Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The administration of glucagon, cAMP [adenosine 3',5'-(cyclic)-monophosphate], BcAMP [6-N-2'-O-dibutyryladenosine 3',5'-(cyclic)-monophosphate] or adrenaline to foetal rats during the last 2 days of gestation evoked the appearance of tyrosine aminotransferase and enhanced the accumulation of glucose 6-phosphatase in the liver. In foetuses 1-2 days younger only BcAMP was effective. After birth liver glucose 6-phosphatase no longer responds to glucagon or BcAMP. Tyrosine aminotransferase is still inducible by these agents in 2-day-old rats, but not in 50-day-old rats. After adrenalectomy of adults glucagon or BcAMP can enhance the induction of the enzyme by hydrocortisone. The results indicate that the ability to synthesize tyrosine aminotransferase and glucose 6-phosphatase when exposed to cAMP develops sooner than the ability to respond to glucagon with an increase in the concentration of cAMP; the responsiveness of enzymes to different hormones changes with age. A scheme illustrating the sequential development of competence in regulating the level of an enzyme is presented. 2. Actinomycin inhibited the effects of glucagon and BcAMP on liver tyrosine aminotransferase and glucose 6-phosphatase in foetal rats. Growth hormone, insulin and hydrocortisone did not enhance the formation of these enzymes. 3. The time-course of accumulation of glucose 6-phosphatase in the kidney is different from that in the liver. Hormones that increase the accumulation in foetal liver do not do so in the kidney of the same foetus or in the livers of postnatal rats.
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PMID:The hormonal regulation of enzymes in penatal and postnatal rat liver. Effects of adenosine 3',5'-(cyclic)-monophosphate. 418 80

The mechanism of triiodothyronine (T3) induction of a thyroid hormone responsive mRNA (mRNAS14) was studied in primary cultures of adult rat hepatocytes. T3 induced mRNAS14 in less than one hour after addition to the cultures. After 24 hours exposure to T3, the level of mRNAS14 was 2.5 to 6 times above the untreated controls. Addition of Actinomycin-D to both induced and control cultures led to similar mRNAS14 disappearance curves, implying that T3 augments the synthesis of mRNAS14 rather than stabilizing pre-formed mature mRNA. Glucagon inhibits the T3 induction of mRNAS14. When added to both induced and control cultures, glucagon leads to similar fractional decay curves for mRNAS14, confirming the Actinomycin-D studies. These findings demonstrate T3 induces mRNAS14 directly in the hepatocyte by increasing the synthesis of the mature mRNA.
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PMID:T3 stimulates the synthesis of a specific mRNA in primary hepatocyte culture. 654 79