Evidence map›Paper›PMID 40136665›Full record

ArticleCells2025

Differential Regulation of PKM2, AMPK, and mTOR in Response to Insulin and Dietary Management.

Emily Broberg, Jillise English, Derek M Clarke, Marley J Shin, Benjamin T Bikman, Paul R Reynolds, Juan A Arroyo

Abstract read
In one paragraph

Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
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

7 authors.

Emily BrobergDepartment of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.
Jillise EnglishDepartment of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.
Derek M ClarkeDepartment of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.
Marley J ShinDepartment of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.
Benjamin T BikmanDepartment of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.
Paul R ReynoldsDepartment of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.ORCID 0000-0002-0931-3025
Juan A ArroyoDepartment of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.ORCID 0000-0002-8818-8786

Funding

RAGE targeting attenuates smoke-induced inflammationR15HL152257 · NHLBI · BRIGHAM YOUNG UNIVERSITY · PI REYNOLDS, PAUL R · 2020 to 2025
$879k
Receptor for advanced glycation end-products signaling induction in the lung and placenta due to secondhand smoke and e-cigarette vaporR15HD108743 · NICHD · BRIGHAM YOUNG UNIVERSITY · PI ARROYO, JUAN A · 2022 to 2022
$455k
NHLBI NIH HHS R15 HL152257NICHD NIH HHS R15 HD108743NIH HHS 1R15HL152257
6 · The paper itself

Abstract

Gestational diabetes mellitus (GDM) affects placental metabolism, influencing both maternal and fetal outcomes. This study investigated the expression of metabolic regulators-Pyruvate Kinase M2 (PKM2), AMP-activated protein kinase (AMPK), and mTOR pathway components-in placental tissues from GDM pregnancies managed with either insulin (GDM-I) or dietary interventions (GDM-D). We hypothesize that metabolic adaptation in GDM is differentially regulated by treatment modality. This study analyzed 30 cases, including 10 control pregnancies,10 GDM-D cases, and 10 GDM-I cases. Analytical methods included immunofluorescence and immunoblotting. We observed an upregulation of PKM2 in both GDM-I and GDM-D placentas, suggesting enhanced glycolytic adaptation under GDM-induced metabolic stress. AMPK expression was significantly elevated in GDM-I and moderately increased in GDM-D placentas, potentially compensating for insulin resistance by promoting glucose uptake and energy homeostasis. Furthermore, mTOR pathway activation differed by treatment type, suggesting a treatment-specific mTOR response. The metabolic changes observed suggest that treatment modality in GDM may have direct implications for maternal and fetal health. Our findings indicate that while insulin and dietary management support metabolic adaptation in GDM, they do so through distinct mechanisms. These findings support a personalized approach in GDM treatment, where patient-specific metabolic responses should guide therapeutic decisions.

Indexed as

AMP-Activated Protein KinasesCarrier ProteinsDiabetes, GestationalInsulinMembrane ProteinsThyroid HormonesTOR Serine-Threonine KinasesAdultFemaleHumansInsulin ResistancePlacentaPregnancySignal TransductionThyroid Hormone-Binding ProteinsAMP-Activated Protein KinasesCarrier ProteinsInsulinMembrane ProteinsMTOR protein, humanThyroid Hormone-Binding ProteinsThyroid HormonesTOR Serine-Threonine KinasesAMPKGDMmTORPKM2placental metabolism

Identifiers

PMID40136665
PMCPMC11940920

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Registered trials

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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.