Evidence map›Paper›PMID 29649104›Full record

ArticleNutrients2018

Coordination of GPR40 and Ketogenesis Signaling by Medium Chain Fatty Acids Regulates Beta Cell Function.

Julien Benjamin Pujol, Nicolas Christinat, Yann Ratinaud, Claudia Savoia, Siobhan E Mitchell, El Hadji M Dioum

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

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  10. The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021
    Review
  11. Article
  12. Review
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  15. TAK-875 MitigatesJournal of diabetes research · 2019
    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

6 authors at 2 institutions in 1 country.

Julien Benjamin PujolIslet Function, Nestlé Institute of Health Sciences (NIHS), EPFL Innovation Park, 1015 Lausanne, Switzerland. JulienBenjamin.Pujol@rd.nestle.com.
Nicolas ChristinatLipidomics, Nestlé Institute of Health Sciences (NIHS), EPFL Innovation Park, 1015 Lausanne, Switzerland. Nicolas.Christinat@rd.nestle.com.
Yann RatinaudNatural Bioactives Screening, Nestlé Institute of Health Sciences (NIHS), EPFL Innovation Park, 1015 Lausanne, Switzerland. Yann.Ratinaud@rd.nestle.com.
Claudia SavoiaIslet Function, Nestlé Institute of Health Sciences (NIHS), EPFL Innovation Park, 1015 Lausanne, Switzerland. Claudia.Savoia@rd.nestle.com.
Siobhan E MitchellBrain Health, Nestlé Institute of Health Sciences (NIHS), EPFL Innovation Park, 1015 Lausanne, Switzerland. esiobhanmitchell@gmail.com.
El Hadji M DioumIslet Function, Nestlé Institute of Health Sciences (NIHS), EPFL Innovation Park, 1015 Lausanne, Switzerland. elhadjimamadou.dioum@rd.nestle.com.ORCID 0000-0001-9486-1124
Nestlé (Switzerland) · CHInstitute for Work and Health · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes prevalence increases with age, and β-cell dysfunction contributes to the incidence of the disease. Dietary lipids have been recognized as contributory factors in the development and progression of the disease. Unlike long chain triglycerides, medium chain triglycerides (MCT) increase fat burning in animal and human subjects as well as serum C-peptide in type 2 diabetes patients. We evaluated the beneficial effects of MCT on β-cells in vivo and in vitro. MCT improved glycemia in aged rats via β-cell function assessed by measuring insulin secretion and content. In β-cells, medium chain fatty acid (MCFA)-C10 activated fatty acid receptor 1 FFAR1/GPR40, while MCFA-C8 induced mitochondrial ketogenesis and the C8:C10 mixture improved β cell function. We showed that GPR40 signaling positively impacts ketone body production in β-cells, and chronic treatment with β-hydroxybutyrate (BHB) improves β-cell function. We also showed that BHB and MCFA help β-cells recover from lipotoxic stress by improving mitochondrial function and increasing the expression of genes involved in β-cell function and insulin biogenesis, such as Glut2, MafA, and NeuroD1 in primary human islets. MCFA offers a therapeutic advantage in the preservation of β-cell function as part of a preventative strategy against diabetes in at risk populations.

Indexed as

Age FactorsAnimalsBlood GlucoseCell Line, TumorDose-Response Relationship, DrugFatty AcidsHumansInsulinInsulin-Secreting CellsKetone BodiesMaleMitochondriaRats, WistarReceptors, G-Protein-CoupledSignal TransductionTissue Culture TechniquesBlood GlucoseFatty AcidsFFAR1 protein, humanG-protein-coupled receptor 40, ratInsulinKetone BodiesReceptors, G-Protein-CoupledTriglyceridesBHBGPR40insulin secretionketogenesislipotoxicitymedium chain fatty acidmitochondria

Identifiers

PMID29649104
PMCPMC5946258
OpenAlexW2798148798

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.