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Article ; Online: The identification of farnesoid X receptor modulators as treatment options for nonalcoholic fatty liver disease.

Fiorucci, Stefano / Biagioli, Michele / Baldoni, Monia / Ricci, Patrizia / Sepe, Valentina / Zampella, Angela / Distrutti, Eleonora

Expert opinion on drug discovery

2021 Volume 16, Issue 10, Page(s) 1193–1208

Abstract: Introduction: The farnesoid-x-receptor (FXR) is a ubiquitously expressed nuclear receptor selectively activated by primary bile acids.: Area covered: FXR is a validated pharmacological target. Herein, the authors review preclinical and clinical data ... ...

Abstract	Introduction: The farnesoid-x-receptor (FXR) is a ubiquitously expressed nuclear receptor selectively activated by primary bile acids. Area covered: FXR is a validated pharmacological target. Herein, the authors review preclinical and clinical data supporting the development of FXR agonists in the treatment of nonalcoholic fatty liver disease. Expert opinion: Development of systemic FXR agonists to treat the metabolic liver disease has been proven challenging because the side effects associated with these agents including increased levels of cholesterol and LDL-c and reduced HDL-c raising concerns over their long-term cardiovascular safety. Additionally, pruritus has emerged as a common, although poorly explained, dose-related side effect with all FXR ligands, but is especially common with OCA. FXR agonists that are currently undergoing phase 2/3 trials are cilofexor, tropifexor, nidufexor and MET409. Some of these agents are currently being developed as combination therapies with other agents including cenicriviroc, a CCR2/CCR5 inhibitor, or firsocostat an acetyl CoA carboxylase inhibitor. Additional investigations are needed to evaluate the beneficial effects of combination of these agents with statins. It is expected that in the coming years, FXR agonists will be developed as a combination therapy to minimize side effects and increase likelihood of success by targeting different metabolic pathways.
MeSH term(s)	Azetidines/therapeutic use ; Chenodeoxycholic Acid/pharmacology ; Chenodeoxycholic Acid/therapeutic use ; Humans ; Isonicotinic Acids/therapeutic use ; Liver/metabolism ; Non-alcoholic Fatty Liver Disease/drug therapy
Chemical Substances	Azetidines ; Isonicotinic Acids ; Chenodeoxycholic Acid (0GEI24LG0J) ; cilofexor (YUN2306954)
Language	English
Publishing date	2021-05-05
Publishing country	England
Document type	Journal Article
ZDB-ID	2259618-5
ISSN	1746-045X ; 1746-0441
ISSN (online)	1746-045X
ISSN	1746-0441
DOI	10.1080/17460441.2021.1916465
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Article ; Online: Bile acid-activated receptors and the regulation of macrophages function in metabolic disorders.

Fiorucci, Stefano / Baldoni, Monia / Ricci, Patrizia / Zampella, Angela / Distrutti, Eleonora / Biagioli, Michele

Current opinion in pharmacology

2020 Volume 53, Page(s) 45–54

Abstract: Bile acids are produced in the liver by the cholesterol breakdown and further metabolized by the intestinal microbiota to generate a group of chemically heterogeneous steroids that bind and activate a family of cells surface and nuclear receptors, ... ...

