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Vol. 96, Issue 24, 13656-13661, November 23, 1999 (sterol regulatory element binding proteins / fatty acid
metabolism / gene transcription)
Department of Molecular Genetics, University of Texas Southwestern
Medical Center, Dallas, TX 75235-9046
Contributed by Michael S. Brown, August 27, 1999
Sterol regulatory element binding proteins (SREBPs) enhance
transcription of genes encoding enzymes of cholesterol and fatty acid
biosynthesis and uptake. In the current experiments, we observed a
decline in the mRNA encoding one SREBP isoform, SREBP-1c, in the livers
of rats that were rendered diabetic by treatment with streptozotocin.
There was no change in the mRNA encoding SREBP-1a, which is derived
from the same gene as SREBP-1c but uses a different promoter. The ratio
of SREBP-1c:1a transcripts fell 25-fold from 5:1 in control rats to
0.2:1 in the diabetic animals. The SREBP-1c mRNA rose nearly to normal,
and the 1c:1a ratio increased 17-fold when the diabetic rats were
treated for 6 h with insulin. These treatments produced no change
in the mRNA for SREBP-2, which is encoded by a separate gene. The
SREBP-1c mRNA also fell selectively in freshly isolated rat hepatocytes
and rose when the cells were treated with insulin. Considered together
with recent data on hepatocytes [Foretz, M., Pacot, C., Dugal, I.,
et al. (1999) Mol. Cell. Biol. 19, 3760-3768], the current in vivo studies suggest that
insulin may stimulate lipid synthesis in the liver by selectively inducing transcription of the SREBP-1c gene.
Copyright © 1999 by The National Academy of Sciences 0027-8424/99/9613656-6$2.00/0
Biochemistry
Insulin selectively increases SREBP-1c mRNA in the livers of rats
with streptozotocin-induced diabetes
, and
*
The first two authors contributed equally to this research.
To whom reprint requests should be addressed. E-mail:
mbrow1{at}mednet.swmed.edu or jgolds{at}mednet.swmed.edu.
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