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Article ; Online: Cardiovascular Protection by Sodium Glucose Cotransporter 2 Inhibitors: Potential Mechanisms.

Staels, Bart

2017 Volume 130, Issue 6S, Page(s) S30–S39

Abstract: The mechanism of action of empagliflozin in reducing the risk of adverse cardiovascular outcomes vs placebo in patients with type 2 diabetes mellitus and a high risk of cardiovascular disease in the Empagliflozin Cardiovascular Outcome Event Trial in ... ...

Abstract	The mechanism of action of empagliflozin in reducing the risk of adverse cardiovascular outcomes vs placebo in patients with type 2 diabetes mellitus and a high risk of cardiovascular disease in the Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients-Removing Excess Glucose (EMPA-REG OUTCOME) trial is currently unknown. An antiatherosclerotic effect is considered unlikely given the speed of the observed decrease in cardiovascular mortality. Hemodynamic effects, such as reductions in blood pressure and intravascular volume, and involving osmotic diuresis, may provide a more plausible explanation. Metabolic effects, such as cardiac fuel energetics, and hormonal effects, such as increased glucagon release, may also contribute to the results observed during EMPA-REG OUTCOME. This review discusses the main hypotheses suggested to date.
MeSH term(s)	Benzhydryl Compounds/therapeutic use ; Cardiovascular Diseases/prevention & control ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Diabetic Angiopathies/prevention & control ; Diabetic Cardiomyopathies/metabolism ; Glucosides/therapeutic use ; Hemodynamics ; Hormones/metabolism ; Humans ; Hyperglycemia/drug therapy ; Hyperglycemia/etiology ; Hypoglycemic Agents/therapeutic use ; Sodium-Glucose Transporter 2/antagonists & inhibitors
Chemical Substances	Benzhydryl Compounds ; Glucosides ; Hormones ; Hypoglycemic Agents ; Sodium-Glucose Transporter 2 ; empagliflozin (HDC1R2M35U)
Language	English
Publishing date	2017-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80015-6
ISSN	1555-7162 ; 1873-2178 ; 0002-9343 ; 1548-2766
ISSN (online)	1555-7162 ; 1873-2178
ISSN	0002-9343 ; 1548-2766
DOI	10.1016/j.amjmed.2017.04.009
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Ua VI Zs.289: Show issues

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Article ; Online: Treating NASH by targeting peroxisome proliferator-activated receptors.

Staels, Bart / Butruille, Laura / Francque, Sven

Journal of hepatology

2023 Volume 79, Issue 5, Page(s) 1302–1316

Abstract: The pathophysiology of non-alcoholic steatohepatitis (NASH) encompasses a complex set of intra- and extrahepatic driving mechanisms, involving numerous metabolic, inflammatory, vascular and fibrogenic pathways. The peroxisome proliferator-activated ... ...

Abstract	The pathophysiology of non-alcoholic steatohepatitis (NASH) encompasses a complex set of intra- and extrahepatic driving mechanisms, involving numerous metabolic, inflammatory, vascular and fibrogenic pathways. The peroxisome proliferator-activated receptors (PPARs) α, β/δ and γ belong to the nuclear receptor family of ligand-activated transcription factors. Activated PPARs modulate target tissue transcriptomic profiles, enabling the body's adaptation to changing nutritional, metabolic and inflammatory environments. PPARs hence regulate several pathways involved in NASH pathogenesis. Whereas single PPAR agonists exert robust anti-NASH activity in several preclinical models, their clinical effects on histological endpoints of NASH resolution and fibrosis regression appear more modest. Simultaneous activation of several PPAR isotypes across different organs and within-organ cell types, resulting in pleiotropic actions, enhances the therapeutic potential of PPAR agonists as pharmacological agents for NASH and NASH-related hepatic and extrahepatic morbidity, with some compounds having already shown clinical efficacy on histological endpoints.
Language	English
Publishing date	2023-07-17
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2023.07.004
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Zs.A 2027: Show issues

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Article ; Online: Cardiovascular Protection by Sodium Glucose Cotransporter 2 Inhibitors: Potential Mechanisms.

