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Start Over Author "Nobili, Valerio" Publication Type Academic Journals
896 results on '"Nobili, Valerio"'

3. Comparison of the Phenotype and Approach to Pediatric vs Adult Patients With Nonalcoholic Fatty Liver Disease

Author

Nobili, Valerio, Alisi, Anna, Newton, Kimberly P, and Schwimmer, Jeffrey B

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Rare Diseases, Hepatitis, Chronic Liver Disease and Cirrhosis, Digestive Diseases, Pediatric Research Initiative, Liver Disease, Pediatric, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Adult, Cardiovascular Diseases, Child, Comorbidity, Disease Progression, Female, Humans, Liver, Male, Metabolic Syndrome, Non-alcoholic Fatty Liver Disease, Phenotype, Prevalence, Risk Factors, Nonalcoholic Fatty Liver Disease, Nonalcoholic Steatohepatitis, Children, Adults, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics
Abstract

Nonalcoholic fatty liver disease (NAFLD) is one of the main chronic noncommunicable diseases in Westernized societies; its worldwide prevalence has doubled during the last 20 years. NAFLD has serious health implications not only for adults, but also for children. However, pediatric NAFLD is not only an important global problem in itself, but it is likely to be associated with increases in comorbidities, such as metabolic syndrome and cardiovascular diseases. There are several differences between NAFLD in children and adults, and it is not clear whether the disease observed in children is the initial phase of a process that progresses with age. The increasing prevalence of pediatric NAFLD has serious implications for the future adult population requiring appropriate action. Studies of NAFLD progression, pathogenesis, and management should evaluate disease phenotypes in children and follow these over the patient's lifetime. We review the similarities and differences of NAFLD between children and adults.

Published
2016

4. Nonalcoholic fatty liver disease.

Author

Brunt, Elizabeth M, Wong, Vincent W-S, Nobili, Valerio, Day, Christopher P, Sookoian, Silvia, Maher, Jacquelyn J, Bugianesi, Elisabetta, Sirlin, Claude B, Neuschwander-Tetri, Brent A, and Rinella, Mary E

Subjects
Liver, Hepatocytes, Humans, Carcinoma, Hepatocellular, Liver Neoplasms, Liver Cirrhosis, Insulin Resistance, Disease Progression, Non-alcoholic Fatty Liver Disease, Carcinoma, Hepatocellular, Hepatitis, Clinical Research, Chronic Liver Disease and Cirrhosis, Rare Diseases, Nutrition, Obesity, Liver Disease, Prevention, Digestive Diseases, 2.1 Biological and endogenous factors, Metabolic and Endocrine, Oral and Gastrointestinal, Clinical Sciences
Abstract

Nonalcoholic fatty liver disease (NAFLD) is a disorder characterized by excess accumulation of fat in hepatocytes (nonalcoholic fatty liver (NAFL)); in up to 40% of individuals, there are additional findings of portal and lobular inflammation and hepatocyte injury (which characterize nonalcoholic steatohepatitis (NASH)). A subset of patients will develop progressive fibrosis, which can progress to cirrhosis. Hepatocellular carcinoma and cardiovascular complications are life-threatening co-morbidities of both NAFL and NASH. NAFLD is closely associated with insulin resistance; obesity and metabolic syndrome are common underlying factors. As a consequence, the prevalence of NAFLD is estimated to be 10-40% in adults worldwide, and it is the most common liver disease in children and adolescents in developed countries. Mechanistic insights into fat accumulation, subsequent hepatocyte injury, the role of the immune system and fibrosis as well as the role of the gut microbiota are unfolding. Furthermore, genetic and epigenetic factors might explain the considerable interindividual variation in disease phenotype, severity and progression. To date, no effective medical interventions exist that completely reverse the disease other than lifestyle changes, dietary alterations and, possibly, bariatric surgery. However, several strategies that target pathophysiological processes such as an oversupply of fatty acids to the liver, cell injury and inflammation are currently under investigation. Diagnosis of NAFLD can be established by imaging, but detection of the lesions of NASH still depend on the gold-standard but invasive liver biopsy. Several non-invasive strategies are being evaluated to replace or complement biopsies, especially for follow-up monitoring.

