Evidence map›Paper›PMID 31410530›Full record

ArticleDiabetologia2019

Fenofibrate increases very-long-chain sphingolipids and improves blood glucose homeostasis in NOD mice.

Laurits J Holm, Martin Haupt-Jorgensen, Jano D Giacobini, Jane P Hasselby, Mesut Bilgin, Karsten Buschard

Open access · hybridAbstract read
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Article in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  4. Lipidomic predictors of residual insulin production in adults with newly diagnosed type 1 diabetes.Metabolomics : Official journal of the Metabolomic Society · 2026
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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 3 institutions in 1 country.

Laurits J HolmThe Bartholin Institute, Department of Pathology, Rigshospitalet, Copenhagen Biocenter, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Martin Haupt-JorgensenThe Bartholin Institute, Department of Pathology, Rigshospitalet, Copenhagen Biocenter, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Jano D GiacobiniCell Death and Metabolism Unit, Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, Copenhagen, Denmark.
Jane P HasselbyDepartment of Pathology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Mesut BilginCell Death and Metabolism Unit, Center for Autophagy, Recycling and Disease, Danish Cancer Society Research Center, Copenhagen, Denmark.
Karsten BuschardThe Bartholin Institute, Department of Pathology, Rigshospitalet, Copenhagen Biocenter, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark. buschard@dadlnet.dk.
Rigshospitalet · DKDanish Cancer Society · DKCopenhagen University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisSphingolipid metabolism regulates beta cell biology and inflammation and is abnormal at the onset of type 1 diabetes. Fenofibrate, a regulator of sphingolipid metabolism, is known to prevent diabetes in NOD mice. Here, we aimed to investigate the effects of fenofibrate on the pancreatic lipidome, pancreas morphology, pancreatic sympathetic nerves and blood glucose homeostasis in NOD mice.

methodsWe treated female NOD mice with fenofibrate from 3 weeks of age. The pancreatic lipidome was analysed using MS. Analysis of pancreas and islet volume was performed by stereology. Islet sympathetic nerve fibre volume was evaluated using tyrosine hydroxylase staining. The effect on blood glucose homeostasis was assessed by measuring non-fasting blood glucose from age 12 to 30 weeks. Furthermore, we measured glucose tolerance, fasting insulin and glucagon levels, and insulin tolerance.

resultsWe found that fenofibrate selectively increases the amount of very-long-chain sphingolipids in the pancreas of NOD mice. In addition, we found that fenofibrate causes a remodelling of the pancreatic lipidome with an increased amount of lysoglycerophospholipids. Fenofibrate did not affect islet or pancreas volume, but led to a higher volume of islet sympathetic nerve fibres and tyrosine hydroxylase-positive cells. Fenofibrate-treated NOD mice had a more stable blood glucose, which was associated with reduced non-fasting and increased fasting blood glucose. Furthermore, fenofibrate improved glucose tolerance, reduced fasting glucagon levels and prevented fasting hyperinsulinaemia. CONCLUSIONS/

interpretationThese data indicate that fenofibrate alters the pancreatic lipidome to a more anti-inflammatory and anti-apoptotic state. The beneficial effects on islet sympathetic nerve fibres and blood glucose homeostasis indicate that fenofibrate could be used as a therapeutic approach to improve blood glucose homeostasis and prevent diabetes-associated pathologies.

Indexed as

AnimalsBlood GlucoseDiabetes Mellitus, Type 1FemaleFenofibrateHomeostasisHypolipidemic AgentsLipid MetabolismMiceMice, Inbred NODPancreasSphingolipidsBlood GlucoseFenofibrateHypolipidemic AgentsSphingolipidsBlood glucose homeostasisCeramideFenofibrateGlycerophospholipidNOD miceSphingolipidSulfatideSympathetic nerve fibresType 1 diabetesTyrosine hydroxylase

Identifiers

PMID31410530
PMCPMC6861358
OpenAlexW2967447175

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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.