Abstract	Bile acids are produced in the liver by the cholesterol breakdown and further metabolized by the intestinal microbiota to generate a group of chemically heterogeneous steroids that bind and activate a family of cells surface and nuclear receptors, collectively known as the bile acid-activated receptors (BARs). The two best characterized members of this family are the farnesoid-x-receptor (FXR) and G protein Bile Acid Receptor (GPBAR1). Both receptors are expressed by cells of innate immunity including liver-resident and intestinal-resident macrophages and monocytes-derived macrophages. Because FXR and GPBAR1 knockout mice are biased toward a pro-inflammatory phenotype, it appears the both receptors might have a role in the development and maintenance of a tolerogenic phenotype. FXR and GPBAR1 ligands have been proven effective in the treatment in inflammatory and metabolic disorders and ligands for these receptors are currently under development for the treatment of non-alcoholic steato-hepatitis and diabetes.
MeSH term(s)	Animals ; Bile Acids and Salts/metabolism ; Gastrointestinal Microbiome ; Humans ; Macrophages/metabolism ; Metabolic Diseases/metabolism ; Receptors, Cytoplasmic and Nuclear/agonists ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, G-Protein-Coupled/agonists ; Receptors, G-Protein-Coupled/metabolism
Chemical Substances	Bile Acids and Salts ; GPBAR1 protein, human ; Receptors, Cytoplasmic and Nuclear ; Receptors, G-Protein-Coupled ; farnesoid X-activated receptor (0C5V0MRU6P)
Language	English
Publishing date	2020-05-29
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2020.04.008
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Article ; Online: Effectiveness of swapping to ustekinumab after vedolizumab failure in patients with multi-refractory Crohn's disease.

Melotti, Laura / Dussias, Nikolas Konstantine / Salice, Marco / Calabrese, Carlo / Baldoni, Monia / Scaioli, Eleonora / Belluzzi, Andrea / Mazzotta, Elena / Gionchetti, Paolo / Rizzello, Fernando

Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver

2022 Volume 55, Issue 2, Page(s) 230–234

Abstract: Background: Ustekinumab (UST) and vedolizumab (VDZ) are biologic therapies for moderate-to-severe Crohn's disease (CD) in patients who failed or had contraindication to anti-TNF treatment.: Aims: To evaluate ustekinumab efficacy as third-line ... ...

Abstract	Background: Ustekinumab (UST) and vedolizumab (VDZ) are biologic therapies for moderate-to-severe Crohn's disease (CD) in patients who failed or had contraindication to anti-TNF treatment. Aims: To evaluate ustekinumab efficacy as third-line treatment after swapping from VDZ for failure. Methods: We conducted a monocentric, retrospective, observational study where CD patients were followed for 12 months from the beginning of UST therapy. We assessed clinical activity (HBI) and laboratory markers (CRP) at the initiation of UST therapy (T0) and after 2(T2), 6(T6) and 12(T12) months. Endoscopic activity was recorded at T0 and T12. We registered data regarding their clinical history and previous biologic treatments. Steroid-free clinical remission was defined as HBI ≤ 4 without need for steroids. Clinical response was defined as HBI reduction of at least three points or the suspension of steroids. Results: 27 CD patients treated with UST after VDZ failure had a minimum follow up of 12 months and were included. All patients had previously been treated with anti-TNF agents. After 12 months, steroid-free clinical remission was evident in 15 (55.5%) patients, 5 (18.5%) had clinical response, while 7 (26%) had suspended for failure or persisted on treatment after optimization. Conclusions: Ustekinumab should be considered as third-line biologic treatment in multi-refractory CD patients.
MeSH term(s)	Humans ; Ustekinumab/adverse effects ; Crohn Disease/drug therapy ; Retrospective Studies ; Tumor Necrosis Factor Inhibitors/therapeutic use ; Biological Products/therapeutic use ; Treatment Outcome ; Remission Induction
Chemical Substances	Ustekinumab (FU77B4U5Z0) ; vedolizumab (9RV78Q2002) ; Tumor Necrosis Factor Inhibitors ; Biological Products
Language	English
Publishing date	2022-07-22
Publishing country	Netherlands
Document type	Observational Study ; Journal Article
ZDB-ID	1459373-7
ISSN	1878-3562 ; 1125-8055
ISSN (online)	1878-3562
ISSN	1125-8055
DOI	10.1016/j.dld.2022.06.029
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Article ; Online: Bile Acid Signaling in Inflammatory Bowel Diseases.

Fiorucci, Stefano / Carino, Adriana / Baldoni, Monia / Santucci, Luca / Costanzi, Emanuele / Graziosi, Luigina / Distrutti, Eleonora / Biagioli, Michele

Digestive diseases and sciences

2020 Volume 66, Issue 3, Page(s) 674–693

Abstract: Bile acids are a group of chemically different steroids generated at the host/microbial interface. Indeed, while primary bile acids are the end-product of cholesterol breakdown in the host liver, secondary bile acids are the products of microbial ... ...