Staels, Bart

The American journal of cardiology

2017 Volume 120, Issue 1S, Page(s) S28–S36

Abstract	The mechanism of action of empagliflozin in reducing the risk of adverse cardiovascular outcomes vs placebo in patients with type 2 diabetes mellitus and a high risk of cardiovascular disease in the Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients-Removing Excess Glucose (EMPA-REG OUTCOME) trial is currently unknown. An antiatherosclerotic effect is considered unlikely given the speed of the observed decrease in cardiovascular mortality. Hemodynamic effects, such as reductions in blood pressure and intravascular volume, and involving osmotic diuresis, may provide a more plausible explanation. Metabolic effects, such as cardiac fuel energetics, and hormonal effects, such as increased glucagon release, may also contribute to the results observed during EMPA-REG OUTCOME. This review discusses the main hypotheses suggested to date.
MeSH term(s)	Benzhydryl Compounds/therapeutic use ; Cardiovascular Diseases/prevention & control ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Diabetic Angiopathies/prevention & control ; Diabetic Cardiomyopathies/metabolism ; Glucosides/therapeutic use ; Hemodynamics ; Hormones/metabolism ; Humans ; Hyperglycemia/drug therapy ; Hyperglycemia/etiology ; Hypoglycemic Agents/therapeutic use ; Sodium-Glucose Transporter 2/antagonists & inhibitors
Chemical Substances	Benzhydryl Compounds ; Glucosides ; Hormones ; Hypoglycemic Agents ; Sodium-Glucose Transporter 2 ; empagliflozin (HDC1R2M35U)
Language	English
Publishing date	2017-05-30
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	80014-4
ISSN	1879-1913 ; 0002-9149
ISSN (online)	1879-1913
ISSN	0002-9149
DOI	10.1016/j.amjcard.2017.05.013
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Ui IV Zs.73: Show issues

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Article ; Online: Hepatic sexual dimorphism - implications for non-alcoholic fatty liver disease.

Lefebvre, Philippe / Staels, Bart

Nature reviews. Endocrinology

2021 Volume 17, Issue 11, Page(s) 662–670

Abstract: The liver is often thought of as a single functional unit, but both its structural and functional architecture make it highly multivalent and adaptable. In any given physiological situation, the liver can maintain metabolic homeostasis, conduct ... ...

Abstract	The liver is often thought of as a single functional unit, but both its structural and functional architecture make it highly multivalent and adaptable. In any given physiological situation, the liver can maintain metabolic homeostasis, conduct appropriate inflammatory responses, carry out endobiotic and xenobiotic transformation and synthesis reactions, as well as store and release multiple bioactive molecules. Moreover, the liver is a very resilient organ. This resilience means that chronic liver diseases can go unnoticed for decades, yet culminate in life-threatening clinical complications once the adaptive capacity of the liver is overwhelmed. Non-alcoholic fatty liver disease (NAFLD) predisposes individuals to cirrhosis and increases liver-related and cardiovascular disease-related mortality. This Review discusses the accumulating evidence of sexual dimorphism in NAFLD, which is currently rarely considered in preclinical and clinical studies. Increased awareness of the mechanistic causes of hepatic sexual dimorphism could lead to improved understanding of the biological processes that are dysregulated in NAFLD, to the identification of relevant therapeutic targets and to improved risk stratification of patients with NAFLD undergoing therapeutic intervention.
MeSH term(s)	Cardiovascular Diseases/complications ; Female ; Humans ; Liver Cirrhosis/complications ; Liver Cirrhosis/pathology ; Male ; Non-alcoholic Fatty Liver Disease/complications ; Non-alcoholic Fatty Liver Disease/pathology ; Sex Characteristics
Language	English
Publishing date	2021-08-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/s41574-021-00538-6
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Zs.A 6336: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 93: Show issues

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Article ; Online: Immune-metabolic interactions in homeostasis and the progression to NASH.

