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Article ; Online: DNA methylation is altered in B and NK lymphocytes in obese and type 2 diabetic human.

Simar, David / Versteyhe, Soetkin / Donkin, Ida / Liu, Jia / Hesson, Luke / Nylander, Vibe / Fossum, Anna / Barrès, Romain

Metabolism: clinical and experimental

2014 Volume 63, Issue 9, Page(s) 1188–1197

Abstract: ... increased methylation levels in B cells from obese and T2D subjects and in natural killer cells from T2D ...

Abstract	Objective: Obesity is associated with low-grade inflammation and the infiltration of immune cells in insulin-sensitive tissues, leading to metabolic impairment. Epigenetic mechanisms control immune cell lineage determination, function and migration and are implicated in obesity and type 2 diabetes (T2D). The aim of this study was to determine the global DNA methylation profile of immune cells in obese and T2D individuals in a cell type-specific manner. Material and methods: Fourteen obese subjects and 11 age-matched lean subjects, as well as 12 T2D obese subjects and 7 age-matched lean subjects were recruited. Global DNA methylation levels were measured in a cell type-specific manner by flow cytometry. We validated the assay against mass spectrometry measures of the total 5-methylcytosine content in cultured cells treated with the hypomethylation agent decitabine (r=0.97, p<0.001). Results: Global DNA methylation in peripheral blood mononuclear cells, monocytes, lymphocytes or T cells was not altered in obese or T2D subjects. However, analysis of blood fractions from lean, obese, and T2D subjects showed increased methylation levels in B cells from obese and T2D subjects and in natural killer cells from T2D patients. In these cell types, DNA methylation levels were positively correlated with insulin resistance, suggesting an association between DNA methylation changes, immune function and metabolic dysfunction. Conclusions: Both obesity and T2D are associated with an altered epigenetic signature of the immune system in a cell type-specific manner. These changes could contribute to the altered immune functions associated with obesity and insulin resistance.
MeSH term(s)	Adolescent ; Adult ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Body Mass Index ; Cells, Cultured ; Cohort Studies ; DNA Methylation ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/immunology ; Diabetes Mellitus, Type 2/metabolism ; Epigenesis, Genetic ; Humans ; Insulin Resistance ; Killer Cells, Natural/metabolism ; Killer Cells, Natural/pathology ; Leukocytes, Mononuclear/metabolism ; Leukocytes, Mononuclear/pathology ; Male ; Middle Aged ; Monocytes/metabolism ; Monocytes/pathology ; Obesity/immunology ; Obesity/metabolism ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology ; Up-Regulation ; Young Adult
Language	English
Publishing date	2014-09
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80230-x
ISSN	1532-8600 ; 0026-0495
ISSN (online)	1532-8600
ISSN	0026-0495
DOI	10.1016/j.metabol.2014.05.014
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Article ; Online: Altered promoter methylation of PDK4, IL1 B, IL6, and TNF after Roux-en Y gastric bypass.

Kirchner, Henriette / Nylen, Carolina / Laber, Samantha / Barrès, Romain / Yan, Jie / Krook, Anna / Zierath, Juleen R / Näslund, Erik

Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery

2014 Volume 10, Issue 4, Page(s) 671–678

Abstract: ... interleukin-1 beta (IL1 B), interleukin-6 (IL6) and tumor necrosis factor-α (TNF) is altered in blood after ... A, TFAM, IL1 B, IL6, and TNF promoters was changed two days after RYGB. Similar changes were also seen ... on day one after cholecystectomy. Moreover, methylation increased in PDK4, IL1 B, IL6, and TNF promoters ...