Published
2015

5. Lipid-Induced Hepatocyte-Derived Extracellular Vesicles Regulate Hepatic Stellate Cells via MicroRNA Targeting Peroxisome Proliferator-Activated Receptor-γ

Author

Povero, Davide, Panera, Nadia, Eguchi, Akiko, Johnson, Casey D, Papouchado, Bettina G, de Araujo Horcel, Lucas, Pinatel, Eva M, Alisi, Anna, Nobili, Valerio, and Feldstein, Ariel E

Subjects
Prevention, Digestive Diseases, Liver Disease, Genetics, Biotechnology, Chronic Liver Disease and Cirrhosis, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Extracellular Vesicles, Hepatic Stellate Cell, Lipotoxicity, Liver Fibrosis, miRNAs
Abstract

Background&aimsHepatic stellate cells (HSCs) play a key role in liver fibrosis in various chronic liver disorders including nonalcoholic fatty liver disease (NAFLD). The development of liver fibrosis requires a phenotypic switch from quiescent to activated HSCs. The triggers for HSCs activation in NAFLD remain poorly understood. We investigated the role and molecular mechanism of extracellular vesicles (EVs) released by hepatocytes during lipotoxicity in modulation of HSC phenotype.MethodsEVs were isolated from fat-laden hepatocytes by differential centrifugation and incubated with HSCs. EV internalization and HSCs activation, migration and proliferation were assessed. Loss- and gain-of-functions studies were performed to explore the potential role of PPAR-γ-targeting miRNAs carried by EVs into HSC.ResultsHepatocyte-derived EVs released during lipotoxicity are efficiently internalized by HSCs resulting in their activation, as shown by marked up-regulation of pro-fibrogenic genes (Collagen-I, α-SMA and TIMP-2), proliferation, chemotaxis and wound healing responses. These changes were associated with miRNAs shuttled by EVs and suppression of PPAR-γ expression in HSC. Hepatocyte-derived EVs miRNA content included various miRNAs that are known inhibitors of PPAR-γ expression with miR-128-3p being the most effectively transferred. Furthermore loss- and gain-of-function studies identified miR-128-3p as a central modulator of the effects of EVs on PPAR-γ inhibition and HSC activation.ConclusionOur findings demonstrate a link between fat-laden hepatocyte-derived EVs and liver fibrosis and have potential implications for the development of novel anti-fibrotic targets for NAFLD and other fibrotic diseases.

Published
2015

6. Lipid-induced hepatocyte-derived extracellular vesicles regulate hepatic stellate cell via microRNAs targeting PPAR-γ.

Author

Povero, Davide, Panera, Nadia, Eguchi, Akiko, Johnson, Casey D, Papouchado, Bettina G, de Araujo Horcel, Lucas, Pinatel, Eva M, Alisi, Anna, Nobili, Valerio, and Feldstein, Ariel E

Subjects
Extracellular Vesicles, Hepatic Stellate Cell, Lipotoxicity, Liver Fibrosis, miRNAs
Abstract

Background&aimsHepatic stellate cells (HSCs) play a key role in liver fibrosis in various chronic liver disorders including nonalcoholic fatty liver disease (NAFLD). The development of liver fibrosis requires a phenotypic switch from quiescent to activated HSCs. The triggers for HSCs activation in NAFLD remain poorly understood. We investigated the role and molecular mechanism of extracellular vesicles (EVs) released by hepatocytes during lipotoxicity in modulation of HSC phenotype.MethodsEVs were isolated from fat-laden hepatocytes by differential centrifugation and incubated with HSCs. EV internalization and HSCs activation, migration and proliferation were assessed. Loss- and gain-of-functions studies were performed to explore the potential role of PPAR-γ-targeting miRNAs carried by EVs into HSC.ResultsHepatocyte-derived EVs released during lipotoxicity are efficiently internalized by HSCs resulting in their activation, as shown by marked up-regulation of pro-fibrogenic genes (Collagen-I, α-SMA and TIMP-2), proliferation, chemotaxis and wound healing responses. These changes were associated with miRNAs shuttled by EVs and suppression of PPAR-γ expression in HSC. Hepatocyte-derived EVs miRNA content included various miRNAs that are known inhibitors of PPAR-γ expression with miR-128-3p being the most effectively transferred. Furthermore loss- and gain-of-function studies identified miR-128-3p as a central modulator of the effects of EVs on PPAR-γ inhibition and HSC activation.ConclusionOur findings demonstrate a link between fat-laden hepatocyte-derived EVs and liver fibrosis and have potential implications for the development of novel anti-fibrotic targets for NAFLD and other fibrotic diseases.