Abstract	Bile acids are a group of chemically different steroids generated at the host/microbial interface. Indeed, while primary bile acids are the end-product of cholesterol breakdown in the host liver, secondary bile acids are the products of microbial metabolism. Primary and secondary bile acids along with their oxo derivatives have been identified as signaling molecules acting on a family of cell membrane and nuclear receptors collectively known as "bile acid-activated receptors." Members of this group of receptors are highly expressed throughout the gastrointestinal tract and mediate the bilateral communications of the intestinal microbiota with the host immune system. The expression and function of bile acid-activated receptors FXR, GPBAR1, PXR, VDR, and RORγt are highly dependent on the structure of the intestinal microbiota and negatively regulated by intestinal inflammation. Studies from gene ablated mice have demonstrated that FXR and GPBAR1 are essential to maintain a tolerogenic phenotype in the intestine, and their ablation promotes the polarization of intestinal T cells and macrophages toward a pro-inflammatory phenotype. RORγt inhibition by oxo-bile acids is essential to constrain Th17 polarization of intestinal lymphocytes. Gene-wide association studies and functional characterizations suggest a potential role for impaired bile acid signaling in development inflammatory bowel diseases (IBD). In this review, we will focus on how bile acids and their receptors mediate communications of intestinal microbiota with the intestinal immune system, describing dynamic changes of bile acid metabolism in IBD and the potential therapeutic application of targeting bile acid signaling in these disorders.
MeSH term(s)	Bile Acids and Salts/immunology ; Bile Acids and Salts/metabolism ; Gastrointestinal Microbiome/immunology ; Humans ; Immune System Phenomena/physiology ; Inflammatory Bowel Diseases/immunology ; Inflammatory Bowel Diseases/metabolism ; Intestinal Mucosa/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/immunology
Chemical Substances	Bile Acids and Salts ; Receptors, Cytoplasmic and Nuclear ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2020-12-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	304250-9
ISSN	1573-2568 ; 0163-2116
ISSN (online)	1573-2568
ISSN	0163-2116
DOI	10.1007/s10620-020-06715-3
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Article ; Online: The Bile Acid Receptor GPBAR1 Modulates CCL2/CCR2 Signaling at the Liver Sinusoidal/Macrophage Interface and Reverses Acetaminophen-Induced Liver Toxicity.

Biagioli, Michele / Carino, Adriana / Fiorucci, Chiara / Marchianò, Silvia / Di Giorgio, Cristina / Bordoni, Martina / Roselli, Rosalinda / Baldoni, Monia / Distrutti, Eleonora / Zampella, Angela / Fiorucci, Stefano

Journal of immunology (Baltimore, Md. : 1950)

2020 Volume 204, Issue 9, Page(s) 2535–2551

Abstract: Drug-induced liver injury caused by acetaminophen (acetyl-para-aminophenol [APAP]) is the main cause of acute liver failure and liver transplantation in several Western countries. Whereas direct toxicity exerted by APAP metabolites is a key determinant ... ...