Abstract	Background: Early benefits of Roux-en Y gastric bypass (RYGB) are partly mediated by the caloric restriction that patients undergo before and acutely after the procedure. Altered DNA methylation occurs in metabolic diseases including obesity, as well as in skeletal, muscle eight months after RYGB. The objective of this study was to test whether promoter methylation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PPARGC1 A), pyruvate dehydrogenase kinase isozyme-4 (PDK4), transcription factor A (TFAM), interleukin-1 beta (IL1 B), interleukin-6 (IL6) and tumor necrosis factor-α (TNF) is altered in blood after a very low calorie diet (VLCD) or RYGB. Methods: Obese nondiabetic patients (n = 18, body mass index [BMI] 42.3 ± 4.9 kg/m(2)) underwent a 14-day VLCD followed by RYGB. Nonobese patients (n = 6, BMI 25.7 ± 2.1 kg/m(2)) undergoing elective cholecystectomy served as controls. DNA methylation of selected promoter regions was measured in whole blood before and after VLCD. A subgroup of seven patients was studied 1-2 days and 12 ± 3 months after RYGB. Promoter methylation was measured using methylated DNA capture and quantitative real-time polymerase chain reaction (PCR). Results: VLCD decreased promoter methylation of PPARGC1 A. Methylation of PPARGC1 A, TFAM, IL1 B, IL6, and TNF promoters was changed two days after RYGB. Similar changes were also seen on day one after cholecystectomy. Moreover, methylation increased in PDK4, IL1 B, IL6, and TNF promoters 12 months after RYGB. Conclusion: RYGB induced more profound epigenetic changes than VLCD in promoters of the tested genes in whole blood. Changes in DNA methylation may contribute to the improved overall metabolic health after RYGB.
MeSH term(s)	Adult ; Caloric Restriction ; Case-Control Studies ; DNA Methylation ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Female ; Gastric Bypass ; Humans ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Male ; Middle Aged ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Obesity, Morbid/genetics ; Obesity, Morbid/metabolism ; Obesity, Morbid/therapy ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	DNA-Binding Proteins ; Interleukin-1beta ; Interleukin-6 ; Mitochondrial Proteins ; PPARGC1A protein, human ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; TFAM protein, human ; Transcription Factors ; Tumor Necrosis Factor-alpha ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; pyruvate dehydrogenase (acetyl-transferring) kinase (EC 2.7.11.2)
Language	English
Publishing date	2014-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2274243-8
ISSN	1878-7533 ; 1550-7289
ISSN (online)	1878-7533
ISSN	1550-7289
DOI	10.1016/j.soard.2013.12.019
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Article ; Online: Emergence and spread of the barley net blotch pathogen coincided with crop domestication and cultivation history.

Taliadoros, Demetris / Feurtey, Alice / Wyatt, Nathan / Barrès, Benoit / Gladieux, Pierre / Friesen, Timothy L / Stukenbrock, Eva H

PLoS genetics

2024 Volume 20, Issue 1, Page(s) e1010884

Abstract: Fungal pathogens cause devastating disease in crops. Understanding the evolutionary origin of pathogens is essential to the prediction of future disease emergence and the potential of pathogens to disperse. The fungus Pyrenophora teres f. teres causes ... ...

Abstract	Fungal pathogens cause devastating disease in crops. Understanding the evolutionary origin of pathogens is essential to the prediction of future disease emergence and the potential of pathogens to disperse. The fungus Pyrenophora teres f. teres causes net form net blotch (NFNB), an economically significant disease of barley. In this study, we have used 104 P. teres f. teres genomes from four continents to explore the population structure and demographic history of the fungal pathogen. We showed that P. teres f. teres is structured into populations that tend to be geographically restricted to different regions. Using Multiple Sequentially Markovian Coalescent and machine learning approaches we demonstrated that the demographic history of the pathogen correlates with the history of barley, highlighting the importance of human migration and trade in spreading the pathogen. Exploring signatures of natural selection, we identified several population-specific selective sweeps that colocalized with genomic regions enriched in putative virulence genes, and loci previously identified as determinants of virulence specificities by quantitative trait locus analyses. This reflects rapid adaptation to local hosts and environmental conditions of P. teres f. teres as it spread with barley. Our research highlights how human activities can contribute to the spread of pathogens that significantly impact the productivity of field crops.
MeSH term(s)	Humans ; Hordeum/genetics ; Hordeum/microbiology ; Domestication ; Ascomycota/genetics ; Plant Diseases/genetics ; Plant Diseases/microbiology ; Quantitative Trait Loci/genetics
Language	English
Publishing date	2024-01-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1010884
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Article ; Online: Distribution of invasive versus native whitefly species and their pyrethroid knock-down resistance allele in a context of interspecific hybridization.

