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Article ; Online: Understanding lipid metabolism through hepatic steat-omics.

Haas, Joel T / Staels, Bart

2019 Volume 15, Issue 6, Page(s) 321–322

MeSH term(s)	Animals ; Humans ; Lipid Metabolism ; Liver
Language	English
Publishing date	2019-04-01
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/s41574-019-0203-9
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Article ; Online: Dysregulated lipid metabolism links NAFLD to cardiovascular disease.

Deprince, Audrey / Haas, Joel T / Staels, Bart

Molecular metabolism

2020 Volume 42, Page(s) 101092

Abstract: Background: Non-alcoholic fatty liver disease (NAFLD) is rapidly becoming a global health problem. Cardiovascular diseases (CVD) are the most common cause of mortality in NAFLD patients. NAFLD and CVD share several common risk factors including obesity, ...

Abstract	Background: Non-alcoholic fatty liver disease (NAFLD) is rapidly becoming a global health problem. Cardiovascular diseases (CVD) are the most common cause of mortality in NAFLD patients. NAFLD and CVD share several common risk factors including obesity, insulin resistance, and type 2 diabetes (T2D). Atherogenic dyslipidemia, characterized by plasma hypertriglyceridemia, increased small dense low-density lipoprotein (LDL) particles, and decreased high-density lipoprotein cholesterol (HDL-C) levels, is often observed in NAFLD patients. Scope of review: In this review, we highlight recent epidemiological studies evaluating the link between NAFLD and CVD risk. We further focus on recent mechanistic insights into the links between NAFLD and altered lipoprotein metabolism. We also discuss current therapeutic strategies for NAFLD and their potential impact on NAFLD-associated CVD risk. Major conclusions: Alterations in hepatic lipid and lipoprotein metabolism are major contributing factors to the increased CVD risk in NAFLD patients, and many promising NASH therapies in development also improve dyslipidemia in clinical trials.
MeSH term(s)	Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/physiopathology ; Dyslipidemias/epidemiology ; Dyslipidemias/physiopathology ; Humans ; Lipid Metabolism/physiology ; Lipids/physiology ; Liver/metabolism ; Non-alcoholic Fatty Liver Disease/epidemiology ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/physiopathology ; Obesity/metabolism ; Risk Factors
Chemical Substances	Lipids
Language	English
Publishing date	2020-10-01
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2020.101092
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Article ; Online: Fasting the Microbiota to Improve Metabolism?

Haas, Joel T / Staels, Bart

Cell metabolism

2017 Volume 26, Issue 4, Page(s) 584–585

Abstract: While intermittent or periodic fasting provides a variety of favorable health benefits, the molecular mediators of these effects are poorly understood. In this issue of Cell Metabolism, Li and colleagues (2017) highlight the role of gut microbiota in ... ...

Abstract	While intermittent or periodic fasting provides a variety of favorable health benefits, the molecular mediators of these effects are poorly understood. In this issue of Cell Metabolism, Li and colleagues (2017) highlight the role of gut microbiota in mediating benefits of intermittent fasting through activation of adipose tissue beiging.
Language	English
Publishing date	2017-10-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2017.09.013
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Article ; Online: An oxidative stress paradox: time for a conceptual change?

Haas, Joel T / Staels, Bart

Diabetologia

2016 Volume 59, Issue 12, Page(s) 2514–2517

Abstract: Oxidative stress has long been considered a key driving factor of many obesity-related health problems. However, recent work by Merry, Tran et al (Diabetologia DOI 10.1007/s00125-016-4084-3 ) challenges this idea with an interesting study using a ... ...

Abstract	Oxidative stress has long been considered a key driving factor of many obesity-related health problems. However, recent work by Merry, Tran et al (Diabetologia DOI 10.1007/s00125-016-4084-3 ) challenges this idea with an interesting study using a hepatocyte-specific Gpx1-knockout (HGKO) mouse. GPX1 is an important detoxification enzyme that converts H
MeSH term(s)	Animals ; Glutathione Peroxidase/metabolism ; Hydrogen Peroxide/metabolism ; Liver/metabolism ; Mice ; Mice, Knockout ; Non-alcoholic Fatty Liver Disease/metabolism ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species ; Hydrogen Peroxide (BBX060AN9V) ; glutathione peroxidase GPX1 (EC 1.11.1.-) ; Glutathione Peroxidase (EC 1.11.1.9)
Language	English
Publishing date	2016-12
Publishing country	Germany
Document type	Editorial
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-016-4117-y
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Article ; Online: Cholesteryl-ester transfer protein (CETP): A Kupffer cell marker linking hepatic inflammation with atherogenic dyslipidemia?

