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    Effect of pinealectomy and melatonin supplementation on metallothionein, ZnT2, ZIP2, ZIP4 and zinc levels in rat small intestine
    (Taylor & Francis Ltd, 2021) Unal, Omer; Baltaci, Abdulkerim Kasim; Mogulkoc, Rasim; Avunduk, Mustafa Cihat
    We investigated the relations among levels of metallothionein (MT); zinc (Zn) transport proteins, ZnT2, ZIP2 (ZRT and IRT-like proteins); and ZIP4, which enable Zn absorption in the small intestine of rats. We also investigated tissue Zn levels in the small intestine. We used four groups of adult male rats: group 1, control; group 2, pinealectomy (Px); group 3, Px + melatonin (MEL); group 4, MEL only. Animals in groups 3 and 4 were administered 5 mg/kg/day MEL for four weeks. At the end of the study, all animals were sacrificed and samples of duodenum, jejunum and ileum were harvested to analyze ZnT2, ZIP2, ZIP4 and MT levels using immunohistochemistry, and tissue Zn levels were measured by atomic absorption spectrophotometry. The lowest ZnT2 levels in the duodenum, jejunum and ileum, and the lowest ZIP2 levels in the duodenum and ileum were found in group 2. The lowest ZIP4 levels were found in the duodenum and jejunum, and the lowest MT levels in the duodenum and ileum were found in group 2. The highest MT values in the ileum were found in group 4. We found that ZnT2, ZIP2, ZIP4 and MT levels were reduced in the ileum compared to controls following Px, but levels approached control values after MEL administration. By its effects on ZnT2, ZIP2, ZIP4 and MT levels, MEL participates in the absorption of Zn in the rat small intestine.
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    The Role of Zinc Status on Spatial Memory, Hippocampal Synaptic Plasticity, and Insulin Signaling in icv-STZ-Induced Sporadic Alzheimer's-Like Disease in Rats
    (Springernature, 2022) Baltaci, Saltuk Bugra; Unal, Omer; Gulbahce-Mutlu, Elif; Gumus, Haluk; Pehlivanoglu, Suray; Yardimci, Ahmet; Mogulkoc, Rasim
    Alzheimer's disease (AD), especially its sporadic form (sAD), is of multifactorial nature. Brain insulin resistance and disrupted zinc homeostasis are two key aspects of AD that remain to be elucidated. Here, we investigated the effects of dietary zinc deficiency and supplementation on memory, hippocampal synaptic plasticity, and insulin signaling in intracerebroventricular streptozotocin (icv-STZ)-induced sAD in rats. The memory performance was evaluated by Morris water maze. The expression of hippocampal protein and mRNA levels of targets related to synaptic plasticity and insulin pathway was assessed by Western blot and real-time quantitative PCR. We found memory deficits in icv-STZ rats, which were fully recovered by zinc supplementation. Western blot analysis revealed that icv-STZ treatment significantly reduced hippocampal PSD95 and p-GSK3 beta, and zinc supplementation restored the normal protein levels. mRNA levels of BDNF, PSD95, SIRT1, GLUT4, insulin receptor, and ZnT3 were found to be reduced by icv-STZ and reestablished by zinc supplementation. Our data suggest that zinc supplementation improves cognitive deficits and rescues the decline in key molecular targets of synaptic plasticity and insulin signaling in hippocampus caused by icv-STZ induced sAD in rats.