Published
2015

8. Prevalence and Risk Factors of Significant Fibrosis in Patients With Nonalcoholic Fatty Liver Without Steatohepatitis

Author

Pelusi, Serena, Cespiati, Annalisa, Rametta, Raffaela, Pennisi, Grazia, Mannisto, Ville, Rosso, Chiara, Baselli, Guido, Dongiovanni, Paola, Fracanzani, Anna Ludovica, Badiali, Sara, Maggioni, Marco, Craxi, Antonio, Fargion, Silvia, Prati, Daniele, Nobili, Valerio, Bugianesi, Elisabetta, Romeo, Stefano, Pihlajamaki, Jussi, Petta, Salvatore, and Valenti, Luca

Published
2019
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23. A “systems medicine” approach to the study of non-alcoholic fatty liver disease

Author

Ferrannini, Ele, Loguercio, Carmela, Lonardo, Amedeo, Marra, Fabio, Mancini, Marcello, Miele, Luca, Nobili, Valerio, Baroni, Gianluca Svegliati, Alessandro, Federico, Ballestri, Stefano, Rossana Brunetto, Maurizia, Coco, Barbara, Grieco, Antonio, Fargion, Silvia, Kondili, Loreta, Nascimbeni, Fabio, Prinster, Anna, Romagnoli, Dante, Taddei, Stefano, Vanni, Ester, Vella, Stefano, Petta, Salvatore, Valenti, Luca, Bugianesi, Elisabetta, Targher, Giovanni, Bellentani, Stefano, and Bonino, Ferruccio

Published
2016
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25. Statin use and non-alcoholic steatohepatitis in at risk individuals

Author

Dongiovanni, Paola, Petta, Salvatore, Mannisto, Ville, Mancina, Rosellina Margherita, Pipitone, Rosaria, Karja, Vesa, Maggioni, Marco, Kakela, Pirjo, Wiklund, Olov, Mozzi, Enrico, Grimaudo, Stefania, Kaminska, Dorota, Rametta, Raffaela, Craxi, Antonio, Fargion, Silvia, Nobili, Valerio, Romeo, Stefano, Pihlajamaki, Jussi, and Valenti, Luca

Published
2015
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27. Similarities and Differences in Allocation Policies for Pediatric Liver Transplantation Across the World

Author

Fischler, Björn, Baumann, Ulrich, D’Agostino, Daniel, D’Antiga, Lorenzo, Dezsofi, Antal, Debray, Dominique, Durmaz, Ozlem, Evans, Helen, Frauca, Esteban, Hadzic, Nedim, Jahnel, Jörg, Loveland, Jerome, McLin, Valérie, Ng, Vicky L., Nobili, Valerio, Pawłowska, Joanna, Sharif, Khalid, Smets, Francoise, Verkade, Henkjan J., Hsu, Evelyn, Horslen, Simon, and Bucuvalas, John

Published
2019
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32. Epidemiology and natural history of NAFLD

Author

Della Corte Claudia, Ferrari Federica, Villani Alberto, and Nobili Valerio

Subjects
nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, children, obesity, metabolic syndrome, Biochemistry, QD415-436
Abstract

Paralleling the growing prevalence of obesity and metabolic syndrome, nonalcoholic fatty liver disease (NAFLD) is emerging as the most frequent hepatopathy in adults and children. The true prevalence of pediatric NAFLD is still unknown, because of the heterogeneity of diagnostic methods used for diagnosis in the available studies and the different characteristics of the populations evaluated. Pediatric NAFLD is typically of primary origin and it is strongly associated with several features of the metabolic syndrome. Age, gender and race/ethnicity are significant determinants of risk, and sex hormones, insulin sensitivity and adipocytokines are implicated in the pathogenesis of pediatric NAFLD. The natural history of NAFLD in children is still poorly understood, because of its complex nature and the scarcity of prospective studies, especially in pediatric populations. Both genetic and environmental factors seem to be implicated in the development and progression of the disease via multiple mechanisms that involve liver crosstalk with other organs and tissues, especially gut and adipose tissue. To evaluate and effectively treat pediatric NAFLD, the pathophysiology and natural history of the disease should be clarified and noninvasive methods for screening, diagnosis, and longitudinal assessment developed.

