Depressed Response of Plasma Iron and Zinc to Endotoxin and LEM in STZ-Diabetic Rat

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Abstract
Laboratory and epidemiological evidence indicate that the enhanced flux of Fe and Zn from the plasma to the storage compartments, such as liver, serves as a protective host response to combat infection. The status of this nonspecific immune response was studied in the diabetic animal since it is commonly held that the diabetic has an increased incidence and susceptibility to infection. Normal rats and rats previously rendered diabetic by streptozotocin (STZ) were injected with saline or Escherichia coli endotoxin; plasma levels of Zn, Fe and Cu were monitored 8 h thereafter. Diabetic rats reduced their plasma Zn and Fe levels by 35 and 25%, respectively, in response to endotoxin injection; control rats had a 70% decrease in Zn and a 46% depression in Fe. Insulin administration to the diabetic rats restored the ability to decrease plasma Zn and Fe to the same degree as control rats. Plasma Cu did not change in any group. Further investigation suggested that the defect in trace metal response occurred after the secretion of leukocytic endogenous mediator (LEM) in the inflammatory response pathway. Thus, STZ-diabetic rats have a diminished ability to decrease plasma Zn and Fe in response to endotoxin; this defect is due to an ineffective response of target tissues to the effects of leukocytic endogenous mediator. Apparently, the hyperinsulinemia associated with the stress of infection functions to lower plasma Zn and possibly Fe, thereby allowing the host to better combat infections.