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Article: Editorial: Intra and inter organ cross-talk and cellular communication.

Denechaud, Pierre-Damien / Rabhi, Nabil

2023 Volume 14, Page(s) 1209436

MeSH term(s)	Cell Communication ; Cell Physiological Phenomena ; Communication
Language	English
Publishing date	2023-05-12
Publishing country	Switzerland
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2023.1209436
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Article ; Online: Hepatic lipid overload triggers biliary epithelial cell activation via E2Fs.

Yildiz, Ece / El Alam, Gaby / Perino, Alessia / Jalil, Antoine / Denechaud, Pierre-Damien / Huber, Katharina / Fajas, Lluis / Auwerx, Johan / Sorrentino, Giovanni / Schoonjans, Kristina

eLife

2023 Volume 12

Abstract: During severe or chronic hepatic injury, biliary epithelial cells (BECs) undergo rapid activation into proliferating progenitors, a crucial step required to establish a regenerative process known as ductular reaction (DR). While DR is a hallmark of ... ...

Abstract	During severe or chronic hepatic injury, biliary epithelial cells (BECs) undergo rapid activation into proliferating progenitors, a crucial step required to establish a regenerative process known as ductular reaction (DR). While DR is a hallmark of chronic liver diseases, including advanced stages of non-alcoholic fatty liver disease (NAFLD), the early events underlying BEC activation are largely unknown. Here, we demonstrate that BECs readily accumulate lipids during high-fat diet feeding in mice and upon fatty acid treatment in BEC-derived organoids. Lipid overload induces metabolic rewiring to support the conversion of adult cholangiocytes into reactive BECs. Mechanistically, we found that lipid overload activates the E2F transcription factors in BECs, which drive cell cycle progression while promoting glycolytic metabolism. These findings demonstrate that fat overload is sufficient to reprogram BECs into progenitor cells in the early stages of NAFLD and provide new insights into the mechanistic basis of this process, revealing unexpected connections between lipid metabolism, stemness, and regeneration.
MeSH term(s)	Animals ; Mice ; Non-alcoholic Fatty Liver Disease/metabolism ; Liver/metabolism ; Epithelial Cells/metabolism ; Cell Division ; Lipids
Chemical Substances	Lipids
Language	English
Publishing date	2023-03-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.81926
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Article: E2F1, a Novel Regulator of Metabolism.

Denechaud, Pierre-Damien / Fajas, Lluis / Giralt, Albert

Frontiers in endocrinology

2017 Volume 8, Page(s) 311

Abstract: In the past years, several lines of evidence have shown that cell cycle regulatory proteins also can modulate metabolic processes. The transcription factor E2F1 is a central player involved in cell cycle progression, DNA-damage response, and apoptosis. ... ...

Abstract	In the past years, several lines of evidence have shown that cell cycle regulatory proteins also can modulate metabolic processes. The transcription factor E2F1 is a central player involved in cell cycle progression, DNA-damage response, and apoptosis. Its crucial role in the control of cell fate has been extensively studied and reviewed before; however, here, we focus on the participation of E2F1 in the regulation of metabolism. We summarize recent findings about the cell cycle-independent roles of E2F1 in various tissues that contribute to global metabolic homeostasis and highlight that E2F1 activity is increased during obesity. Finally, coming back to the pivotal role of E2F1 in cancer development, we discuss how E2F1 links cell cycle progression with different metabolic adaptations required for cell growth and survival.
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2017.00311
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Article ; Online: DietSee: An on-hand, portable, strip-type biosensor for lipolysis monitoring via real-time amperometric determination of glycerol in blood.

Degrelle, Séverine A / Delile, Sébastien / Moog, Sophie / Mouisel, Etienne / O'Gorman, Donal / Moro, Cédric / Denechaud, Pierre-Damien / Torre, Cyril

Analytica chimica acta

2021 Volume 1155, Page(s) 338358

Abstract: Glycerol is a clinical biomarker of lipolysis that is mainly produced by adipose tissues. Blood glycerol content increases in pathological conditions such as metabolic and cardiovascular diseases or cancer cachexia, but also in response to energetic ... ...

Abstract	Glycerol is a clinical biomarker of lipolysis that is mainly produced by adipose tissues. Blood glycerol content increases in pathological conditions such as metabolic and cardiovascular diseases or cancer cachexia, but also in response to energetic stress such as physical exercise. Accurate glycerol monitoring is therefore important in a range of healthcare contexts. However, current methods available for the quantification of glycerol are expensive, time-consuming, and require the extraction of plasma from blood, from which blood glycerol content is then extrapolated. Here, we report the development of a new point-of-care glycerometer device, DietSee, based on a strip-type biosensor that enables the quantification of glycerol directly from whole blood in 6 s. The performance of the biosensor was first evaluated using buffer solutions and spiked human and mouse plasma samples, and its response was compared with that of the gold-standard colorimetric method. The results obtained using DietSee correlated strongly with those from the reference method and demonstrated a linear response to glycerol levels across a wide range of concentrations (40-750 μM) that were representative of those in the human body. Next, the biosensor was validated using spiked human blood samples over a range of 30-55% hematocrit; it also demonstrated a strong correlation with reference measurements under these conditions (R
MeSH term(s)	Animals ; Biosensing Techniques ; Colorimetry ; Glycerol ; Lipolysis ; Mice
Chemical Substances	Glycerol (PDC6A3C0OX)
Language	English
Publishing date	2021-02-27
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1483436-4
ISSN	1873-4324 ; 0003-2670
ISSN (online)	1873-4324
ISSN	0003-2670
DOI	10.1016/j.aca.2021.338358
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Article ; Online: Contrôle de l’homéostasie glucido-lipidique par les facteurs du cycle cellulaire CDK4 et E2F1.