Abstract	Drug-induced liver injury caused by acetaminophen (acetyl-para-aminophenol [APAP]) is the main cause of acute liver failure and liver transplantation in several Western countries. Whereas direct toxicity exerted by APAP metabolites is a key determinant for early hepatocytes injury, the recruitment of cells of innate immunity exerts a mechanistic role in disease progression, determining the clinical outcomes. GPBAR1 is a G protein-coupled receptor for secondary bile acids placed at the interface between liver sinusoidal cells and innate immunity. In this report, using genetic and pharmacological approaches, we demonstrate that whereas Gpbar1 gene deletion worsens the severity of liver injury, its pharmacological activation by 6β-ethyl-3a,7b-dihydroxy-5b-cholan-24-ol rescues mice from liver injury caused by APAP. This protective effect was supported by a robust attenuation of liver recruitment of monocyte-derived macrophages and their repolarization toward an anti-inflammatory phenotype. Macrophage depletion by gadolinium chloride pretreatment abrogated disease development, whereas their reconstitution by spleen-derived macrophage transplantation restored the sensitivity to APAP in a GPBAR1-dependent manner. RNA sequencing analyses demonstrated that GPBAR1 agonism modulated the expression of multiple pathways, including the chemokine CCL2 and its receptor, CCR2. Treating wild-type mice with an anti-CCL2 mAb attenuated the severity of liver injury. We demonstrated that negative regulation of CCL2 production by GPBAR1 agonism was promoter dependent and involved FOXO1. In conclusion, we have shown that GPBAR1 is an upstream modulator of CCL2/CCR2 axis at the sinusoidal cell/macrophage interface, providing a novel target in the treatment of liver damage caused by APAP.
MeSH term(s)	Acetaminophen/pharmacology ; Animals ; Bile Acids and Salts/metabolism ; Capillaries/metabolism ; Cell Line ; Cell Line, Tumor ; Chemical and Drug Induced Liver Injury/metabolism ; Chemokine CCL2/metabolism ; Forkhead Box Protein O1/metabolism ; Hep G2 Cells ; Humans ; Liver/drug effects ; Liver/metabolism ; Macrophages/metabolism ; Mice ; Promoter Regions, Genetic/physiology ; RAW 264.7 Cells ; Receptors, CCR2/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/physiology ; Spleen/drug effects ; Spleen/metabolism ; THP-1 Cells
Chemical Substances	Bile Acids and Salts ; Ccl2 protein, mouse ; Ccr2 protein, mouse ; Chemokine CCL2 ; Forkhead Box Protein O1 ; Gpbar1 protein, mouse ; Receptors, CCR2 ; Receptors, G-Protein-Coupled ; Acetaminophen (362O9ITL9D)
Language	English
Publishing date	2020-03-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1901427
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Article ; Online: Identification of cysteinyl-leukotriene-receptor 1 antagonists as ligands for the bile acid receptor GPBAR1.

Biagioli, Michele / Carino, Adriana / Marchianò, Silvia / Roselli, Rosalinda / Di Giorgio, Cristina / Bordoni, Martina / Fiorucci, Chiara / Sepe, Valentina / Conflitti, Paolo / Limongelli, Vittorio / Distrutti, Eleonora / Baldoni, Monia / Zampella, Angela / Fiorucci, Stefano

Biochemical pharmacology

2020 Volume 177, Page(s) 113987

Abstract: The cysteinyl leukotrienes (CysLTs), i.e. ... ...

Abstract	The cysteinyl leukotrienes (CysLTs), i.e. LTC
MeSH term(s)	Acetates/pharmacology ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Bile Acids and Salts/pharmacology ; Colitis/drug therapy ; Colitis/genetics ; Colitis/metabolism ; Colitis/pathology ; Disease Models, Animal ; Gene Expression ; Genes, Reporter ; HEK293 Cells ; Hep G2 Cells ; Humans ; Leukotriene Antagonists/pharmacology ; Leukotriene C4/metabolism ; Leukotriene D4/metabolism ; Leukotriene E4/metabolism ; Luciferases/genetics ; Luciferases/metabolism ; Mice ; Mice, Knockout ; Molecular Docking Simulation ; Quinolines/pharmacology ; RAW 264.7 Cells ; Receptors, G-Protein-Coupled/antagonists & inhibitors ; Receptors, G-Protein-Coupled/chemistry ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Leukotriene/chemistry ; Receptors, Leukotriene/genetics ; Receptors, Leukotriene/metabolism ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism
Chemical Substances	6-ethyl-24-norcholane-3,7,23-triol-23 sulfate ; Acetates ; Anti-Inflammatory Agents, Non-Steroidal ; Bile Acids and Salts ; GPBAR1 protein, human ; Leukotriene Antagonists ; Quinolines ; Receptors, G-Protein-Coupled ; Receptors, Leukotriene ; Recombinant Fusion Proteins ; alpha-pentyl-3-(2-quinolinylmethoxy)benzenemethanol (101910-24-1) ; Leukotriene C4 (2CU6TT9V48) ; Leukotriene D4 (73836-78-9) ; Leukotriene E4 (75715-89-8) ; Luciferases (EC 1.13.12.-) ; leukotriene D4 receptor (LRF7RW46ID) ; montelukast (MHM278SD3E)
Language	English
Publishing date	2020-04-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2020.113987
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Article ; Online: Duodenal submucosal tunnelization by fishbone.