Taquet, Alizée / Jourdan-Pineau, Hélène / Simiand, Christophe / Grondin, Martial / Barrès, Benoit / Delatte, Hélène

Scientific reports

2022 Volume 12, Issue 1, Page(s) 8448

Abstract: The invasion success of a species in an agrosystem is greatly influenced by environmental factors such as the use of insecticides, by the intrinsic evolutionary capabilities of the species, and also by interactions with resident species. On the island of ...

Abstract	The invasion success of a species in an agrosystem is greatly influenced by environmental factors such as the use of insecticides, by the intrinsic evolutionary capabilities of the species, and also by interactions with resident species. On the island of La Réunion, the successive invasions of MEAM1 and MED whitefly species over the last 20 years have not only led an increased use of insecticides, but have also challenged the resident IO species. To trace the evolution of the 3 species, and the distribution of the kdr mutation (resistance to pyrethroid) in the para-type voltage-gated sodium channel, we genotyped 41 populations (using neutral nuclear markers) and look at the prevalence of the kdr allele. MEAM1 was predominantly present in agrosystems showing quasi fixation of the resistant kdr allele whereas IO was mainly in natural environments and did not have any resistant allele. Hybridization between the two former species was detected in low frequency but has not led to introgression of resistant alleles in the resident species so far. MED showed a limited distribution in agrosystems but all individuals displayed a resistant allele. These highly contrasting patterns of distribution and resistant mutations between invasive and resident whitefly species are further discussed.
MeSH term(s)	Alleles ; Animals ; Hemiptera/genetics ; Humans ; Insecticide Resistance/genetics ; Insecticides/pharmacology ; Mutation ; Pyrethrins/pharmacology
Chemical Substances	Insecticides ; Pyrethrins
Language	English
Publishing date	2022-05-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-12373-4
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Article ; Online: Butyrate inhibits IL-1β-induced inflammatory gene expression by suppression of NF-κB activity in pancreatic beta cells.

Pedersen, Signe Schultz / Prause, Michala / Williams, Kristine / Barrès, Romain / Billestrup, Nils

The Journal of biological chemistry

2022 Volume 298, Issue 9, Page(s) 102312

Abstract: Cytokine-induced beta cell dysfunction is a hallmark of type 2 diabetes (T2D). Chronic exposure of beta cells to inflammatory cytokines affects gene expression and impairs insulin secretion. Thus, identification of anti-inflammatory factors that preserve ...

