Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Query: EC:3.1.3.9 (
glucose-6-phosphatase
)
3,081
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Administration of L-thyroxine (T4) to thyroidectomized Calotes versicolor significantly increased the activity of
glucose-6-phosphatase
(
G-6-Pase
) (liver and kidney), the concentrations of blood glucose and total protein (liver and kidney), and decreased hepatic cholesterol when compared to thyroidectomized lizards.
Propranolol
injections in thyroidectomized lizards increased the cholesterol concentration and did not change the other parameters. The activity of
G-6-Pase
and blood glucose content was stimulated, whereas the total protein and cholesterol contents were decreased after alloxan treatment. Administration of T4 to thyroidectomized animals pretreated with propranolol or alloxan significantly elevated the activity of
G-6-Pase
, the concentrations of blood glucose, and total protein, and reduced hepatic cholesterol level when compared to drug-treated lizards. From the results, it is evident that thyroid hormone has an independent stimulatory influence on intermediary metabolism in C. versicolor irrespective of the involvement of adrenaline or insulin.
...
PMID:Role of thyroid hormone in intermediary metabolism of propranolol or alloxan-treated Calotes versicolor. 132 45
Glucagon increased the activities of alanine amino transferase (AAT), fructose-1:6-bisphosphatase (fru-P2ase) and
glucose-6-phosphatase
(
G-6-Pase
) in goat brain tissue by about 100%, 150% and 50% respectively. These increase in activities were reversed by beta-antagonists propranolol. Well known alpha-agonist and antagonist like phenylephrine and phenoxybenzamine also increased AAT and
G-6-Pase
activities and these increased activities were reversed by propranolol. Phenylephrine and phenoxybenzamine however did not increase brain Fru-P2ase activity. However the most interesting finding is that cerebral cortical slices could produce glucose from alanine and this glucose production was enhanced by glucagon, phenylephrine and phenoxybenzamine.
Propranolol
reversed the effects of these agonists and antagonist to a great extent. From all these experiments we suggest brain to be a gluconeogenic organ although much less efficient than liver.
...
PMID:Is brain a gluconeogenic organ? 826 72