Denechaud, Pierre-Damien / Lopez-Mejia, Isabel C / Fajas, Lluis

Medecine sciences : M/S

2016 Volume 32, Issue 10, Page(s) 815–818

Title translation	Cell cycle regulators CDK4 and E2F1 control glucose and lipid homeostasis.
MeSH term(s)	Adipose Tissue/metabolism ; Cyclin-Dependent Kinase 4/physiology ; E2F1 Transcription Factor/physiology ; Fatty Liver ; Glucose/metabolism ; Glycolysis/physiology ; Homeostasis ; Humans ; Insulin/metabolism ; Lipid Metabolism/physiology ; Lipogenesis/physiology ; Liver/metabolism ; Obesity/metabolism ; Signal Transduction/physiology
Chemical Substances	E2F1 Transcription Factor ; E2F1 protein, human ; Insulin ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Glucose (IY9XDZ35W2)
Language	French
Publishing date	2016-10
Publishing country	France
Document type	Journal Article
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/20163210008
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Article ; Online: CDK4 is an essential insulin effector in adipocytes.

The Journal of clinical investigation

2023 Volume 133, Issue 6

Language	English
Publishing date	2023-03-15
Publishing country	United States
Document type	Retraction of Publication
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI170315
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Article ; Online: CDK4 is an essential insulin effector in adipocytes

The Journal of Clinical Investigation, Vol 133, Iss

2023 Volume 6

Keywords	Medicine ; R
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	American Society for Clinical Investigation
Document type	Article ; Online
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Article ; Online: β-Cell-Specific E2f1 Deficiency Impairs Glucose Homeostasis, β-Cell Identity, and Insulin Secretion.

Oger, Frédérik / Bourouh, Cyril / Friano, Marika Elsa / Courty, Emilie / Rolland, Laure / Gromada, Xavier / Moreno, Maeva / Carney, Charlène / Rabhi, Nabil / Durand, Emmanuelle / Amanzougarene, Souhila / Berberian, Lionel / Derhourhi, Mehdi / Blanc, Etienne / Hannou, Sarah Anissa / Denechaud, Pierre-Damien / Benfodda, Zohra / Meffre, Patrick / Fajas, Lluis /

Kerr-Conte, Julie / Pattou, François / Froguel, Philippe / Pourcet, Benoit / Bonnefond, Amélie / Collombat, Patrick / Annicotte, Jean-Sébastien

Diabetes

2023 Volume 72, Issue 8, Page(s) 1112–1126

Abstract: The loss of pancreatic β-cell identity has emerged as an important feature of type 2 diabetes development, but the molecular mechanisms are still elusive. Here, we explore the cell-autonomous role of the cell-cycle regulator and transcription factor E2F1 ...

Abstract	The loss of pancreatic β-cell identity has emerged as an important feature of type 2 diabetes development, but the molecular mechanisms are still elusive. Here, we explore the cell-autonomous role of the cell-cycle regulator and transcription factor E2F1 in the maintenance of β-cell identity, insulin secretion, and glucose homeostasis. We show that the β-cell-specific loss of E2f1 function in mice triggers glucose intolerance associated with defective insulin secretion, altered endocrine cell mass, downregulation of many β-cell genes, and concomitant increase of non-β-cell markers. Mechanistically, epigenomic profiling of the promoters of these non-β-cell upregulated genes identified an enrichment of bivalent H3K4me3/H3K27me3 or H3K27me3 marks. Conversely, promoters of downregulated genes were enriched in active chromatin H3K4me3 and H3K27ac histone marks. We find that specific E2f1 transcriptional, cistromic, and epigenomic signatures are associated with these β-cell dysfunctions, with E2F1 directly regulating several β-cell genes at the chromatin level. Finally, the pharmacological inhibition of E2F transcriptional activity in human islets also impairs insulin secretion and the expression of β-cell identity genes. Our data suggest that E2F1 is critical for maintaining β-cell identity and function through sustained control of β-cell and non-β-cell transcriptional programs. Article highlights: β-Cell-specific E2f1 deficiency in mice impairs glucose tolerance. Loss of E2f1 function alters the ratio of α- to β-cells but does not trigger β-cell conversion into α-cells. Pharmacological inhibition of E2F activity inhibits glucose-stimulated insulin secretion and alters β- and α-cell gene expression in human islets. E2F1 maintains β-cell function and identity through control of transcriptomic and epigenetic programs.
MeSH term(s)	Animals ; Humans ; Mice ; Chromatin/metabolism ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Glucose/metabolism ; Histones/metabolism ; Homeostasis/genetics ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Mice, Knockout
Chemical Substances	Chromatin ; Glucose (IY9XDZ35W2) ; Histones ; Insulin ; E2F1 protein, human ; E2f1 protein, mouse
Language	English
Publishing date	2023-05-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db22-0604
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Article ; Online: ChREBPβ is dispensable for the control of glucose homeostasis and energy balance.