Abstract	Cytokine-induced beta cell dysfunction is a hallmark of type 2 diabetes (T2D). Chronic exposure of beta cells to inflammatory cytokines affects gene expression and impairs insulin secretion. Thus, identification of anti-inflammatory factors that preserve beta cell function represents an opportunity to prevent or treat T2D. Butyrate is a gut microbial metabolite with anti-inflammatory properties for which we recently showed a role in preventing interleukin-1β (IL-1β)-induced beta cell dysfunction, but how prevention is accomplished is unclear. Here, we investigated the mechanisms by which butyrate exerts anti-inflammatory activity in beta cells. We exposed mouse islets and INS-1E cells to a low dose of IL-1β and/or butyrate and measured expression of inflammatory genes and nitric oxide (NO) production. Additionally, we explored the molecular mechanisms underlying butyrate activity by dissecting the activation of the nuclear factor-κB (NF-κB) pathway. We found that butyrate suppressed IL-1β-induced expression of inflammatory genes, such as Nos2, Cxcl1, and Ptgs2, and reduced NO production. Butyrate did not inhibit IκBα degradation nor NF-κB p65 nuclear translocation. Furthermore, butyrate did not affect binding of NF-κB p65 to target sequences in synthetic DNA but inhibited NF-κB p65 binding and RNA polymerase II recruitment to inflammatory gene promoters in the context of native DNA. We found this was concurrent with increased acetylation of NF-κB p65 and histone H4, suggesting butyrate affects NF-κB activity via inhibition of histone deacetylases. Together, our results show butyrate inhibits IL-1β-induced inflammatory gene expression and NO production through suppression of NF-κB activation and thereby possibly preserves beta cell function.
MeSH term(s)	Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Butyrates/pharmacology ; Cyclooxygenase 2/metabolism ; Diabetes Mellitus, Type 2/immunology ; Diabetes Mellitus, Type 2/pathology ; Gene Expression Regulation ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/metabolism ; Histones/metabolism ; Inflammation/genetics ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Interleukin-1beta/antagonists & inhibitors ; Interleukin-1beta/metabolism ; Interleukin-1beta/pharmacology ; Mice ; NF-KappaB Inhibitor alpha/metabolism ; NF-kappa B/metabolism ; Nitric Oxide/biosynthesis ; RNA Polymerase II/metabolism
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Butyrates ; Histone Deacetylase Inhibitors ; Histones ; Interleukin-1beta ; NF-kappa B ; NF-KappaB Inhibitor alpha (139874-52-5) ; Nitric Oxide (31C4KY9ESH) ; Cyclooxygenase 2 (EC 1.14.99.1) ; RNA Polymerase II (EC 2.7.7.-) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2022-07-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2022.102312
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Article ; Online: Investigation of the sensitivity of Plasmopara viticola to amisulbrom and ametoctradin in French vineyards using bioassays and molecular tools.

Fontaine, Séverine / Remuson, Florent / Caddoux, Laëtitia / Barrès, Benoit

Pest management science

2019 Volume 75, Issue 8, Page(s) 2115–2123

Abstract: ... by a single point mutation in the cytochrome b gene, leading to the S34L substitution. The role ...

Abstract	Background: Complex III inhibitors are key compounds in the control of Plasmopara viticola. They are prone to the development of resistance, as demonstrated by the emergence of resistance to quinone-outside inhibitors. By using a combination of bioassays and molecular methods, we monitored sensitivity to amisulbrom and ametoctradin in P. viticola populations in French vineyards from 2012 to 2017. Results: We found that the alternative oxidase (AOX)-related resistance mechanism was common in French P. viticola populations. Target-site resistance to ametoctradin was first detected in 2015 and is likely caused by a single point mutation in the cytochrome b gene, leading to the S34L substitution. The role of this substitution in resistance to ametoctradin was corroborated by another study using an experimental model. A molecular biology method has been developed to detect the mutant allele. To date, the frequency of this mutation is low in French P. viticola populations and it is often co-detected with the wild-type allele. Conclusion: Populations of P. viticola displaying evidence of AOX-related resistance were detected for every surveyed year, and their occurrence in French vineyards seems to be increasing over time. This resistance mechanism is currently threatening the efficacy of complex III inhibitors in the field. The low frequency of the S34L allele conferring resistance to ametoctradin, and the instability of resistant phenotypes in some populations, suggest that a fitness cost may be associated with the mutation. © 2019 Society of Chemical Industry.
MeSH term(s)	Fungicides, Industrial ; Halogenation ; Indoles ; Oomycetes ; Pest Control ; Pyrimidines ; Triazoles
Chemical Substances	Fungicides, Industrial ; Indoles ; Pyrimidines ; Triazoles ; ametoctradin (J84P40P7BV)
Language	English
Publishing date	2019-06-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2001705-4
ISSN	1526-4998 ; 1526-498X
ISSN (online)	1526-4998
ISSN	1526-498X
DOI	10.1002/ps.5461
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Article: Host plants and insecticides shape the evolution of genetic and clonal diversity in a major aphid crop pest.