Hoogerland, Joanne A / Staels, Bart / Dombrowicz, David

Trends in endocrinology and metabolism: TEM

2022 Volume 33, Issue 10, Page(s) 690–709

Abstract: The incidence of non-alcoholic fatty liver disease (NAFLD) has increased significantly over the past two decades. NAFLD ranges from simple steatosis (NAFL) to nonalcoholic steatohepatitis (NASH) and predisposes to fibrosis and hepatocellular carcinoma ( ... ...

Abstract	The incidence of non-alcoholic fatty liver disease (NAFLD) has increased significantly over the past two decades. NAFLD ranges from simple steatosis (NAFL) to nonalcoholic steatohepatitis (NASH) and predisposes to fibrosis and hepatocellular carcinoma (HCC). The importance of the immune system in hepatic physiology and in the progression of NAFLD is increasingly recognized. At homeostasis, the liver participates in immune defense against pathogens and in tolerance of gut-derived microbial compounds. Hepatic immune cells also respond to metabolic stimuli and have a role in NAFLD progression to NASH. In this review, we discuss how metabolic perturbations affect immune cell phenotype and function in NAFL and NASH, and then focus on the role of immune cells in liver homeostasis and in the development of NASH.
MeSH term(s)	Carcinoma, Hepatocellular/epidemiology ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Disease Progression ; Homeostasis ; Humans ; Liver/metabolism ; Liver Cirrhosis/genetics ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Liver Neoplasms/epidemiology ; Liver Neoplasms/genetics ; Liver Neoplasms/pathology ; Non-alcoholic Fatty Liver Disease/metabolism
Language	English
Publishing date	2022-08-10
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2022.07.001
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Zs.A 2999: Show issues

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Article ; Online: An optimized protocol with a stepwise approach to identify specific nuclear receptor ligands from cultured mammalian cells.

Berthier, Alexandre / Staels, Bart / Lefebvre, Philippe

STAR protocols

2021 Volume 2, Issue 3, Page(s) 100658

Abstract: Here, we describe an optimized protocol to identify specific nuclear receptor ligands. First, to rule out any compound interference with luciferase activity per se, we describe ... ...

Abstract	Here, we describe an optimized protocol to identify specific nuclear receptor ligands. First, to rule out any compound interference with luciferase activity per se, we describe an
MeSH term(s)	Animals ; Cells, Cultured ; Constitutive Androstane Receptor ; Cytological Techniques/methods ; Drug Discovery/methods ; Ligands ; Pregnane X Receptor ; Receptors, Cytoplasmic and Nuclear/agonists ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors ; Receptors, Cytoplasmic and Nuclear/chemistry ; Receptors, Cytoplasmic and Nuclear/metabolism
Chemical Substances	Constitutive Androstane Receptor ; Ligands ; Pregnane X Receptor ; Receptors, Cytoplasmic and Nuclear
Language	English
Publishing date	2021-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2021.100658
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Article ; Online: Intestine-liver crosstalk in Type 2 Diabetes and non-alcoholic fatty liver disease.

Nawrot, Margaux / Peschard, Simon / Lestavel, Sophie / Staels, Bart

Metabolism: clinical and experimental

2021 Volume 123, Page(s) 154844

Abstract: Type 2 diabetes (T2D) and Non-Alcoholic Fatty Liver Disease (NAFLD) are pathologies whose prevalence continues to increase worldwide. Both diseases are precipitated by an excessive caloric intake, which promotes insulin resistance and fatty liver. The ... ...

