Evidence map›Paper›PMID 36516926›Full record

ArticleMitochondrion2023

β-Hydroxybutyrate preferentially enhances neuron over astrocyte respiration while signaling cellular quiescence.

Scott J Koppel, Heather M Wilkins, Ian W Weidling, Xiaowan Wang, Blaise W Menta, Russell H Swerdlow

Open access · greenAbstract read
In one paragraph

Article in Mitochondrion, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Scott J KoppelUniversity of Kansas Alzheimer's Disease Center, Kansas City, KS, USA; Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA.
Heather M WilkinsUniversity of Kansas Alzheimer's Disease Center, Kansas City, KS, USA; Department of Neurology, University of Kansas Medical Center, Kansas City, KS, USA; Department of Biochemistry, University of Kansas Medical Center, Kansas City, KS, USA.
Ian W WeidlingUniversity of Kansas Alzheimer's Disease Center, Kansas City, KS, USA; Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA.
Xiaowan WangUniversity of Kansas Alzheimer's Disease Center, Kansas City, KS, USA; Department of Neurology, University of Kansas Medical Center, Kansas City, KS, USA.
Blaise W MentaUniversity of Kansas Alzheimer's Disease Center, Kansas City, KS, USA; Department of Biochemistry, University of Kansas Medical Center, Kansas City, KS, USA.
Russell H SwerdlowUniversity of Kansas Alzheimer's Disease Center, Kansas City, KS, USA; Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA; Department of Neurology, University of Kansas Medical Center, Kansas City, KS, USA; Department of Biochemistry, University of Kansas Medical Center, Kansas City, KS, USA. Electronic address: rswerdlow@kumc.edu.
University of Kansas · USUniversity of Kansas Medical Center · US

Funding

University of Kansas Alzheimer's Disease Research Center (KU ADRC)P30AG072973 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI JEFFREY Murray BURNS, RUSSELL H. SWERDLOW · 2021 to 2026
$25.3M
University of Kansas Alzheimer's Disease Core CentersP30AG035982 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI SWERDLOW, RUSSELL H. · 2011 to 2020
$16.6M
Novel Approaches for the Control of Microbial PathogensP30GM103326 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUTKENHAUS, JOSEPH F · 2012 to 2016
$5.3M
Kansas University Training Program in Neurological and Rehabilitation SciencesT32HD057850 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI Jacob J. Sosnoff · 2009 to 2026
$3.4M
The role of ketogenic diet metabolites in molecular signaling within distinct brain cell populations.F30AG058397 · NIA · UNIVERSITY OF KANSAS MEDICAL CENTER · PI KOPPEL, SCOTT JOSHUA · 2018 to 2021
$164k
NIA NIH HHS F30 AG058397NIA NIH HHS P30 AG035982NIA NIH HHS P30 AG072973NICHD NIH HHS T32 HD057850NIGMS NIH HHS P30 GM103326
6 · The paper itself

Abstract

While ketone bodies support overall brain energy metabolism, it is increasingly clear specific brain cell types respond differently to ketone body availability. Here, we characterized how SH-SY5Y neuroblastoma cell, primary neuron, and primary astrocyte bioenergetics and nutrient sensing pathways respond to β-hydroxybutyrate (βOHB). SH-SY5Y cells and primary neurons, but not astrocytes, exposed to βOHB increased respiration and decreased PI3K-Akt-mTOR signaling. Despite increased carbon availability and respiration, SH-SY5Y cells treated with βOHB reduced their overall metabolic activity and cell cycling rate. Levels of the quiescence-regulating Yamanaka factors increased to a broader extent in SH-SY5Y cells and primary neurons. We propose a βOHB-induced increase in neuron respiration, accompanied by activation of quiescence associated pathways, could alleviate bioenergetic stress and limit cell senescence. This in turn could potentially benefit conditions, including brain aging and neurodegenerative diseases, that feature bioenergetic decline and cell senescence.

Indexed as

NeuroblastomaPhosphatidylinositol 3-Kinases3-Hydroxybutyric AcidCell Line, TumorHumansKetone BodiesNeurons3-Hydroxybutyric AcidKetone BodiesPhosphatidylinositol 3-KinasesAgingBioenergeticsKetonesMitochondriaQuiescenceSenescence

Identifiers

PMID36516926
PMCPMC9805520
OpenAlexW4313251924

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.