Abstract
Phosphoglucomutase catalyses the reversible conversion of glucose-6-P and glucose-1-P. Lithium is a potent inhibitor of phosphoglucomutase in vitro, however, it is not known if phosphoglucomutase was significantly inhibited by Li+ in Li+-treated bipolar patients. Here, we demonstrate that phosphoglucomutase inhibition by chronic Li+ treatment causes alterations of glucose-phosphate levels in various tissues of rats. Also, phosphoglucomutase inhibition results in compensatory elevation of phosphoglucomutase activity in rat tissues and in leukocytes isolated from Li+-treated bipolar patients. The increase of uninhibited phosphoglucomutase activity in leukocytes of Li+-treated bipolar patients is due to the increased expression of the PGM1 gene.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antimanic Agents / pharmacology*
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Bipolar Disorder / pathology*
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Brain / drug effects
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Brain / enzymology
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Calcium / metabolism
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Glucose-6-Phosphate / metabolism
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Glucosephosphates / metabolism
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Humans
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Leukocytes / drug effects*
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Lithium Chloride / metabolism
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Lithium Chloride / pharmacology*
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Liver / drug effects
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Liver / enzymology
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Magnesium / metabolism
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Male
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Muscle, Skeletal / drug effects
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Muscle, Skeletal / enzymology
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Myocardium / enzymology
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Phosphoglucomutase / genetics
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Phosphoglucomutase / metabolism*
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RNA, Messenger / metabolism
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Rats
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Rats, Wistar
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Reverse Transcriptase Polymerase Chain Reaction / methods
Substances
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Antimanic Agents
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Glucosephosphates
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RNA, Messenger
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Glucose-6-Phosphate
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glucose-1-phosphate
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Phosphoglucomutase
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Lithium Chloride
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Magnesium
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Calcium