Curcumin adds spice to the debate: lipid metabolism in liver disease

Research output: Contribution to journalArticle

Abstract

Activated hepatic stellate cells (HSCs), the major source of the collagens involved in fibrosis and non-alcoholic fatty liver disease (NAFLD), undergo a profound loss of lipid and vitamin A storage capacity, as a consequence of a decline in expression of ‘adipogenic’ transcription factors such as peroxisome proliferator-activated receptor-¿ (PPAR¿). By contrast, hepatocytes undergo a micro- and macro-vesicular steatosis, reflecting the accumulation of triacylglycerol, and associated with chronic inflammation and fibrosis. These paradoxical findings are extended in this issue: Kang and Chen demonstrate that while low-density lipoproteins (LDL) can activate HSCs, curcumin can inhibit this process by activation of PPAR¿, which not only represses gene expression of SREBP-2 and LDLR, but via induction of expression of SREBP-1c, restores the lipid storage capacity characteristic of quiescent HSCs, suggesting that curcumin may be of therapeutic usage in protecting against liver steatosis and fibrosis.

Original languageEnglish
Pages (from-to)1352-1353
Number of pages2
JournalBritish Journal of Pharmacology
Volume157
Issue number8
DOIs
Publication statusPublished - 1 Aug 2009

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Hepatic Stellate Cells
Spices
Curcumin
Lipid Metabolism
Liver Diseases
Peroxisome Proliferator-Activated Receptors
Fibrosis
Sterol Regulatory Element Binding Protein 1
Lipid A
Fatty Liver
Vitamin A
LDL Lipoproteins
Liver Cirrhosis
Hepatocytes
Triglycerides
Transcription Factors
Collagen
Inflammation
Lipids
Gene Expression

Keywords

  • adipogenesis
  • lipid metabolism
  • liver disease

Cite this

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title = "Curcumin adds spice to the debate: lipid metabolism in liver disease",
abstract = "Activated hepatic stellate cells (HSCs), the major source of the collagens involved in fibrosis and non-alcoholic fatty liver disease (NAFLD), undergo a profound loss of lipid and vitamin A storage capacity, as a consequence of a decline in expression of ‘adipogenic’ transcription factors such as peroxisome proliferator-activated receptor-¿ (PPAR¿). By contrast, hepatocytes undergo a micro- and macro-vesicular steatosis, reflecting the accumulation of triacylglycerol, and associated with chronic inflammation and fibrosis. These paradoxical findings are extended in this issue: Kang and Chen demonstrate that while low-density lipoproteins (LDL) can activate HSCs, curcumin can inhibit this process by activation of PPAR¿, which not only represses gene expression of SREBP-2 and LDLR, but via induction of expression of SREBP-1c, restores the lipid storage capacity characteristic of quiescent HSCs, suggesting that curcumin may be of therapeutic usage in protecting against liver steatosis and fibrosis.",
keywords = "adipogenesis, lipid metabolism, liver disease",
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Curcumin adds spice to the debate: lipid metabolism in liver disease. / Graham, Annette.

In: British Journal of Pharmacology, Vol. 157, No. 8, 01.08.2009, p. 1352-1353.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Curcumin adds spice to the debate: lipid metabolism in liver disease

AU - Graham, Annette

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AB - Activated hepatic stellate cells (HSCs), the major source of the collagens involved in fibrosis and non-alcoholic fatty liver disease (NAFLD), undergo a profound loss of lipid and vitamin A storage capacity, as a consequence of a decline in expression of ‘adipogenic’ transcription factors such as peroxisome proliferator-activated receptor-¿ (PPAR¿). By contrast, hepatocytes undergo a micro- and macro-vesicular steatosis, reflecting the accumulation of triacylglycerol, and associated with chronic inflammation and fibrosis. These paradoxical findings are extended in this issue: Kang and Chen demonstrate that while low-density lipoproteins (LDL) can activate HSCs, curcumin can inhibit this process by activation of PPAR¿, which not only represses gene expression of SREBP-2 and LDLR, but via induction of expression of SREBP-1c, restores the lipid storage capacity characteristic of quiescent HSCs, suggesting that curcumin may be of therapeutic usage in protecting against liver steatosis and fibrosis.

KW - adipogenesis

KW - lipid metabolism

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