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J. Biol. Chem., Vol. 276, Issue 13, 9800-9807, March 30, 2001
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From the The reduction in hepatic abundance of
sterol regulatory element binding protein-1
(SREBP-1) mRNA and protein associated with the
ingestion of polyunsaturated fatty acids (PUFA) appears to be largely
responsible for the PUFA-dependent inhibition of lipogenic gene transcription. Our initial studies indicated that the induction of
SREBP-1 expression by insulin and glucose was blocked by
PUFA. Nuclear run-on assays suggested PUFA reduced SREBP-1
mRNA by post-transcriptional mechanisms. In this report we
demonstrate that PUFA enhance the decay of both SREBP-1a
and -1c. When rat hepatocytes in monolayer culture were
treated with albumin-bound 20:4(n-6) or
20:5(n-3) the half-life of total SREBP-1
mRNA was reduced by 50%. Ribonuclease protection assays revealed
that the decay of SREBP-1c mRNA was more sensitive to
PUFA than was SREBP-1a, i.e. the half-life of SREBP-1c and -1a was reduced from 10.0 to
4.6 h and 11.6 to 7.6 h, respectively. Interestingly,
treating the hepatocytes with the translational inhibitor,
cycloheximide, prevented the PUFA-dependent decay of
SREBP-1. This suggests that SREBP-1 mRNA
may need to undergo translation to enter the decay process, or that the
decay process requires the synthesis of a rapidly turning over protein. Although the mechanism by which PUFA accelerate SREBP-1
mRNA decay remains to be determined, cloning and sequencing of the
3'-untranslated region for the rat SREBP-1 transcript
revealed the presence of an A-U-rich region that is characteristic of a
destablizing element.
Polyunsaturated Fatty Acids Suppress Hepatic Sterol
Regulatory Element-binding Protein-1 Expression by
Accelerating Transcript Decay*
,,, and¶
Division of Nutritional Sciences, and the
Institute for Cellular and Molecular Biology, The University of Texas
at Austin, Austin, Texas 78712 and the § Division of Life
Sciences, Hallym University, Chunchon, 200-702, Korea
*
This work was supported by National Institutes of Health
Grants DK 53872 (to S. D. C.) and DK 09723 (to M. T. N.), the Universidad Nacional Autonoma de Mexico (to M. T. G.), and by the sponsors of the M. M. Love Chair in
Nutritional, Cellular and Molecular Sciences at The University of Texas
at Austin (to S. D. C.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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