Abstract	Type 2 diabetes (T2D) and Non-Alcoholic Fatty Liver Disease (NAFLD) are pathologies whose prevalence continues to increase worldwide. Both diseases are precipitated by an excessive caloric intake, which promotes insulin resistance and fatty liver. The role of the intestine and its crosstalk with the liver in the development of these metabolic diseases is receiving increasing attention. Alterations in diet-intestinal microbiota interactions lead to the dysregulation of intestinal functions, resulting in altered metabolite and energy substrate production and increased intestinal permeability. Connected through the portal circulation, these changes in intestinal functions impact the liver and other metabolic organs, such as visceral adipose tissue, hence participating in the development of insulin resistance, and worsening T2D and NAFLD. Thus, targeting the intestine may be an efficient therapeutic approach to cure T2D and NAFLD. In this review, we will first introduce the signaling pathways linking T2D and NAFLD. Next, we will address the role of the gut-liver crosstalk in the development of T2D and NAFLD, with a particular focus on the gut microbiota and the molecular pathways behind the increased intestinal permeability and inflammation. Finally, we will summarize the therapeutic strategies which target the gut and its functions and are currently used or under development to treat T2D and NAFLD.
MeSH term(s)	Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/therapy ; Dyslipidemias/metabolism ; Gastrointestinal Microbiome ; Humans ; Intestines/physiopathology ; Lipid Metabolism ; Liver/metabolism ; Liver/physiopathology ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/therapy ; Signal Transduction
Language	English
Publishing date	2021-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80230-x
ISSN	1532-8600 ; 0026-0495
ISSN (online)	1532-8600
ISSN	0026-0495
DOI	10.1016/j.metabol.2021.154844
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Article ; Online: PPAR control of metabolism and cardiovascular functions.

Montaigne, David / Butruille, Laura / Staels, Bart

Nature reviews. Cardiology

2021 Volume 18, Issue 12, Page(s) 809–823

Abstract: Peroxisome proliferator-activated receptor-α (PPARα), PPARδ and PPARγ are transcription factors that regulate gene expression following ligand activation. PPARα increases cellular fatty acid uptake, esterification and trafficking, and regulates ... ...

Abstract	Peroxisome proliferator-activated receptor-α (PPARα), PPARδ and PPARγ are transcription factors that regulate gene expression following ligand activation. PPARα increases cellular fatty acid uptake, esterification and trafficking, and regulates lipoprotein metabolism genes. PPARδ stimulates lipid and glucose utilization by increasing mitochondrial function and fatty acid desaturation pathways. By contrast, PPARγ promotes fatty acid uptake, triglyceride formation and storage in lipid droplets, thereby increasing insulin sensitivity and glucose metabolism. PPARs also exert antiatherogenic and anti-inflammatory effects on the vascular wall and immune cells. Clinically, PPARγ activation by glitazones and PPARα activation by fibrates reduce insulin resistance and dyslipidaemia, respectively. PPARs are also physiological master switches in the heart, steering cardiac energy metabolism in cardiomyocytes, thereby affecting pathological heart failure and diabetic cardiomyopathy. Novel PPAR agonists in clinical development are providing new opportunities in the management of metabolic and cardiovascular diseases.
MeSH term(s)	Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/prevention & control ; Humans ; PPAR alpha/metabolism ; PPAR delta/metabolism ; PPAR gamma/metabolism
Chemical Substances	PPAR alpha ; PPAR delta ; PPAR gamma
Language	English
Publishing date	2021-06-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2490375-9
ISSN	1759-5010 ; 1759-5002
ISSN (online)	1759-5010
ISSN	1759-5002
DOI	10.1038/s41569-021-00569-6
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Zs.A 6019: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 98: Show issues

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Article: The Circadian Clock and Obesity.

Sebti, Yasmine / Hebras, Aurore / Pourcet, Benoit / Staels, Bart / Duez, Hélène

Handbook of experimental pharmacology

2022 Volume 274, Page(s) 29–56

Abstract: The modern way of life has dramatically affected our biological rhythms. Circadian rhythms, which are generated by an endogenous circadian clock, are observed in a large number of physiological functions including metabolism. Proper peripheral clock ... ...