Castellani, Danilo / Nardi, Elisabetta / Baldoni, Monia / Bassotti, Gabrio

Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver

2011 Volume 43, Issue 4, Page(s) e7

MeSH term(s)	Abdominal Pain/etiology ; Duodenoscopy ; Duodenum/injuries ; Foreign Bodies/complications ; Foreign Bodies/therapy ; Humans ; Intestinal Mucosa/injuries ; Male ; Middle Aged ; Weight Loss
Language	English
Publishing date	2011-04
Publishing country	Netherlands
Document type	Case Reports ; Journal Article
ZDB-ID	1459373-7
ISSN	1878-3562 ; 1125-8055
ISSN (online)	1878-3562
ISSN	1125-8055
DOI	10.1016/j.dld.2010.07.002
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Article ; Online: Opposite effects of the FXR agonist obeticholic acid on Mafg and Nrf2 mediate the development of acute liver injury in rodent models of cholestasis.

Carino, Adriana / Biagioli, Michele / Marchianò, Silvia / Fiorucci, Chiara / Bordoni, Martina / Roselli, Rosalinda / Di Giorgio, Cristina / Baldoni, Monia / Ricci, Patrizia / Monti, Maria Chiara / Morretta, Elva / Zampella, Angela / Distrutti, Eleonora / Fiorucci, Stefano

Biochimica et biophysica acta. Molecular and cell biology of lipids

2020 Volume 1865, Issue 9, Page(s) 158733

Abstract: The farnesoid-X-receptor (FXR) is validated target in the cholestatic disorders treatment. Obeticholic acid (OCA), the first in class of FXR agonist approved for clinical use, causes side effects including acute liver decompensation when administered to ... ...

Abstract	The farnesoid-X-receptor (FXR) is validated target in the cholestatic disorders treatment. Obeticholic acid (OCA), the first in class of FXR agonist approved for clinical use, causes side effects including acute liver decompensation when administered to cirrhotic patients with primary biliary cholangitis at higher than recommended doses. The V-Maf avian-musculoaponeurotic-fibrosarcoma-oncogene-homolog-G (Mafg) and nuclear factor-erythroid-2-related-factor-2 (Nrf2) mediates some of the downstream effects of FXR. In the present study we have investigated the role of FXR/MafG/NRF2 pathway in the development of liver toxicity caused by OCA in rodent models of cholestasis. Cholestasis was induced by bile duct ligation (BDL) or administration of α-naphtyl-isothiocyanate (ANIT) to male Wistar rats and FXR
MeSH term(s)	Animals ; Chenodeoxycholic Acid/analogs & derivatives ; Chenodeoxycholic Acid/pharmacology ; Cholestasis/complications ; Cholestasis/genetics ; Cholestasis/metabolism ; Hep G2 Cells ; Humans ; Liver/drug effects ; Liver/metabolism ; Liver Diseases/etiology ; Liver Diseases/genetics ; Liver Diseases/metabolism ; MafG Transcription Factor/antagonists & inhibitors ; MafG Transcription Factor/genetics ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; NF-E2-Related Factor 2/agonists ; NF-E2-Related Factor 2/genetics ; Rats, Wistar ; Receptors, Cytoplasmic and Nuclear/agonists ; Receptors, Cytoplasmic and Nuclear/antagonists & inhibitors ; Receptors, Cytoplasmic and Nuclear/genetics
Chemical Substances	MafG Transcription Factor ; NF-E2-Related Factor 2 ; Receptors, Cytoplasmic and Nuclear ; obeticholic acid (0462Z4S4OZ) ; farnesoid X-activated receptor (0C5V0MRU6P) ; Chenodeoxycholic Acid (0GEI24LG0J)
Language	English
Publishing date	2020-05-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbalip.2020.158733
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Article ; Online: Sonographic diagnosis of benign pneumoretroperitoneum following colonoscopy in Crohn's disease.

