Evidence map›Paper›PMID 31767173›Full record

ArticleMolecular metabolism2019

Steroidogenic control of liver metabolism through a nuclear receptor-network.

Alexandra Milona, Vittoria Massafra, Harmjan Vos, Jyoti Naik, Natalia Artigas, Helen A B Paterson, Ingrid T G W Bijsmans, Ellen C L Willemsen, Jose M Ramos Pittol, Irene Miguel-Aliaga and 7 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

7 citing papers in PubMed, 32 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

17 authors at 5 institutions in 2 countries.

Alexandra MilonaMRC London Institute of Medical Sciences (LMS), London, United Kingdom; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, London, United Kingdom.
Vittoria MassafraCenter for Molecular Medicine, University Medical Center Utrecht and Utrecht University, Utrecht, the Netherlands.
Harmjan VosCenter for Molecular Medicine, University Medical Center Utrecht and Utrecht University, Utrecht, the Netherlands.
Jyoti NaikAmsterdam UMC, University of Amsterdam, Tytgat Institute for Liver and Intestinal Research, AG&M, Meibergdreef 69-71, 1105 BK, Amsterdam, the Netherlands.
Natalia ArtigasMRC London Institute of Medical Sciences (LMS), London, United Kingdom; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, London, United Kingdom.
Helen A B PatersonMRC London Institute of Medical Sciences (LMS), London, United Kingdom; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, London, United Kingdom.
Ingrid T G W BijsmansCenter for Molecular Medicine, University Medical Center Utrecht and Utrecht University, Utrecht, the Netherlands.
Ellen C L WillemsenCenter for Molecular Medicine, University Medical Center Utrecht and Utrecht University, Utrecht, the Netherlands.
Jose M Ramos PittolCenter for Molecular Medicine, University Medical Center Utrecht and Utrecht University, Utrecht, the Netherlands.
Irene Miguel-AliagaMRC London Institute of Medical Sciences (LMS), London, United Kingdom; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, London, United Kingdom.
Piter BosmaAmsterdam UMC, University of Amsterdam, Tytgat Institute for Liver and Intestinal Research, AG&M, Meibergdreef 69-71, 1105 BK, Amsterdam, the Netherlands.
Boudewijn M T BurgeringCenter for Molecular Medicine, University Medical Center Utrecht and Utrecht University, Utrecht, the Netherlands.
Catherine WilliamsonSchool of Life Course Science, Kings College London, London, United Kingdom.
Santiago VerniaMRC London Institute of Medical Sciences (LMS), London, United Kingdom; Institute of Clinical Sciences (ICS), Faculty of Medicine, Imperial College London, London, United Kingdom.
Waljit S DhilloSection of Endocrinology & Investigative Medicine, Division of Diabetes, Endocrinology, and Metabolism, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, United Kingdom.
Saskia W C van MilCenter for Molecular Medicine, University Medical Center Utrecht and Utrecht University, Utrecht, the Netherlands; Amsterdam UMC, University of Amsterdam, Tytgat Institute for Liver and Intestinal Research, AG&M, Meibergdreef 69-71, 1105 BK, Amsterdam, the Netherlands. Electronic address: S.W.C.vanmil@umcutrecht.nl.
Bryn M OwenSection of Endocrinology & Investigative Medicine, Division of Diabetes, Endocrinology, and Metabolism, Department of Metabolism, Digestion, and Reproduction, Imperial College London, London, United Kingdom. Electronic address: bryn.owen05@imperial.ac.uk.
Utrecht University · NLMRC London Institute of Medical Sciences · GBAmsterdam University Medical Centers · NLImperial College London · GBKing's College London · GB

Funding

Medical Research Council MC_EX_MR/S300008/1Medical Research Council MC_UP_1102/18Wellcome Trust
6 · The paper itself

Abstract

objectiveCoupling metabolic and reproductive pathways is essential for the survival of species. However, the functions of steroidogenic enzymes expressed in metabolic tissues are largely unknown. METHODS AND

resultsHere, we show that in the liver, the classical steroidogenic enzyme Cyp17a1 forms an essential nexus for glucose and ketone metabolism during feed-fast cycles. Both gain- and loss-of-function approaches are used to show that hepatic Cyp17a1 is induced by fasting, catalyzes the production of at least one hormone-ligand (DHEA) for the nuclear receptor PPARα, and is ultimately required for maintaining euglycemia and ketogenesis during nutrient deprivation. The feedback-loop that terminates Cyp17a1-PPARα activity, and re-establishes anabolic liver metabolism during re-feeding is mapped to postprandial bile acid-signaling, involving the receptors FXR, SHP and LRH-1.

conclusionsTogether, these findings represent a novel paradigm of homeostatic control in which nutritional cues feed-forward on to metabolic pathways by influencing extragonadal steroidogenesis.

Indexed as

AnimalsBile Acids and SaltsGlucoseHEK293 CellsHepatocytesHomeostasisHumansKetonesLipogenesisLiverMaleMiceMice, Inbred C57BLMice, TransgenicOxidation-ReductionPPAR alphaBile Acids and SaltsCYP17A1 protein, humanGlucoseKetonesPPAR alphaReceptors, Cytoplasmic and NuclearSteroid 17-alpha-HydroxylaseBile acidsCyp17a1DiabetesFastingFGF21FXRGluconeogenesisLiverMetabolismSteroidogenesis

Identifiers

PMID31767173
PMCPMC6819870
OpenAlexW2979284629

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.