Abstract	The modern way of life has dramatically affected our biological rhythms. Circadian rhythms, which are generated by an endogenous circadian clock, are observed in a large number of physiological functions including metabolism. Proper peripheral clock synchronization by different signals including appropriate feeding/fasting cycles is essential to coordinate and temporally gate metabolic processes. In this chapter, we emphasize the importance of nutrient sensing by peripheral clocks and highlight the major role of peripheral and central clock communication to locally regulate metabolic processes and ensure optimal energy storage and expenditure. As a consequence, changes in eating behavior and/or bedtime, as occurs upon shift work and jet lag, have direct consequences on metabolism and participate in the increasing prevalence of obesity and associated metabolic diseases such as type 2 diabetes and non-alcoholic fatty liver disease. In this setting, time-restricted feeding has been suggested as an efficient approach to ameliorate metabolic parameters and control body weight.
MeSH term(s)	Circadian Clocks/physiology ; Circadian Rhythm/physiology ; Diabetes Mellitus, Type 2 ; Feeding Behavior ; Humans ; Obesity
Language	English
Publishing date	2022-03-02
Publishing country	Germany
Document type	Journal Article
ISSN	0171-2004
ISSN	0171-2004
DOI	10.1007/164_2021_579
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Sign. bis Bd. 125 (1997): 1982 A 2146: Show issues
danach: Sign. bei den Einzelbänden: Show issues

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Article ; Online: Benzopyran hydrazones with dual PPARα/γ or PPARα/δ agonism and an anti-inflammatory effect on human THP-1 macrophages.

García, Ainhoa / Vila, Laura / Duplan, Isabelle / Schiel, María Ayelén / Enriz, Ricardo D / Hennuyer, Nathalie / Staels, Bart / Cabedo, Nuria / Cortes, Diego

European journal of medicinal chemistry

2024 Volume 265, Page(s) 116125

Abstract: Peroxisome proliferator-activated receptors (PPARs) play a major role in regulating inflammatory processes, and dual or pan-PPAR agonists with PPARγ partial activation have been recognised to be useful to manage both metabolic syndrome and metabolic ... ...

Abstract	Peroxisome proliferator-activated receptors (PPARs) play a major role in regulating inflammatory processes, and dual or pan-PPAR agonists with PPARγ partial activation have been recognised to be useful to manage both metabolic syndrome and metabolic dysfunction-associated fatty liver disease (MAFLD). Previous works have demonstrated the capacity of 2-prenylated benzopyrans as PPAR ligands. Herein, we have replaced the isoprenoid bond by hydrazone, a highly attractive functional group in medicinal chemistry. In an attempt to discover novel and safety PPAR activators, we efficiently prepared benzopyran hydrazone/hydrazine derivatives containing benzothiazole (series 1) or 5-chloro-3-(trifluoromethyl)-2-pyridine moiety (series 2) with a 3- or 7-carbon side chain at the 2-position of the benzopyran nucleus. Benzopyran hydrazones 4 and 5 showed dual hPPARα/γ agonism, while hydrazone 14 exerted dual hPPARα/δ agonism. These three hydrazones greatly attenuated inflammatory markers such as IL-6 and MCP-1 on the THP-1 macrophages via NF-κB activation. Therefore, we have discovered novel hits (4, 5 and 14), containing a hydrazone framework with dual PPARα/γ or PPARα/δ partial agonism, depending on the length of the side chain. Benzopyran hydrazones emerge as potential lead compounds which could be useful for treating metabolic diseases.
MeSH term(s)	Humans ; PPAR alpha/agonists ; Benzopyrans/chemistry ; Hydrazones/pharmacology ; Hypoglycemic Agents ; PPAR gamma/agonists ; Anti-Inflammatory Agents
Chemical Substances	PPAR alpha ; Benzopyrans ; Hydrazones ; Hypoglycemic Agents ; PPAR gamma ; Anti-Inflammatory Agents
Language	English
Publishing date	2024-01-04
Publishing country	France
Document type	Journal Article
ZDB-ID	188597-2
ISSN	1768-3254 ; 0009-4374 ; 0223-5234
ISSN (online)	1768-3254
ISSN	0009-4374 ; 0223-5234
DOI	10.1016/j.ejmech.2024.116125
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