Roy, Lise / Barrès, Benoit / Capderrey, Cécile / Mahéo, Frédérique / Micoud, Annie / Hullé, Maurice / Simon, Jean-Christophe

Evolutionary applications

2022 Volume 15, Issue 10, Page(s) 1653–1669

Abstract: Understanding the spatiotemporal dynamics of pesticide resistance at the landscape scale is essential to anticipate the evolution and spread of new resistance phenotypes. In crop mosaics, host plant specialization in pest populations is likely to dampen ... ...

Abstract	Understanding the spatiotemporal dynamics of pesticide resistance at the landscape scale is essential to anticipate the evolution and spread of new resistance phenotypes. In crop mosaics, host plant specialization in pest populations is likely to dampen the spread of pesticide resistance between different crops even in mobile pests such as aphids. Here, we assessed the contribution of host-based genetic differentiation to the dynamics of resistance alleles in
Language	English
Publishing date	2022-07-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2405496-3
ISSN	1752-4563 ; 1752-4571
ISSN (online)	1752-4563
ISSN	1752-4571
DOI	10.1111/eva.13417
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Article ; Online: Insecticide resistance and fitness cost in Bemisia tabaci (Hemiptera: Aleyrodidae) invasive and resident species in La Réunion Island.

Taquet, Alizée / Delatte, Hélène / Barrès, Benoit / Simiand, Christophe / Grondin, Martial / Jourdan-Pineau, Hélène

Pest management science

2019 Volume 76, Issue 4, Page(s) 1235–1244

Abstract: ... of the susceptibility to insecticides for B. tabaci IO species. For the time being, no resistance to the tested ...

Abstract	Background: Global and intensive use of insecticides has led to the emergence and rapid evolution of resistance in the major pest Bemisia tabaci (Gennadius). In La Réunion, an island of the South West Indian Ocean, three whitefly species coexist, two of which are predominant, the indigenous Indian Ocean (IO) and the invasive Middle East Asia Minor 1 (MEAM1) species. To assess the resistance level of both of these species to acetamiprid and pymetrozine, whitefly populations were sampled at 15 collection sites located all over the island in agroecosystems and natural areas, and tested using leaf-dip bioassays. We also investigated the potential cost of resistance to acetamiprid by measuring six fitness-related traits for MEAM1 populations that displayed different resistance levels. Results: IO was mainly found in natural areas and was susceptible to both acetamiprid and pymetrozine. MEAM1 populations displayed evidence of high resistance to pymetrozine, whereas resistance to acetamiprid was more variable. No fitness-related costs were associated with this resistance in MEAM1 populations. Conclusion: This is the first assessment of the susceptibility to insecticides for B. tabaci IO species. For the time being, no resistance to the tested insecticides has evolved in this species despite (i) its presence in agroecosystems and their surroundings, and (ii) its close proximity to, and possible hybridization with, the MEAM1 species. In contrast, with continuous selection pressure of insecticide treatments and in the absence of fitness cost to resistance, the invasive exotic species MEAM1 will continue to threaten agriculture in La Réunion. © 2019 Society of Chemical Industry.
MeSH term(s)	Animals ; Far East ; Hemiptera ; Insecticide Resistance ; Insecticides ; Reunion
Chemical Substances	Insecticides
Language	English
Publishing date	2019-11-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2001705-4
ISSN	1526-4998 ; 1526-498X
ISSN (online)	1526-4998
ISSN	1526-498X
DOI	10.1002/ps.5633
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Article ; Online: Ablation of DNA-methyltransferase 3A in skeletal muscle does not affect energy metabolism or exercise capacity.

