Gene/Protein Disease Symptom Drug Enzyme Compound
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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)

The effect of regucalcin, a calcium-binding protein isolated from rat liver cytosol, on glucose-6-phosphatase in the microsomes of rat liver was investigated. Addition of Ca2+ up to 2.5 microM to the enzyme reaction mixture caused a significant increase of glucose-6-phosphatase activity in hepatic microsomes, while Ni2+, Zn2+, Cd2+, Cu2+, Mn2+ and Co2+ (20 microM) did not have an appreciable effect. Vanadate (V5+) markedly inhibited the enzyme activity; a significant inhibitory effect was seen at 10 microM V5+. The Ca2+-induced increase of glucose-6-phosphatase activity was reversed by the presence of regucalcin; the effect was complete at 1.0 microM of the protein. Regucalcium had no effect on the basal activity of the enzyme. Meanwhile, the inhibitory effect of V5+ (10-100 microM) on glucose-6-phosphatase was not appreciably blocked by the presence of regucalcin (up to 2.0 microM). The present data suggest that hepatic microsomal glucose-6-phosphatase is uniquely regulated by Ca2+ and V5+, of various metals, and that the Ca2+ effect is reversed by regucalcin. The present study supports the view that regucalcin plays an important role as a regulatory protein in liver cell function related to Ca2+.
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PMID:Effects of Ca2+ and V5+ on glucose-6-phosphatase activity in rat liver microsomes: the Ca2+ effect is reversed by regucalcin. 254 64

In order to determine the specific action of cadmium on bone metabolism, the effect of cadmium on alkaline phosphatase activity, a marker enzyme of osteoblasts, was compared with that of other divalent heavy metal ions, i.e., zinc, manganese, lead, copper, nickel and mercury (10 microM each), using cloned osteoblast-like cells, MC3T3-E1. Cadmium had the strongest inhibitory effect on alkaline phosphatase activity of the cells among the metals tested. At the same dose, however, cadmium failed to inhibit cellular glucose-6-phosphatase and lactate dehydrogenase activities, suggesting that the inhibitory effect of cadmium on alkaline phosphatase was specific and was not dependent on cell injury. Cadmium treatment caused a significant decrease in cellular zinc level, but mercury treatment had no such effect at the dose inhibiting alkaline phosphatase activity. There was a good correlation between decrease of cellular zinc level and inhibition of alkaline phosphatase activity in cadmium-treated cells. Concomitant treatment of the cells with zinc prevented the cadmium-induced inhibition of alkaline phosphatase activity. However, this was not the case in the mercury-induced inhibition. Cadmium also inhibited the mineralization of osteoblasts. When 10 or 20 microM zinc was concomitantly added to the cultures, the inhibition of mineralization was prevented. These data suggest that the inhibitory effect of cadmium in osteoblasts may be closely related to its influence on the cellular zinc metabolism.
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PMID:Preventive effects of zinc on cadmium-induced inhibition of alkaline phosphatase activity and mineralization activity in osteoblast-like cells, MC3T3-E1. 274 54

The effect of daily intraperitoneal administration of Mn2+(4 mg/kg) was investigated on the metabolism of carbohydrates and certain enzymes involved in the oxidation of glucose in the rat liver and blood at the intervals of 30, 60 and 90 days after exposure. Mn2+ had no effect on the contents of blood reducing sugars and proteins, however the levels of pyruvic and lactic acids were reduced at 60 and 90 days after the metal treatment. The contents of liver glycogen and proteins remained unaffected while pyruvic acid content was decreased in Mn2+ treated rat liver throughout the experimental period. The activities of glycogen phosphorylase and lactate dehydrogenase decreased while that of phosphoglucoisomerase and glucose-6-phosphatase increased in the post mitochondrial supernatant at 60 and 90 days of Mn2+ exposure. The levels of hexokinase decreased and FDP-aldolase and fructose-1, 6-diphosphatase increased throughout the experimental period. The magnitude of alteration was found to be greater with the increase in the duration of Mn2+ treatment. Several of the mitochondrial enzymes in the liver were inhibited in the manganese exposed rats which may be responsible to inhibit the rate of dehydrogenation of Kreb cycle's intermediates along with the linked respiratory chain and eventually oxidation in the rat liver.
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PMID:Effects of manganese on carbohydrate metabolism and mitochondrial enzymes in rats. 713 26