Recazens, Emeline / Tavernier, Geneviève / Dufau, Jérémy / Bergoglio, Camille / Benhamed, Fadila / Cassant-Sourdy, Stéphanie / Marques, Marie-Adeline / Caspar-Bauguil, Sylvie / Brion, Alice / Monbrun, Laurent / Dentin, Renaud / Ferrier, Clara / Leroux, Mélanie / Denechaud, Pierre-Damien / Moro, Cedric / Concordet, Jean-Paul / Postic, Catherine / Mouisel, Etienne / Langin, Dominique

JCI insight

2022 Volume 7, Issue 4

Abstract: Impaired glucose metabolism is observed in obesity and type 2 diabetes. Glucose controls gene expression through the transcription factor ChREBP in liver and adipose tissues. Mlxipl encodes 2 isoforms: ChREBPα, the full-length form (translocation into ... ...

Abstract	Impaired glucose metabolism is observed in obesity and type 2 diabetes. Glucose controls gene expression through the transcription factor ChREBP in liver and adipose tissues. Mlxipl encodes 2 isoforms: ChREBPα, the full-length form (translocation into the nucleus is under the control of glucose), and ChREBPβ, a constitutively nuclear shorter form. ChREBPβ gene expression in white adipose tissue is strongly associated with insulin sensitivity. Here, we investigated the consequences of ChREBPβ deficiency on insulin action and energy balance. ChREBPβ-deficient male and female C57BL6/J and FVB/N mice were produced using CRISPR/Cas9-mediated gene editing. Unlike global ChREBP deficiency, lack of ChREBPβ showed modest effects on gene expression in adipose tissues and the liver, with variations chiefly observed in brown adipose tissue. In mice fed chow and 2 types of high-fat diets, lack of ChREBPβ had moderate effects on body composition and insulin sensitivity. At thermoneutrality, ChREBPβ deficiency did not prevent the whitening of brown adipose tissue previously reported in total ChREBP-KO mice. These findings revealed that ChREBPβ is dispensable for metabolic adaptations to nutritional and thermic challenges.
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/biosynthesis ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Blood Glucose/metabolism ; Cells, Cultured ; Diabetes Mellitus, Experimental ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Energy Metabolism/genetics ; Female ; Gene Expression Regulation ; Male ; Mice ; Mice, Inbred C57BL ; RNA/genetics
Chemical Substances	Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Blood Glucose ; Mlxipl protein, mouse ; RNA (63231-63-0)
Language	English
Publishing date	2022-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.153431
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Article: Untargeted Lipidomic Profiling of Dry Blood Spots Using SFC-HRMS.

Le Faouder, Pauline / Soullier, Julia / Tremblay-Franco, Marie / Tournadre, Anthony / Martin, Jean-François / Guitton, Yann / Carlé, Caroline / Caspar-Bauguil, Sylvie / Denechaud, Pierre-Damien / Bertrand-Michel, Justine

Metabolites

2021 Volume 11, Issue 5

Abstract: Lipids are essential cellular constituents that have many critical roles in physiological functions. They are notably involved in energy storage and cell signaling as second messengers, and they are major constituents of cell membranes, including lipid ... ...

Abstract	Lipids are essential cellular constituents that have many critical roles in physiological functions. They are notably involved in energy storage and cell signaling as second messengers, and they are major constituents of cell membranes, including lipid rafts. As a consequence, they are implicated in a large number of heterogeneous diseases, such as cancer, diabetes, neurological disorders, and inherited metabolic diseases. Due to the high structural diversity and complexity of lipid species, the presence of isomeric and isobaric lipid species, and their occurrence at a large concentration scale, a complete lipidomic profiling of biological matrices remains challenging, especially in clinical contexts. Using supercritical fluid chromatography coupled with high-resolution mass spectrometry, we have developed and validated an untargeted lipidomic approach to the profiling of plasma and blood. Moreover, we have tested the technique using the Dry Blood Spot (DBS) method and found that it allows for the easy collection of blood for analysis. To develop the method, we performed the optimization of the separation and detection of lipid species on pure standards, reference human plasma (SRM1950), whole blood, and DBS. These analyses allowed an in-house lipid data bank to be built. Using the MS-Dial software, we developed an automatic process for the relative quantification of around 500 lipids species belonging to the 6 main classes of lipids (including phospholipids, sphingolipids, free fatty acids, sterols, and fatty acyl-carnitines). Then, we compared the method using the published data for SRM 1950 and a mouse blood sample, along with another sample of the same blood collected using the DBS method. In this study, we provided a method for blood lipidomic profiling that can be used for the easy sampling of dry blood spots.
Language	English
Publishing date	2021-05-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo11050305
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