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Vol. 13, No. 4, pp. 495-504, February 15, 1999
affects glucose homeostasis and islet glucagon gene expression in vivo
1 Department of Genetics, University of Pennsylvania School
of Medicine, Philadelphia, Pennsylvania 19104-6145 USA;
2 Division of Gastroenterology, Department of Medicine,
University of Pennsylvania School of Medicine, Philadelphia,
Pennsylvania 19104-6144 USA; 3 Department of Medicine, Banting
and Best Diabetes Center, Toronto Hospital, University of Toronto,
Ontario M5G 2C4, Canada; 4 Division Molecular Biology of the
Cell I, German Cancer Research Center, D-69120 Heidelberg, Germany
Mice homozygous for a null mutation in the winged helix
transcription factor HNF3
showed severe
postnatal growth retardation followed by death between P2 and P12.
Homozygous mutant mice were hypoglycemic despite unchanged expression
of HNF3 target genes involved in hepatic gluconeogenesis. Whereas
insulin and corticosteroid levels were altered as expected, plasma
glucagon was reduced markedly in the mutant animals despite the
hypoglycemia that should be expected to increase glucagon levels. This
correlated with a 70% reduction in pancreatic proglucagon gene
expression. We also showed that HNF3 could bind to and transactivate
the proglucagon gene promoter. These observations invoke a central role
for HNF3 in the regulatory control of islet
genes essential for glucose homeostasis in vivo.
[Key Words: Hepatocyte nuclear factor; endoderm development; metabolic regulation]
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