Evidence map›Paper›PMID 37960342›Full record

ArticleNutrients2023

Heptanoate Improves Compensatory Mechanism of Glucose Homeostasis in Mitochondrial Long-Chain Fatty Acid Oxidation Defect.

Siti Nurjanah, Albert Gerding, Marcel A Vieira-Lara, Bernard Evers, Miriam Langelaar-Makkinje, Ute Spiekerkoetter, Barbara M Bakker, Sara Tucci

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nutrients, 2023. 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
0.8field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Four novel variants identified in theFrontiers in genetics · 2024
    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

8 authors at 2 institutions in 2 countries.

Siti NurjanahDepartment of General Pediatrics, Adolescent Medicine and Neonatology, Medical Centre, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.
Albert GerdingLaboratory of Pediatrics, Systems Medicine of Metabolism and Signaling, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands.
Marcel A Vieira-LaraLaboratory of Pediatrics, Systems Medicine of Metabolism and Signaling, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands.
Bernard EversLaboratory of Pediatrics, Systems Medicine of Metabolism and Signaling, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands.
Miriam Langelaar-MakkinjeLaboratory of Pediatrics, Systems Medicine of Metabolism and Signaling, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands.
Ute SpiekerkoetterDepartment of General Pediatrics, Adolescent Medicine and Neonatology, Medical Centre, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.ORCID 0000-0002-5385-6705
Barbara M BakkerLaboratory of Pediatrics, Systems Medicine of Metabolism and Signaling, University Medical Center Groningen, University of Groningen, 9700 RB Groningen, The Netherlands.ORCID 0000-0001-6274-3633
Sara TucciPharmacy, Medical Center, University of Freiburg, 79106 Freiburg, Germany.ORCID 0000-0003-3851-4843
University Medical Center Groningen · NLUniversity of Freiburg · DE

Funding

Deutsche Forschungsgemeinschaft (DFG) TU492/3-1European Union's Horizon 2020 research and innovation program PoLiMeR - 812616
6 · The paper itself

Abstract

Defects in mitochondrial fatty acid β-oxidation (FAO) impair metabolic flexibility, which is an essential process for energy homeostasis. Very-long-chain acyl-CoA dehydrogenase (VLCADD; OMIM 609575) deficiency is the most common long-chain mitochondrial FAO disorder presenting with hypoglycemia as a common clinical manifestation. To prevent hypoglycemia, triheptanoin-a triglyceride composed of three heptanoates (C7) esterified with a glycerol backbone-can be used as a dietary treatment, since it is metabolized into precursors for gluconeogenesis. However, studies investigating the effect of triheptanoin on glucose homeostasis are limited. To understand the role of gluconeogenesis in the pathophysiology of long-chain mitochondrial FAO defects, we injected VLCAD-deficient (VLCAD

Indexed as

HypoglycemiaLipid Metabolism, Inborn ErrorsMitochondrial DiseasesAcyl-CoA Dehydrogenase, Long-ChainAnimalsFatty AcidsGlucoseGlycerolHeptanoatesHomeostasisMiceAcyl-CoA Dehydrogenase, Long-ChainFatty AcidsGlucoseGlycerolHeptanoatesfatty acid oxidation disorderglucose homeostasisglycerolheptanoatestable isotopevery long-chain acyl-CoA dehydrogenaseVLCAD deficiency

Identifiers

PMID37960342
PMCPMC10649308
OpenAlexW4388380161

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.