| Autor: |
Arciprete, Francesca, Carotti, Simone, Zingariello, Maria, Zalfa, Francesca, Lettieri-Barbato, Daniele, Piemonte, Fiorella, Francesconi, Maria, Perrone, Giuseppe, Aquilano, Katia, Vespasiani-Gentilucci, Umberto, Morini, Sergio |
| Předmět: |
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| Zdroj: |
Italian Journal of Anatomy & Embryology / Archivio Italiano di Anatomia Ed Embriologia; 2021 Supplement, Vol. 125, p55-55, 1p |
| Abstrakt: |
Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in Western countries and is correlated with altered lipid metabolism and impaired lipophagy [1]. LAL is a lysosomal enzyme that hydrolyzes cholesterol esters and triglycerides and in general plays an important role in lipid disposal. The impairment of LAL activity was proposed as an underlying mechanism in the pathogenesis of NAFLD [2]. In order to find a correlation between LAL alteration and NAFLD, we examined LAL expression and localization in pre-clinical cellular and animal models of NAFLD and in NAFLD patients. In Huh7 cells exposed to high-glucose/high-lipid (HGHL) medium and in the liver of C57BL/6 mice fed with high-fat-diet (HFD), a reduced LAL activity together with decreased functional/notubiquitinated LAL protein levels was evidenced. Moreover, the accumulation of dysfunctional/ubiquitinated LAL, the high rate of ubiquitination and extra-lysosomal localization was demonstrated. Lastly, a lower level of functional/not-ubiquitinated LAL protein correlating with disease progression was detected in NAFLD patients. All these findings strongly suggest that the reduced hepatic fat disposal and NAFLD progression are promoted by impaired LAL function. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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