Dual effect of glucose on macrophage nadph oxidase activity: a possible link between diabetes and tuberculosis
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Glucose is known to stimulate NADPH oxidase, an enzyme responsible for respiratory burst and intracellular killing of pathogens; but hyperglycemic state is associated with enhanced infections by invading microorganisms. In the present work we have examined the effect of glucose on macrophage NADPH oxidase activity. THP-1 cells and monocytes obtained from normal human subjects are incubated in different concentrations of glucose for a given period before and after conversion into macrophages by PMA treatment. Macrophage NADPH oxidase activity is measured and glycation of the membrane fraction is estimated in both the cases. The derived macrophages show enhanced glycation and significantly less enzyme activity when it is incubated in glucose for four days but the enzyme activity increases significantly when the macrophage precursor cells are incubated in high concentrations of glucose. This is supported by cell free experiment.
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Glucose is known to stimulate NADPH oxidase, an enzyme responsible for respiratory burst and intracellular killing of pathogens; but hyperglycemic state is associated with enhanced infections by invading microorganisms. In the present work we have examined the effect of glucose on macrophage NADPH oxidase activity. THP-1 cells and monocytes obtained from normal human subjects are incubated in different concentrations of glucose for a given period before and after conversion into macrophages by PMA treatment. Macrophage NADPH oxidase activity is measured and glycation of the membrane fraction is estimated in both the cases. The derived macrophages show enhanced glycation and significantly less enzyme activity when it is incubated in glucose for four days but the enzyme activity increases significantly when the macrophage precursor cells are incubated in high concentrations of glucose. This is supported by cell free experiment.
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