Giuliano, Vittorio / Malaspina, Corrado / Galuppo, Carla / Baldoni, Monia / Bassotti, Gabrio

Clinics and research in hepatology and gastroenterology

2013 Volume 37, Issue 1, Page(s) e1–2

MeSH term(s)	Adult ; Colonoscopy/adverse effects ; Crohn Disease/diagnosis ; Female ; Humans ; Male ; Retropneumoperitoneum/diagnostic imaging ; Retropneumoperitoneum/etiology ; Ultrasonography
Language	English
Publishing date	2013-02
Publishing country	France
Document type	Case Reports ; Journal Article
ZDB-ID	2594333-9
ISSN	2210-741X ; 2210-7401
ISSN (online)	2210-741X
ISSN	2210-7401
DOI	10.1016/j.clinre.2012.05.006
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Article: The Aryl Hydrocarbon Receptor (AhR) Mediates the Counter-Regulatory Effects of Pelargonidins in Models of Inflammation and Metabolic Dysfunctions

Biagioli, Michele / Carino, Adriana / Fiorucci, Chiara / Annunziato, Giannamaria / Marchianò, Silvia / Bordoni, Martina / Roselli, Rosalinda / Giorgio, Cristina Di / Castiglione, Federica / Ricci, Patrizia / Bruno, Agostino / Faccini, Andrea / Distrutti, Eleonora / Baldoni, Monia / Costantino, Gabriele / Fiorucci, Stefano

Nutrients. 2019 Aug. 07, v. 11, no. 8

2019

Abstract: Pelargonidins are anthocyanidins thought to be beneficial for the human health, although controversies exist over the doses needed and the unclear mechanism of action, along with poor systemic bioavailability. One putative target of pelargonidins is the ... ...

Abstract	Pelargonidins are anthocyanidins thought to be beneficial for the human health, although controversies exist over the doses needed and the unclear mechanism of action, along with poor systemic bioavailability. One putative target of pelargonidins is the aryl hydrocarbon receptor (AhR). A synthetic pelargonidin (Mt-P) was synthesized by the methylation of the pelargonidin (the natural compound indicated as P). Mt-P transactivated the AhR with an EC<inf>50</inf> of 1.97 μM and was ~2-fold more potent than the natural compound. In vitro Mt-P attenuated pro-inflammatory activities of Raw264.7 macrophage cells in an AhR-dependent manner. In vivo, administration of the Mt-P in Balb/c mice resulted in a dose-dependent attenuation of signs and symptoms of colitis induced by TNBS. A dose of 5 mg/kg Mt-P, but not the natural compound P, reversed intestinal inflammation and increased expression of Tnf-α, Ifn-ƴ, and Il-6, while promoted the expansion of regulatory T cells and M2 macrophages. In C57BL/6J mice fed a high fat diet (HFD), Mt-P attenuated body weight gain, intestinal and liver inflammation, and ameliorated insulin sensitivity, while worsened liver steatosis by up-regulating the liver expression of Cd36 and Apo100b. These effects were abrogated by AhR gene ablation. Mt-P is a synthetic pelargonidin endowed with robust AhR agonist activity that exerts beneficial effects in murine models of inflammation and metabolic dysfunction.
Keywords	T-lymphocytes ; agonists ; animal models ; bioavailability ; body weight changes ; colitis ; dose response ; fatty liver ; genes ; high fat diet ; human health ; inflammation ; insulin resistance ; interleukin-6 ; intestines ; liver ; macrophages ; mechanism of action ; methylation ; mice ; pelargonidin ; receptors ; tumor necrosis factor-alpha
Language	English
Dates of publication	2019-0807
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu11081820
Database	NAL-Catalogue (AGRICOLA)

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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