Haas, Joel T / Staels, Bart

Hepatology (Baltimore, Md.)

2015 Volume 62, Issue 6, Page(s) 1659–1661

MeSH term(s)	Animals ; Cholesterol Ester Transfer Proteins/metabolism ; Female ; Humans ; Kupffer Cells/metabolism ; Male
Chemical Substances	Cholesterol Ester Transfer Proteins
Language	English
Publishing date	2015-12
Publishing country	United States
Document type	Comment ; Editorial ; Research Support, Non-U.S. Gov't
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.28125
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Article ; Online: Pathophysiology and Mechanisms of Nonalcoholic Fatty Liver Disease.

Haas, Joel T / Francque, Sven / Staels, Bart

Annual review of physiology

2016 Volume 78, Page(s) 181–205

Abstract: Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver disorders characterized by abnormal hepatic fat accumulation, inflammation, and hepatocyte dysfunction. Importantly, it is also closely linked to obesity and the metabolic syndrome. ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) encompasses a spectrum of liver disorders characterized by abnormal hepatic fat accumulation, inflammation, and hepatocyte dysfunction. Importantly, it is also closely linked to obesity and the metabolic syndrome. NAFLD predisposes susceptible individuals to cirrhosis, hepatocellular carcinoma, and cardiovascular disease. Although the precise signals remain poorly understood, NAFLD pathogenesis likely involves actions of the different hepatic cell types and multiple extrahepatic signals. The complexity of this disease has been a major impediment to the development of appropriate metrics of its progression and effective therapies. Recent clinical data place increasing importance on identifying fibrosis, as it is a strong indicator of hepatic disease-related mortality. Preclinical modeling of the fibrotic process remains challenging, particularly in the contexts of obesity and the metabolic syndrome. Future studies are needed to define the molecular pathways determining the natural progression of NAFLD, including key determinants of fibrosis and disease-related outcomes. This review covers the evolving concepts of NAFLD from both human and animal studies. We discuss recent clinical and diagnostic methods assessing NAFLD diagnosis, progression, and outcomes; compare the features of genetic and dietary animal models of NAFLD; and highlight pharmacological approaches for disease treatment.
MeSH term(s)	Animals ; Disease Progression ; Humans ; Liver/pathology ; Liver Cirrhosis/pathology ; Metabolic Syndrome/pathology ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/pathology ; Obesity/pathology ; Risk Factors
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	207933-1
ISSN	1545-1585 ; 0066-4278
ISSN (online)	1545-1585
ISSN	0066-4278
DOI	10.1146/annurev-physiol-021115-105331
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Article ; Online: Shotgun metagenomics and systemic targeted metabolomics highlight indole-3-propionic acid as a protective gut microbial metabolite against influenza infection.

Heumel, Séverine / de Rezende Rodovalho, Vinícius / Urien, Charlotte / Specque, Florian / Brito Rodrigues, Patrícia / Robil, Cyril / Delval, Lou / Sencio, Valentin / Descat, Amandine / Deruyter, Lucie / Ferreira, Stéphanie / Gomes Machado, Marina / Barthelemy, Adeline / Angulo, Fabiola Silva / Haas, Joel T / Goosens, Jean François / Wolowczuk, Isabelle / Grangette, Corinne / Rouillé, Yves /

Grimaud, Ghjuvan / Lenski, Marie / Hennart, Benjamin / Ramirez Vinolo, Marco Aurélio / Trottein, François

Gut microbes

2024 Volume 16, Issue 1, Page(s) 2325067

Abstract: The gut-to-lung axis is critical during respiratory infections, including influenza A virus (IAV) infection. In the present study, we used high-resolution shotgun metagenomics and targeted metabolomic analysis to characterize influenza-associated changes ...

