Abstract
Abstract
An in vitro study was conducted to determine whether bovine mammary glucose-6-phosphate dehydrogenase (G6PD) activity was regulated by palmitoyl coenzyme A (CoA), acetate, spermidine, and putrescine and whether these effects were dependent upon stage of lactation. Early lactation explants incubated in media containing palmitoyl CoA or acetate had reduced (P < 0.01) G6PD activity compared with incubated control explants. G6PD activity in early lactation explants was reduced (P < 0.05) when incubated with 5 μM palmitoyl CoA or 1 mM acetate compared with 25 μM palmitoyl CoA or 10 mM acetate. Spermidine (0.4 mM) reversed (P < 0.05) palmitoyl CoA-induced inhibition of early lactation G6PD activity at 5 μM, but not at 25 μM palmitoyl CoA. G6PD activity in early lactation explants was decreased (P < 0.05) when treated with putrescine (0.4 mM) compared with explants treated with spermidine. Addition of acetate in combination with 5 μM palmitoyl CoA reversed G6PD inhibition (P < 0.05 for 1 mM and P < 0.01 for 10 mM) while addition of either level of acetate in combination with 25 μM palmitoyl CoA failed to reverse G6PD inhibition. G6PD activity was higher (P < 0.01) in early lactation than mid-lactation explants. No statistical differences (P > 0.1) were found among any treatments in explants from mid-lactation cows. We conclude that palmitoyl CoA and acetate will inhibit G6PD activity in early lactation, but not mid-lactation explants; addition of spermidine will reverse this inhibition.
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