Zinc supplementation improves ZIP14 (SLC39A14) levels in cerebral cortex suppressed by icv-STZ injection

Abstract

Introduction: Metabolic dysfunctions are critical in the pathology of Alzheimer’s disease. Impaired zinc homeostasis, in particular, is a significant issue in this disease that has yet to be explained. Gene expression of ZIP14 in brain tissue has been previously reported. But to date, only one study has reported reduced ZIP14 levels in aged brain tissue. We investigated how dietary zinc deprivation and supplementation impact ZIP14 levels in the cerebral cortex in rats with sporadic Alzheimer’s disease (sAH) produced by intracerebroventricular streptozotocin (icv-STZ). Impaired zinc homeostasis, in particular, is a significant issue with this condition that has yet to be elucidated. Methods: Animals were divided into 5 groups in equal numbers (n=8): Sham 1 group: icv received artificial cerebrospinal fluid (aCSF); Sham 2 group: retrieved icv aCSF and intraperitoneal (ip) saline, STZ group: received 3 mg/kg icv-STZ; STZ-Zn-Deficient group: received 3 mg/ kg icv-STZ and fed a zinc-deprived diet; STZ-Zn-Supplemented: It received 3 mg/kg icv-STZ and ip zinc sulfate (5 mg/kg/day ZIP 14 levels (ng/L) in cortex tissue samples taken from animals sacrificed under general anesthesia were determined by ELISA at the final stage of the experimental applications. Results: Decreased ZIP14 levels in the sporadic Alzheimer’s group were severely by zinc deficiency. Zinc supplementation treated the reduction in ZIP14 levels. Conclusion: The results of the current study show that ZIP14 levels in cerebral cortex tissue, which are suppressed in the experimental rat Alzheimer model and are even more critically reduced in zinc deficiency, can be restored by zinc supplementation.