Abstract	The gut-to-lung axis is critical during respiratory infections, including influenza A virus (IAV) infection. In the present study, we used high-resolution shotgun metagenomics and targeted metabolomic analysis to characterize influenza-associated changes in the composition and metabolism of the mouse gut microbiota. We observed several taxonomic-level changes on day (D)7 post-infection, including a marked reduction in the abundance of members of the
MeSH term(s)	Humans ; Animals ; Mice ; Propionates ; Influenza, Human ; Gastrointestinal Microbiome ; Tryptophan ; Actinobacteria ; Inflammation ; Polyamines
Chemical Substances	propionic acid (JHU490RVYR) ; Propionates ; Tryptophan (8DUH1N11BX) ; Polyamines
Language	English
Publishing date	2024-03-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2575755-6
ISSN	1949-0984 ; 1949-0984
ISSN (online)	1949-0984
ISSN	1949-0984
DOI	10.1080/19490976.2024.2325067
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Article ; Online: Time-of-day-dependent variation of the human liver transcriptome and metabolome is disrupted in MASLD.

JHEP reports : innovation in hepatology

2023 Volume 6, Issue 1, Page(s) 100948

Abstract: Background & aims: Liver homeostasis is ensured in part by time-of-day-dependent processes, many of them being paced by the molecular circadian clock. Liver functions are compromised in metabolic dysfunction-associated steatotic liver disease (MASLD) ... ...

Abstract	Background & aims: Liver homeostasis is ensured in part by time-of-day-dependent processes, many of them being paced by the molecular circadian clock. Liver functions are compromised in metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH), and clock disruption increases susceptibility to MASLD progression in rodent models. We therefore investigated whether the time-of-day-dependent transcriptome and metabolome are significantly altered in human steatotic and MASH livers. Methods: Liver biopsies, collected within an 8 h-window from a carefully phenotyped cohort of 290 patients and histologically diagnosed to be either normal, steatotic or MASH hepatic tissues, were analyzed by RNA sequencing and unbiased metabolomic approaches. Time-of-day-dependent gene expression patterns and metabolomes were identified and compared between histologically normal, steatotic and MASH livers. Results: Herein, we provide a first-of-its-kind report of a daytime-resolved human liver transcriptome-metabolome and associated alterations in MASLD. Transcriptomic analysis showed a robustness of core molecular clock components in steatotic and MASH livers. It also revealed stage-specific, time-of-day-dependent alterations of hundreds of transcripts involved in cell-to-cell communication, intracellular signaling and metabolism. Similarly, rhythmic amino acid and lipid metabolomes were affected in pathological livers. Both TNFα and PPARγ signaling were predicted as important contributors to altered rhythmicity. Conclusion: MASLD progression to MASH perturbs time-of-day-dependent processes in human livers, while the differential expression of core molecular clock components is maintained. Impact and implications: This work characterizes the rhythmic patterns of the transcriptome and metabolome in the human liver. Using a cohort of well-phenotyped patients (n = 290) for whom the time-of-day at biopsy collection was known, we show that time-of-day variations observed in histologically normal livers are gradually perturbed in liver steatosis and metabolic dysfunction-associated steatohepatitis. Importantly, these observations, albeit obtained across a restricted time window, provide further support for preclinical studies demonstrating alterations of rhythmic patterns in diseased livers. On a practical note, this study indicates the importance of considering time-of-day as a critical biological variable which may significantly affect data interpretation in animal and human studies of liver diseases.
Language	English
Publishing date	2023-10-27
Publishing country	Netherlands
Document type	Journal Article
ISSN	2589-5559
ISSN (online)	2589-5559
DOI	10.1016/j.jhepr.2023.100948
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Article ; Online: Dissecting the role of insulin resistance in the metabolic syndrome.

Haas, Joel T / Biddinger, Sudha B

Current opinion in lipidology

2009 Volume 20, Issue 3, Page(s) 206–210

Abstract: Purpose of review: Over 20 years ago, insulin resistance was postulated to play a central role in the pathogenesis of the metabolic syndrome. However, this has been difficult to prove, leading to a great deal of controversy within the field. Recent ... ...

