in metabolic studies. However, inherent differences between the species, notably their blood glucose levels, hampered data translation into clinical settings. In this study, we confirmed GLUT1 to be the predominantly expressed glucose transporter in both adult and fetal human β-cells. In comparison, GLUT2 is detected in a small yet significant subpopulation of adult β-cells and is expressed to a greater extent in fetal β-cells. Notably, GLUT1/2 expression in INS+ cells from human stem cell-derived islet-like clusters (SC-islets) exhibited a closer resemblance to that observed in fetal islets. Transplantation of primary human islets or SC-islets, but not murine islets, lowered murine blood glucose to the human glycemic range, emphasizing the critical role of β-cells in establishing species-specific glycemia. We further demonstrate the functional requirements of GLUT1 and GLUT2 in glucose uptake and insulin secretion through chemically inhibiting GLUT1 in primary islets and SC-islets and genetically disrupting GLUT2 in SC-islets. Finally, we developed a mathematical model to predict changes in glucose uptake and insulin secretion as a function of GLUT1/2 expression. Collectively, our findings illustrate the crucial roles of GLUTs in human β-cells, and identify them as key components in establishing species-specific glycemic set points. ARTICLE HIGHLIGHTS:

Indexed as

Glucose Transporter Type 1Glucose Transporter Type 2Insulin-Secreting CellsAnimalsBlood GlucoseGlucoseHumansInsulinInsulin SecretionIslets of LangerhansIslets of Langerhans TransplantationMiceBlood GlucoseGlucoseGlucose Transporter Type 1Glucose Transporter Type 2InsulinSLC2A1 protein, humanSLC2A2 protein, human

Identifiers

PMID38775784
PMCPMC11262048

What Socratic holds

Textmetadata
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.