Small, Lewin / Ingerslev, Lars R / Manitta, Eleonora / Laker, Rhianna C / Hansen, Ann N / Deeney, Brendan / Carrié, Alain / Couvert, Philippe / Barrès, Romain

PLoS genetics

2021 Volume 17, Issue 1, Page(s) e1009325

Abstract: In response to physical exercise and diet, skeletal muscle adapts to energetic demands through large transcriptional changes. This remodelling is associated with changes in skeletal muscle DNA methylation which may participate in the metabolic adaptation ...

Abstract	In response to physical exercise and diet, skeletal muscle adapts to energetic demands through large transcriptional changes. This remodelling is associated with changes in skeletal muscle DNA methylation which may participate in the metabolic adaptation to extracellular stimuli. Yet, the mechanisms by which muscle-borne DNA methylation machinery responds to diet and exercise and impacts muscle function are unknown. Here, we investigated the function of de novo DNA methylation in fully differentiated skeletal muscle. We generated muscle-specific DNA methyltransferase 3A (DNMT3A) knockout mice (mD3AKO) and investigated the impact of DNMT3A ablation on skeletal muscle DNA methylation, exercise capacity and energy metabolism. Loss of DNMT3A reduced DNA methylation in skeletal muscle over multiple genomic contexts and altered the transcription of genes known to be influenced by DNA methylation, but did not affect exercise capacity and whole-body energy metabolism compared to wild type mice. Loss of DNMT3A did not alter skeletal muscle mitochondrial function or the transcriptional response to exercise however did influence the expression of genes involved in muscle development. These data suggest that DNMT3A does not have a large role in the function of mature skeletal muscle although a role in muscle development and differentiation is likely.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA Methylation/genetics ; Energy Metabolism/genetics ; Exercise Tolerance/genetics ; Humans ; Mice ; Mice, Knockout ; Muscle Development/genetics ; Muscle, Skeletal/growth & development ; Muscle, Skeletal/metabolism ; Physical Conditioning, Animal
Chemical Substances	DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; DNA methyltransferase 3A (EC 2.1.1.37)
Language	English
Publishing date	2021-01-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1009325
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Article ; Online: Association of apolipoprotein M and sphingosine-1-phosphate with brown adipose tissue after cold exposure in humans.

Borup, Anna / Donkin, Ida / Boon, Mariëtte R / Frydland, Martin / Martinez-Tellez, Borja / Loft, Annika / Keller, Sune H / Kjaer, Andreas / Kjaergaard, Jesper / Hassager, Christian / Barrès, Romain / Rensen, Patrick C N / Christoffersen, Christina

Scientific reports

2022 Volume 12, Issue 1, Page(s) 18753

Abstract: The HDL-associated apolipoprotein M (apoM) and its ligand sphingosine-1-phosphate (S1P) may control energy metabolism. ApoM deficiency in mice is associated with increased vascular permeability, brown adipose tissue (BAT) mass and activity, and ... ...

Abstract	The HDL-associated apolipoprotein M (apoM) and its ligand sphingosine-1-phosphate (S1P) may control energy metabolism. ApoM deficiency in mice is associated with increased vascular permeability, brown adipose tissue (BAT) mass and activity, and protection against obesity. In the current study, we explored the connection between plasma apoM/S1P levels and parameters of BAT as measured via
MeSH term(s)	Animals ; Humans ; Adipose Tissue, Brown/metabolism ; Apolipoproteins M/metabolism ; Lysophospholipids/metabolism ; Positron Emission Tomography Computed Tomography ; Sphingosine/metabolism
Chemical Substances	Apolipoproteins M ; Lysophospholipids ; Sphingosine (NGZ37HRE42) ; sphingosine 1-phosphate (26993-30-6)
Language	English
Publishing date	2022-11-05
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-21938-2
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