Abstract	Purpose of review: Over 20 years ago, insulin resistance was postulated to play a central role in the pathogenesis of the metabolic syndrome. However, this has been difficult to prove, leading to a great deal of controversy within the field. Recent studies on mice and humans with genetic defects in insulin signaling have allowed us, for the first time, to dissect which features of the metabolic syndrome can be caused by insulin resistance. Recent findings: Liver insulin receptor knockout mice show that hepatic insulin resistance can produce hyperglycemia, increased apolipoprotein B secretion and atherosclerosis, and increased biliary cholesterol secretion and cholesterol gallstones. Many of these changes may be due to disinhibition of the transcription factor, forkhead box O1. Yet, neither liver insulin receptor knockout mice nor humans with insulin receptor mutations develop the hypertriglyceridemia or hepatic steatosis associated with the metabolic syndrome. Summary: These data point to a central role for insulin resistance in the pathogenesis of the metabolic syndrome, as hyperglycemia, atherosclerosis, and cholesterol gallstones can all be caused by insulin resistance. However, hypertriglyceridemia and hepatic steatosis are not due directly to insulin resistance and should be considered pathogenically distinct features of the metabolic syndrome.
MeSH term(s)	Animals ; Humans ; Insulin/metabolism ; Metabolic Syndrome/metabolism ; Signal Transduction
Chemical Substances	Insulin
Language	English
Publishing date	2009-10-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1045394-5
ISSN	1473-6535 ; 0957-9672
ISSN (online)	1473-6535
ISSN	0957-9672
DOI	10.1097/MOL.0b013e32832b2024
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Article ; Online: The ubiquitin-like modifier FAT10 is induced in MASLD and impairs the lipid-regulatory activity of PPARα.

Metabolism: clinical and experimental

2023 Volume 151, Page(s) 155720

Abstract: Background and aims: Peroxisome Proliferator-Activated Receptor α (PPARα) is a key regulator of hepatic lipid metabolism and therefore a promising therapeutic target against Metabolic-dysfunction Associated Steatotic Liver Diseases (MASLD). However, its ...

Abstract	Background and aims: Peroxisome Proliferator-Activated Receptor α (PPARα) is a key regulator of hepatic lipid metabolism and therefore a promising therapeutic target against Metabolic-dysfunction Associated Steatotic Liver Diseases (MASLD). However, its expression and activity decrease during disease progression and several of its agonists did not achieve sufficient efficiency in clinical trials with, surprisingly, a lack of steatosis improvement. Here, we identified the Human leukocyte antigen-F Adjacent Transcript 10 (FAT10) as an inhibitor of PPARα lipid metabolic activity during MASLD progression. Approach and results: In vivo, the expression of FAT10 is upregulated in human and murine MASLD livers upon disease progression and correlates negatively with PPARα expression. The increase of FAT10 occurs in hepatocytes in which both proteins interact. FAT10 silencing in vitro in hepatocytes increases PPARα target gene expression, promotes fatty acid oxidation and decreases intra-cellular lipid droplet content. In line, FAT10 overexpression in hepatocytes in vivo inhibits the lipid regulatory activity of PPARα in response to fasting and agonist treatment in conditions of physiological and pathological hepatic lipid overload. Conclusions: FAT10 is induced during MASLD development and interacts with PPARα resulting in a decreased lipid metabolic response of PPARα to fasting or agonist treatment. Inhibition of the FAT10-PPARα interaction may provide a means to design potential therapeutic strategies against MASLD.
MeSH term(s)	Animals ; Humans ; Mice ; Disease Progression ; Fatty Acids/metabolism ; Fatty Liver/metabolism ; Lipid Metabolism/genetics ; Liver/metabolism ; Metabolic Diseases/metabolism ; PPAR alpha/metabolism ; Ubiquitin/metabolism ; Ubiquitins/metabolism
Chemical Substances	FAT10 protein, mouse ; Fatty Acids ; PPAR alpha ; Ubiquitin ; Ubiquitins ; UBD protein, human
Language	English
Publishing date	2023-11-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	80230-x
ISSN	1532-8600 ; 0026-0495
ISSN (online)	1532-8600
ISSN	0026-0495
DOI	10.1016/j.metabol.2023.155720
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