PMID- 26005675
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150525
LR  - 20220311
IS  - 2304-3881 (Print)
IS  - 2304-389X (Electronic)
IS  - 2304-3881 (Linking)
VI  - 4
IP  - 2
DP  - 2015 Apr
TI  - Sirtuin 1 signaling and alcoholic fatty liver disease.
PG  - 88-100
LID - 10.3978/j.issn.2304-3881.2014.12.06 [doi]
AB  - Alcoholic fatty liver disease (AFLD) is one of the most prevalent forms of liver 
      disease worldwide and can progress to inflammation (hepatitis), 
      fibrosis/cirrhosis, and ultimately lead to end stage liver injury. The 
      mechanisms, by which ethanol consumption leads to AFLD, are complicated and 
      multiple, and remain incompletely understood. Nevertheless, understanding its 
      pathogenesis will facilitate the development of effective pharmacological or 
      nutritional therapies for treating human AFLD. Chronic ethanol consumption causes 
      steatosis and inflammation in rodents or humans by disturbing several important 
      hepatic transcriptional regulators, including AMP-activated kinase (AMPK), 
      lipin-1, sterol regulatory element binding protein 1 (SREBP-1), PPARgamma 
      co-activator-1alpha (PGC-1alpha), and nuclear transcription factor-kappaB (NF-kappaB). 
      Remarkably, the effects of ethanol on these regulators are mediated in whole or 
      in part by inhibition of a central signaling molecule, sirtuin 1 (SIRT1), which 
      is a nicotinamide adenine dinucleotide (NAD(+), NADH)-dependent class III protein 
      deacetylase. In recent years, SIRT1 has emerged as a pivotal molecule controlling 
      the pathways of hepatic lipid metabolism, inflammatory responses and in the 
      development of AFLD in rodents and in humans. Ethanol-mediated SIRT1 inhibition 
      suppresses or stimulates the activities of above described transcriptional 
      regulators and co-regulators, thereby deregulating diverse lipid metabolism and 
      inflammatory response pathways including lipogenesis, fatty acid beta-oxidation, 
      lipoprotein uptake and secretion and expression of pro-inflammatory cytokines in 
      the liver. This review aims to highlight our current understanding of SIRT1 
      regulatory mechanisms and its response to ethanol-induced toxicity, thus, 
      affirming significant role of SIRT1 signaling in the development of AFLD.
FAU - You, Min
AU  - You M
AD  - Department of Pharmaceutical Sciences, College of Pharmacy, Northeast Ohio 
      Medical University, Rootstown, OH 44272, USA.
FAU - Jogasuria, Alvin
AU  - Jogasuria A
AD  - Department of Pharmaceutical Sciences, College of Pharmacy, Northeast Ohio 
      Medical University, Rootstown, OH 44272, USA.
FAU - Taylor, Charles
AU  - Taylor C
AD  - Department of Pharmaceutical Sciences, College of Pharmacy, Northeast Ohio 
      Medical University, Rootstown, OH 44272, USA.
FAU - Wu, Jiashin
AU  - Wu J
AD  - Department of Pharmaceutical Sciences, College of Pharmacy, Northeast Ohio 
      Medical University, Rootstown, OH 44272, USA.
LA  - eng
GR  - R01 AA013623/AA/NIAAA NIH HHS/United States
GR  - R01 AA015951/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - China (Republic : 1949- )
TA  - Hepatobiliary Surg Nutr
JT  - Hepatobiliary surgery and nutrition
JID - 101600750
PMC - PMC4405418
OTO - NOTNLM
OT  - Sirtuin 1 (SIRT1)
OT  - alcoholic fatty liver
OT  - inflammation
OT  - lipid metabolism
OT  - signal transduction
OT  - transcriptional regulators
EDAT- 2015/05/26 06:00
MHDA- 2015/05/26 06:01
PMCR- 2015/04/01
CRDT- 2015/05/26 06:00
PHST- 2014/09/06 00:00 [received]
PHST- 2014/10/29 00:00 [accepted]
PHST- 2015/05/26 06:00 [entrez]
PHST- 2015/05/26 06:00 [pubmed]
PHST- 2015/05/26 06:01 [medline]
PHST- 2015/04/01 00:00 [pmc-release]
AID - hbsn-04-02-088 [pii]
AID - 10.3978/j.issn.2304-3881.2014.12.06 [doi]
PST - ppublish
SO  - Hepatobiliary Surg Nutr. 2015 Apr;4(2):88-100. doi: 
      10.3978/j.issn.2304-3881.2014.12.06.