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(Received for publication, March 27, 1997, and in revised form, August 6, 1997)
,
,
,
and
From the The gene for phosphoenolpyruvate carboxykinase
(PEPCK), a target of CCAAT/enhancer-binding protein-
Department of Biochemistry, Case Western
Reserve University School of Medicine, Cleveland, Ohio 44106-4935, the
¶ Department of Developmental Biochemistry, Hebrew
University-Hadassah Medical School, Jerusalem 991120, Israel, the
Department of Pathology and Human Genetics, Baylor Medical
College, Houston, Texas 77030, and the ** Istituto di Ricerche di
Biologia Molecolare, P. Angeletti, Pomezia, Italy
(C/EBP) and
-
(C/EBP), begins to be expressed in the liver at birth. Mice
homozygous for a deletion in the gene for CEBP
(C/EBP
/ mice) die shortly after
birth of hypoglycemia, with no detectable hepatic PEPCK mRNA and
negligible hepatic glycogen stores. Half of the mice homozygous for a
deletion in the gene for CEBP (C/EBP/
mice) have normal glucose homeostasis (phenotype A), and the other half
die at birth of hypoglycemia due to a failure to express the gene for
PEPCK and to mobilize hepatic glycogen (phenotype B). Insulin
deficiency induces C/EBP and PEPCK gene transcription in the livers
of 19-day fetal rats, whereas dibutyryl cyclic AMP
(Bt2cAMP) increases the expression of the gene for C/EBP
and causes a transient burst of PEPCK mRNA. Bt2cAMP
induces PEPCK mRNA in the livers of fetal
C/EBP/ mice, but at only 20% of the
level of control animals; however, there is no induction of PEPCK
mRNA if the cyclic nucleotide is injected into
C/EBP/ mice immediately after delivery.
The expression of the gene for C/EBP is markedly induced in the
livers of C/EBP/ mice within 2 h
after the administration of Bt2cAMP. C/EBP/ mice injected at 20 days of fetal
life with Bt2cAMP have a normal pattern of induction of
hepatic PEPCK mRNA. In C/EBP/ mice
with phenotype B, the administration of Bt2cAMP immediately
after delivery induces PEPCK mRNA, causes the mobilization of
hepatic glycogen, and maintains normal glucose homeostasis for up to
4 h (duration of the experiment). We conclude that C/EBP is
required for the cAMP induction of PEPCK gene expression in the liver
and that C/EBP can compensate for the loss of C/EBP if its
concentration is induced to appropriate levels.
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