Alcohol and lipid metabolism

Research output: Contribution to journalArticle

72 Citations (Scopus)

Abstract

Hepatic lipid metabolism is controlled by several master transcription factors, in particular peroxisome proliferator-activated receptor-α (PPAR-α) and sterol response element binding protein-1 (SREBP-1). Peroxisome proliferator-activated receptor-α is a receptor for free fatty acids (FFA), and can activate genes involved in transport, oxidation, and export of FFA. Sterol response element binding protein-1 is a sensor for the level of cholesterol in the liver, and is able to activate genes involved in synthesis of cholesterol and FFA. Chronic ethanol treatment of cells or animals inhibited PPAR-α function and activated SREBP. In addition, ethanol inhibited adenosine monophosphate-dependent protein kinase (AMPK). The AMPK controls fatty acid metabolism by inhibiting acetyl-coenzyme A carboxylase, reducing malonyl-coenzyme A, and thereby permitting fatty acid transport into and oxidation in the mitochondrion. Adenosine monophosphate-dependent protein kinase was inhibited in alcohol-treated animals and cells. The mechanisms by which ethanol affects AMPK and the transcription factors are as yet incompletely understood.

Original languageEnglish
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume21
Issue numberSUPPL. 3
DOIs
StatePublished - 2006

Fingerprint

Adenosine Monophosphate
Lipid Metabolism
Protein Kinases
Peroxisome Proliferator-Activated Receptors
Alcohols
Nonesterified Fatty Acids
Ethanol
Response Elements
Sterols
Carrier Proteins
Transcription Factors
Fatty Acids
Cholesterol
Malonyl Coenzyme A
Acetyl-CoA Carboxylase
Liver
Genes
Mitochondria

Keywords

  • Ethanol
  • Fatty liver
  • Kinase
  • Transcription factor

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

Alcohol and lipid metabolism. / Crabb, David; Liangpunsakul, Suthat.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 21, No. SUPPL. 3, 2006.

Research output: Contribution to journalArticle

@article{6076472cc9484e488048968fd9ed9cae,
title = "Alcohol and lipid metabolism",
abstract = "Hepatic lipid metabolism is controlled by several master transcription factors, in particular peroxisome proliferator-activated receptor-α (PPAR-α) and sterol response element binding protein-1 (SREBP-1). Peroxisome proliferator-activated receptor-α is a receptor for free fatty acids (FFA), and can activate genes involved in transport, oxidation, and export of FFA. Sterol response element binding protein-1 is a sensor for the level of cholesterol in the liver, and is able to activate genes involved in synthesis of cholesterol and FFA. Chronic ethanol treatment of cells or animals inhibited PPAR-α function and activated SREBP. In addition, ethanol inhibited adenosine monophosphate-dependent protein kinase (AMPK). The AMPK controls fatty acid metabolism by inhibiting acetyl-coenzyme A carboxylase, reducing malonyl-coenzyme A, and thereby permitting fatty acid transport into and oxidation in the mitochondrion. Adenosine monophosphate-dependent protein kinase was inhibited in alcohol-treated animals and cells. The mechanisms by which ethanol affects AMPK and the transcription factors are as yet incompletely understood.",
keywords = "Ethanol, Fatty liver, Kinase, Transcription factor",
author = "David Crabb and Suthat Liangpunsakul",
year = "2006",
doi = "10.1111/j.1440-1746.2006.04582.x",
language = "English",
volume = "21",
journal = "Journal of Gastroenterology and Hepatology (Australia)",
issn = "0815-9319",
publisher = "Wiley-Blackwell",
number = "SUPPL. 3",

}

TY - JOUR

T1 - Alcohol and lipid metabolism

AU - Crabb, David

AU - Liangpunsakul, Suthat

PY - 2006

Y1 - 2006

N2 - Hepatic lipid metabolism is controlled by several master transcription factors, in particular peroxisome proliferator-activated receptor-α (PPAR-α) and sterol response element binding protein-1 (SREBP-1). Peroxisome proliferator-activated receptor-α is a receptor for free fatty acids (FFA), and can activate genes involved in transport, oxidation, and export of FFA. Sterol response element binding protein-1 is a sensor for the level of cholesterol in the liver, and is able to activate genes involved in synthesis of cholesterol and FFA. Chronic ethanol treatment of cells or animals inhibited PPAR-α function and activated SREBP. In addition, ethanol inhibited adenosine monophosphate-dependent protein kinase (AMPK). The AMPK controls fatty acid metabolism by inhibiting acetyl-coenzyme A carboxylase, reducing malonyl-coenzyme A, and thereby permitting fatty acid transport into and oxidation in the mitochondrion. Adenosine monophosphate-dependent protein kinase was inhibited in alcohol-treated animals and cells. The mechanisms by which ethanol affects AMPK and the transcription factors are as yet incompletely understood.

AB - Hepatic lipid metabolism is controlled by several master transcription factors, in particular peroxisome proliferator-activated receptor-α (PPAR-α) and sterol response element binding protein-1 (SREBP-1). Peroxisome proliferator-activated receptor-α is a receptor for free fatty acids (FFA), and can activate genes involved in transport, oxidation, and export of FFA. Sterol response element binding protein-1 is a sensor for the level of cholesterol in the liver, and is able to activate genes involved in synthesis of cholesterol and FFA. Chronic ethanol treatment of cells or animals inhibited PPAR-α function and activated SREBP. In addition, ethanol inhibited adenosine monophosphate-dependent protein kinase (AMPK). The AMPK controls fatty acid metabolism by inhibiting acetyl-coenzyme A carboxylase, reducing malonyl-coenzyme A, and thereby permitting fatty acid transport into and oxidation in the mitochondrion. Adenosine monophosphate-dependent protein kinase was inhibited in alcohol-treated animals and cells. The mechanisms by which ethanol affects AMPK and the transcription factors are as yet incompletely understood.

KW - Ethanol

KW - Fatty liver

KW - Kinase

KW - Transcription factor

UR - http://www.scopus.com/inward/record.url?scp=33747626296&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33747626296&partnerID=8YFLogxK

U2 - 10.1111/j.1440-1746.2006.04582.x

DO - 10.1111/j.1440-1746.2006.04582.x

M3 - Article

VL - 21

JO - Journal of Gastroenterology and Hepatology (Australia)

JF - Journal of Gastroenterology and Hepatology (Australia)

SN - 0815-9319

IS - SUPPL. 3

ER -