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 language | English |
|---|---|
| Pages (from-to) | 1352-1353 |
| Number of pages | 2 |
| Journal | British Journal of Pharmacology |
| Volume | 157 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - 1 Aug 2009 |
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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 journal › Article
TY - JOUR
T1 - Curcumin adds spice to the debate: lipid metabolism in liver disease
AU - Graham, Annette
N1 - Originally published in: British Journal of Pharmacology (2009), 157 (9), pp.1352-1353.
PY - 2009/8/1
Y1 - 2009/8/1
N2 - 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.
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
KW - liver disease
U2 - 10.1111/j.1476-5381.2009.00335.x
DO - 10.1111/j.1476-5381.2009.00335.x
M3 - Article
VL - 157
SP - 1352
EP - 1353
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
SN - 0007-1188
IS - 8
ER -