Non-alcoholic fatty liver disease (NAFLD) stands nowadays as a leading cause of progressive impairment of liver function. The role of bile acids in the modulation of hepatic lipid metabolism is interesting and controversial; previous evidence showed an inhibitory effect of bile acids on lipogenesis, which was attributed to the activation of the FXR-SHP axis and consequent depression of the LXRα-SREBP-1c lipogenic pathway. Evidence from our research group has shown that both exogenous administration of bile acids and endogenous exposure to bile acid overload (as in cholestasis) may reduce hepatic fat accumulation in rat models, although by different mechanisms. The findings in the paper by Nagahashi et al are quite surprising, showing the development of fatty liver disease in SphK2 -/- mice, in association with a decreased expression of SREBP1c and lipogenic enzymes like FAS. The metabolic effects of bile acids on hepatic lipid metabolism seem to be strictly dependent on the experimental model utilized to induce fat liver accumulation, as well as on the modality of bile acid exposure (exogenous vs endogenous) and the relative activation of the LXR/FXR pathways. Experimental evidence like that brought by Nagahashi et al1 may bring an enormous contribution in this field, in the perspective of novel pharmacological targets for the treatment of NAFLD.

Bile acids and nonalcoholic fatty liver disease: An intriguing relationship / Carulli, Lucia; Gabbi, Chiara; Bertolotti, Marco. - In: HEPATOLOGY. - ISSN 0270-9139. - ELETTRONICO. - 63:5(2016), pp. 1739-1740. [10.1002/hep.27963]

Bile acids and nonalcoholic fatty liver disease: An intriguing relationship

CARULLI, Lucia;GABBI, Chiara;BERTOLOTTI, Marco
2016

Abstract

Non-alcoholic fatty liver disease (NAFLD) stands nowadays as a leading cause of progressive impairment of liver function. The role of bile acids in the modulation of hepatic lipid metabolism is interesting and controversial; previous evidence showed an inhibitory effect of bile acids on lipogenesis, which was attributed to the activation of the FXR-SHP axis and consequent depression of the LXRα-SREBP-1c lipogenic pathway. Evidence from our research group has shown that both exogenous administration of bile acids and endogenous exposure to bile acid overload (as in cholestasis) may reduce hepatic fat accumulation in rat models, although by different mechanisms. The findings in the paper by Nagahashi et al are quite surprising, showing the development of fatty liver disease in SphK2 -/- mice, in association with a decreased expression of SREBP1c and lipogenic enzymes like FAS. The metabolic effects of bile acids on hepatic lipid metabolism seem to be strictly dependent on the experimental model utilized to induce fat liver accumulation, as well as on the modality of bile acid exposure (exogenous vs endogenous) and the relative activation of the LXR/FXR pathways. Experimental evidence like that brought by Nagahashi et al1 may bring an enormous contribution in this field, in the perspective of novel pharmacological targets for the treatment of NAFLD.
2016
31-lug-2015
63
5
1739
1740
Bile acids and nonalcoholic fatty liver disease: An intriguing relationship / Carulli, Lucia; Gabbi, Chiara; Bertolotti, Marco. - In: HEPATOLOGY. - ISSN 0270-9139. - ELETTRONICO. - 63:5(2016), pp. 1739-1740. [10.1002/hep.27963]
Carulli, Lucia; Gabbi, Chiara; Bertolotti, Marco
File in questo prodotto:
File Dimensione Formato  
heptolog carulli 2016.pdf

Accesso riservato

Tipologia: Versione pubblicata dall'editore
Dimensione 482.55 kB
Formato Adobe PDF
482.55 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
Hepato Letter 2015-final.pdf

Open access

Tipologia: Versione dell'autore revisionata e accettata per la pubblicazione
Dimensione 19.24 kB
Formato Adobe PDF
19.24 kB Adobe PDF Visualizza/Apri
Pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1082283
Citazioni
  • ???jsp.display-item.citation.pmc??? 1
  • Scopus 2
  • ???jsp.display-item.citation.isi??? 1
social impact