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| 1 | Relationship between adipose tissue dysfunction, vitamin D deficiency and the pathogenesis of non-alcoholic fatty liver disease显示文摘Non-alcoholic fatty liver disease(NAFLD)is the most common chronic liver disease worldwide.Its pathogenesis is complex and not yet fully understood.Over the years many studies have proposed various pathophysiological hypotheses,among which the currently most widely accepted is the'multiple parallel hits'theory.According to this model,lipid accumulation in the hepatocytes and insulin resistance increase the vulnerability of the liver to many factors that act in a coordinated and cooperative manner to promote hepatic injury,inflammation and fibrosis.Among these factors,adipose tissue dysfunction and subsequent chronic low grade inflammation play a crucial role.Recent studies have shown that vitamin D exerts an immune-regulating action on adipose tissue,and the growing wealth of epidemiological data is demonstrating that hypovitaminosis D is associated with both obesity and NAFLD.Furthermore,given the strong association between these conditions,current findings suggest that vitamin D may be involved in the relationship between adipose tissue dysfunction and NAFLD.The purpose of this review is to provide an overview of recent advances in the pathogenesis of NAFLD in relation to adipose tissue dysfunction,and in the pathophysiology linking vitamin D deficiency with NAFLD and adiposity,together with an overview of the evidence available on the clinical utility of vitamin D supplementation in cases of NAFLD. | Flavia A Cimini Ilaria Barchetta Simone Carotti Laura Bertoccini Marco G Baroni Umberto Vespasiani-Gentilucci Maria-Gisella Cavallo Sergio Morini | 2017 | World Journal of Gastroenterology2017，23，19： | 9 |
| 2 | Starring role of toll-like receptor-4 activation in the gutliver axis显示文摘Since the introduction of the term 'gut-liver axis', many studies have focused on the functional links of intestinal microbiota, barrier function and immune responses to liver physiology. Intestinal and extra-intestinal diseases alter microbiota composition and lead to dysbiosis, which aggravates impaired intestinal barrier function via increased lipopolysaccharide translocation. The subsequent increased passage of gut-derived product from the intestinal lumen to the organ wall and bloodstream affects gut motility and liver biology. The activation of the toll-like receptor 4(TLR-4) likely plays a key role in both cases. This review analyzed the most recent literature on the gut-liver axis, with a particular focus on the role of TLR-4 activation. Findings that linked liver disease with dysbiosis are evaluated, and links between dysbiosis and alterations of intestinal permeability and motility are discussed. We also examine the mechanisms of translocated gut bacteria and/or the bacterial product activation of liver inflammation and fibrogenesis via activity on different hepatic cell types. | Simone Carotti Michele Pier Luca Guarino Umberto Vespasiani-Gentilucci Sergio Morini | 2015 | World Journal of Gastrointestinal Pathophysiology2015，6，4： | 8 |
| 3 | Overview of studies of the vitamin D/vitamin D receptor system in the development of non-alcoholic fatty liver disease显示文摘Non-alcoholic fatty liver disease(NAFLD)is the most common chronic liver disease in the world.NAFLD is known to be associated with obesity,type 2 diabetes,metabolic syndrome and increased cardiovascular events:for these reasons,it is becoming a global public health problem and represents an important challenge in terms of prevention and treatment.The mechanisms behind the pathogenesis of NAFLD are multiple and have not yet been completely unraveled;consequently,at moment there are not effective treatments.In the past few years a large body of evidence has been assembled that attributes an important role in hepatic aberrant fat accumulation,inflammation and fibrosis,to the vitamin D/vitamin D receptor(VD/VDR)axis,showing a strong association between hypovitaminosis D and the diagnosis of NAFLD.However,the data currently available,including clinical trials with VD supplementation,still provides a contrasting picture.The purpose of this editorial is to provide an overview of recent advances in the pathogenesis of NAFLD in relation to VD/VDR.Based on recent data from literature,we focused in particular on the hypothesis that VDR itself,independently from its traditional ligand VD,may have a crucial function in promoting hepatic fat accumulation.This might also offer new possibilities for future innovative therapeutic approaches in the management of NAFLD. | Flavia Agata Cimini Ilaria Barchetta Simone Carotti Sergio Morini Maria Gisella Cavallo | 2019 | World Journal of Gastrointestinal Pathophysiology2019，10，2： | 4 |
| 4 | Portal inflammation during NAFLD is frequent and associated with the early phases of putative hepatic progenitor cell activation显示文摘 | Carotti Simone Vespasiani-Gentilucci Umberto Perrone Giuseppe Picardi Antonio Morini Sergio | 2015 | Journal of Clinical Pathology2015，，11： | 1 |
| 5 | Hepatic toll‐like receptor 4 expression is associated with portal inflammation and fibrosis in patients with NAFLD显示文摘 | Umberto Vespasiani‐Gentilucci Simone Carotti Giuseppe Perrone Chiara Mazzarelli Giovanni Galati Andrea Onetti‐Muda Antonio Picardi Sergio Morini | 2015 | Liver Int2015，，2： | 1 |
| 6 | Matrix metalloproteinase‐10 expression is induced during hepatic injury and plays a fundamental role in liver tissue repair显示文摘 | Oihane Garcia‐Irigoyen Simone Carotti Maria U. Latasa Iker Uriarte Maite G. Fernández‐Barrena Maria Elizalde Raquel Urtasun Umberto Vespasiani‐Gentilucci Sergio Morini Jesús M. Banales William C. Parks Jose A. Rodriguez Josune Orbe Jesús Prieto Jose A. Pá | 2014 | Liver Int2014，，7： | 1 |
| 7 | Human colonic myogenic dysfunction induced by mucosal lipopolysaccharide translocation and oxidative stress显示文摘 | Michele Pier Luca Guarino Rosa Sessa Annamaria Altomare Silvia Cocca Marisa Di Pietro Simone Carotti Giovanni Schiavoni Rossana Alloni Sara Emerenzian Sergio Morini Carola Severi Michele Cicala | 2013 | Digestive and Liver Disease2013，，： | 1 |
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