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(Received for publication, February 3, 1997, and in revised form, March 4, 1997)
From the Glucose-6-phosphatase (G6Pase) catalyzes the
final step in the gluconeogenic and glycogenolytic pathways. The
transcription of the gene encoding the catalytic subunit of G6Pase is
stimulated by glucocorticoids, whereas insulin strongly inhibits both
basal G6Pase gene transcription and the stimulatory effect of
glucocorticoids. To identify the insulin response sequence (IRS) in the
G6Pase promoter through which insulin mediates its action, we have
analyzed the effect of insulin on the basal expression of mouse
G6Pase-chloramphenicol acetyltransferase (CAT) fusion genes transiently
expressed in hepatoma cells. Deletion of the G6Pase promoter sequence
between
Volume 272, Number 18,
Issue of May 2, 1997
pp. 11698-11701
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
,
,
,
Department of Molecular Physiology and
Biophysics, Vanderbilt University Medical School, Nashville, Tennessee
37232 and the § Department of Genetics, University of
Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104
271 and 199 partially reduces the inhibitory effect of
insulin, whereas deletion of additional sequence between 198 and
159 completely abolishes the insulin response. The presence of this multicomponent IRS may explain why insulin potently inhibits basal G6Pase-CAT expression. The G6Pase promoter region between 198 and
159 contains an IRS, since it can confer an inhibitory effect of
insulin on the expression of a heterologous fusion gene. This region
contains three copies of the T(G/A)TTTTG sequence, which is the core
motif of the phosphoenolpyruvate carboxykinase (PEPCK) gene IRS. This
suggests that a coordinate increase in both G6Pase and PEPCK gene
transcription is likely to contribute to the increased hepatic glucose
production characteristic of patients with
non-insulin-dependent diabetes mellitus.
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R. S. Streeper, S. C. Chapman, J. E. Ayala, C. A. Svitek, J. K. Goldman, A. Cave, and R. M. O’Brien A Phorbol Ester-Insensitive AP-1 Motif Mediates the Stimulatory Effect of Insulin on Rat Malic Enzyme Gene Transcription Mol. Endocrinol., November 1, 1998; 12(11): 1778 - 1791. [Abstract] [Full Text]
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M. Dickens, C. A. Svitek, A. A. Culbert, R. M. O'Brien, and J. M. Tavare Central Role for Phosphatidylinositide 3-Kinase in the Repression of Glucose-6-phosphatase Gene Transcription by Insulin J. Biol. Chem., August 7, 1998; 273(32): 20144 - 20149. [Abstract] [Full Text] [PDF]
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