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The diagnosis of some cases of neonatal jaundice is complicated because of inability to identify the gallbladder, which makes it very difficult to differentiate biliary atresia from neonatal hepatitis even by serial ultrasonic (US) examination. Serial (US) examination after the administration of phenobarbital as a cholagogue at a dosage of 5 mg/kg/day for 5 days was performed to evaluate nine patients with neonatal jaundice. In five of the nine patients, the gallbladder was identified by a change in size following oral feeding. These patients were diagnosed as having neonatal hepatitis. The gallbladders of the other four patients were not identified before, during, or after feeding. They were diagnosed as having biliary atresia and the diagnoses were confirmed by surgery. Administration of phenobarbital for 5 days before serial US examination is very useful in the diagnosis of neonatal hepatitis when differentiation between neonatal hepatitis and biliary atresia is impossible because of inability to identify the gallbladder by US alone.
To investigate the regulational interaction of hepatocyte nuclear factor-1alpha (HNF-1alpha) and insulin promoter factor 1 (IPF1) on insulin gene expression, either or both of the expression vectors carrying each transcription factor were transiently transfected into HeLa cells, RINm5F cells and MIN6 cells together with the luciferase reporter construct driven by a human preproinsulin gene promoter (-1998 to +237) designated as, pINS-1998/luc. IPF1-transfection into HeLa cells strongly stimulated the luciferase activity to 725 fold that of the basal level. In contrast, HNF-1alpha-transfection resulted in only a 6.7 fold increase. In co-transfection experiments, increasing the amount of HNF-1alpha resulted in an 84.5% and 74.4% decrease in IPF1-stimulated luciferase activity in HeLa and RINm5F cells, respectively. Deletion constructs designated as pINS-248/luc, pINS-213/luc and pINS-185/luc were transfected into RINm5F cells to determine the role of the A3 element and its 5' flanking sequence in the inhibitory effect of HNF-1alpha. The results showed that the inhibiting effects of HNF-1alpha with pINS-213/luc and pINS-185/luc were significantly smaller than those with both pINS-1998/luc and pINS-248/luc. Transfection into MN6 cells with pINS-1998/luc in the absence of IPF1 resulted in constitutional transactivation of the insulin gene, and this transactivation was abolished by the co-transfection with HNF-1alpha. The present data indicate that IPF1 rather than HNF-1alpha predominantly transactivates the insulin gene, and that HNF-1alpha inhibits IPF1-dependent insulin gene transactivation mediated through the 5' flanking sequence of the A3 element. It is suggested that HNF-1alpha may be involved in insulin gene expression as a negative regulator.