Published
2015

35. Wilsonʼs Disease in Children: A Position Paper by the Hepatology Committee of the European Society for Paediatric Gastroenterology, Hepatology and Nutrition

Author

Socha, Piotr, Janczyk, Wojciech, Dhawan, Anil, Baumann, Ulrich, D’Antiga, Lorenzo, Tanner, Stuart, Iorio, Raffaele, Vajro, Pietro, Houwen, Roderick, Fischler, Björn, Dezsofi, Antal, Hadzic, Nedim, Hierro, Loreto, Jahnel, Jörg, McLin, Valérie, Nobili, Valerio, Smets, Francoise, Verkade, Henkjan J., and Debray, Dominique

Published
2018
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40. Early and Late Factors Impacting Patient and Graft Outcome in Pediatric Liver Transplantation: Summary of an ESPGHAN Monothematic Conference

Author

McLin, Valérie A., Allen, Upton, Boyer, Olivia, Bucuvalas, John, Colledan, Michele, Cuturi, Maria-Cristina, d’Antiga, Lorenzo, Debray, Dominique, Dezsofi, Antal, Goyet, Jean de Ville de, Dhawan, Anil, Durmaz, Ozlem, Falk, Christine, Feng, Sandy, Fischler, Björn, Franchi-Abella, Stéphanie, Frauca, Esteban, Ganschow, Rainer, Gottschalk, Stephen, Hadzic, Nedim, Hierro, Loreto, Horslen, Simon, Hubscher, Stefan, Karam, Vincent, Kelly, Deirdre, Maecker-Kolhoff, Britta, Mazariegos, George, McKiernan, Patrick, Melk, Anette, Nobili, Valerio, Ozgenç, Funda, Reding, Raymond, Sciveres, Marco, Sharif, Khalid, Socha, Piotr, Toso, Christian, Vajro, Pietro, Verma, Anita, Wildhaber, Barbara E., and Baumann, Ulrich

Published
2017
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41. Diagnosis, treatment and prevention of pediatric obesity: consensus position statement of the Italian Society for Pediatric Endocrinology and Diabetology and the Italian Society of Pediatrics

Author

Valerio, Giuliana, Maffeis, Claudio, Saggese, Giuseppe, Ambruzzi, Maria Amalia, Balsamo, Antonio, Bellone, Simonetta, Bergamini, Marcello, Bernasconi, Sergio, Bona, Gianni, Calcaterra, Valeria, Canali, Teresa, Caroli, Margherita, Chiarelli, Francesco, Corciulo, Nicola, Crinò, Antonino, Di Bonito, Procolo, Di Pietrantonio, Violetta, Di Pietro, Mario, Di Sessa, Anna, Diamanti, Antonella, Doria, Mattia, Fintini, Danilo, Franceschi, Roberto, Franzese, Adriana, Giussani, Marco, Grugni, Graziano, Iafusco, Dario, Iughetti, Lorenzo, Lamborghini, Adima, Licenziati, Maria Rosaria, Limauro, Raffaele, Maltoni, Giulio, Manco, Melania, Reggiani, Leonardo Marchesini, Marcovecchio, Loredana, Marsciani, Alberto, del Giudice, Emanuele Miraglia, Morandi, Anita, Morino, Giuseppe, Moro, Beatrice, Nobili, Valerio, Perrone, Laura, Picca, Marina, Pietrobelli, Angelo, Privitera, Francesco, Purromuto, Salvatore, Ragusa, Letizia, Ricotti, Roberta, Santamaria, Francesca, Sartori, Chiara, Stilli, Stefano, Street, Maria Elisabeth, Tanas, Rita, Trifiró, Giuliana, Umano, Giuseppina Rosaria, Vania, Andrea, Verduci, Elvira, and Zito, Eugenio

Published
2018
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