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    Marginal Maternal Zinc Deficiency Produces Liver Damage and Altered Zinc Transporter Expression in Offspring Male Rats
    (Springernature, 2024) Gumus, Meltem; Gulbahce-Mutlu, Elif; Unal, Omer; Baltaci, Saltuk Bugra; Unlukal, Nejat; Mogulkoc, Rasim; Baltaci, Abdulkerim Kasim
    The aim of this study was to investigate how zinc deficiency and supplementation affect liver markers including autotaxin, kallistatin, endocan, and zinc carrier proteins ZIP14 and ZnT9 in rats exposed to maternal zinc deficiency. Additionally, the study aimed to assess liver tissue damage through histological examination. A total of forty male pups were included in the research, with thirty originating from mothers who were given a zinc-deficient diet (Groups 1, 2, and 3), and the remaining ten born to mothers fed a standard diet (Group 4). Subsequently, Group 1 was subjected to a zinc-deficient diet, Group 2 received a standard diet, Group 3 received zinc supplementation, and Group 4 served as the control group without any supplementation. Upon completion of the experimental phases of the study, all animals were sacrificed under general anesthesia, and samples of liver tissue were obtained. The levels of autotaxin, kallistatin, endocan, ZIP 14, and ZnT9 in these liver tissue samples were determined using the ELISA technique. In addition, histological examination was performed to evaluate tissue damage in the liver samples. In the group experiencing zinc deficiency, both endocan and autotaxin levels increased compared to the control group. With zinc supplementation, the levels of endocan and autotaxin returned to the values observed in the control group. Similarly, the suppressed levels of kallistatin, ZIP14, and ZnT9 observed in the zinc deficiency group were reversed with zinc supplementation. Likewise, the reduced levels of kallistatin, ZIP14, and ZnT9 seen in the zinc deficiency group were rectified with zinc supplementation. Moreover, the application of zinc partially ameliorated the heightened liver tissue damage triggered by zinc deficiency. This study is the pioneering one to demonstrate that liver tissue dysfunction induced by a marginal zinc-deficient diet in rats with marginal maternal zinc deficiency can be alleviated through zinc supplementation.
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    The effects of resveratrol and melatonin on biochemical and molecular parameters in diabetic old female rat hearts
    (Pergamon-Elsevier Science Ltd, 2023) Akgun-Unal, Nilufer; Ozyildirim, Serhan; Unal, Omer; Gulbahce-Mutlu, Elif; Mogulkoc, Rasim; Baltaci, Abdulkerim Kasim
    The roles of melatonin and resveratrol-enhanced activation of SIRT1 (silent information regulator 1), GLUT4 (glucose transporter type 4), and PGC-1 alpha (peroxisome proliferator-activated receptor gamma coactivator 1 -alpha) in mediating the protective effects on the heart in aged female rats with streptozotocin-induced dia-betes were investigated. 16-month-old 48 Wistar female rats were separated into 8 groups with equal numbers. Group 1: Control, Group 2: Resveratrol Control, Group 3: Melatonin Control, Group 4: Resveratrol and Melatonin Control, Group 5: Diabetes, Group 6: Diabetes Resveratrol, Group 7: Diabetes Melatonin, Group 8: Diabetes Resveratrol and Melatonin. A single dose of 40 mg/kg intraperitoneal streptozotocin was injected into the rats of Groups 5, 6, 7, and 8 to induce experimental diabetes. Blood glucose levels were measured from the tail veins of the animals six days after the injections, using a diagnostic glucose kit. Rats with a blood glucose levels >= 300 mg/dl were considered diabetic. 5 mg/kg/day of resveratrol (intraperitoneal) and melatonin (subcutaneous) were administered for four weeks. At the end of the applications, SIRT1, GLUT4, PGC-1 alpha gene expression as well as MDA and GSH levels in the heart tissues were determined by the PCR method from heart tissue samples taken under general anesthesia.The findings of our study show that suppressed antioxidant activity and decreased GLUT4, SIRT1, and PGC-1 alpha gene expression in heart tissue can be reversed by the combination of resveratrol, melatonin, and resveratrol + melatonin in a diabetic aged female rat model. Resveratrol and melatonin supplementation may have a pro-tective effect on cardiac functions in the diabetic aged female rat model.
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    Zinc Ameliorates Nogo-A Receptor and Osteocalcin Gene Expression in Memory-Sensitive Rat Hippocampus Impaired by Intracerebroventricular Injection of Streptozotocin
    (Springernature, 2023) Gumus, Haluk; Baltaci, Saltuk Bugra; Unal, Omer; Gulbahce-Mutlu, Elif; Mogulkoc, Rasim; Baltaci, Abdulkerim Kasim
    Metabolic dysfunction is a critical step in the etiopathogenesis of Alzheimer's disease. In this progressive neurological disorder, impaired zinc homeostasis has a key role that needs to be clarified. The aim of this study was to investigate the effect of zinc deficiency and administration on hippocampal Nogo-A receptor and osteocalcin gene expression in rats injected with intracerebroventricular streptozotocin (icv-STZ). Forty male Wistar rats were divided into 5 groups in equal numbers: Sham 1 group received icy artificial cerebrospinal fluid (aCSF); Sham 2 group received icy a CSF and i.p. saline; STZ group received 3 mg/kg icy STZ; STZ-Zn-deficient group received 3 mg/kg icy STZ and fed a zinc-deprived diet; STZ-Zn-supplemented group received 3 mg/kg icy STZ and i.p. zinc sulfate (5 mg/kg/day). Hippocampus tissue samples were taken following the cervical dislocation of the animals under general anesthesia. Nogo-A receptor and osteocalcin gene expression levels were determined by real-time-PCR method. Zinc supplementation attenuated the increase in hippocampal Nogo-A receptor gene expression, which was significantly increased in zinc deficiency. Again, zinc supplementation upregulated the intrinsic protective mechanisms of the brain by activating osteocalcin-expressing cells in the brain. The results of the study show that zinc has critical effects on Nogo-A receptor gene expression and hippocampal osteocalcin gene expression levels in the memory-sensitive rat hippocampus that is impaired by icv-STZ injection. These results are the first to examine the effect of zinc deficiency and supplementation on hippocampal Nogo-A receptor and osteocalcin gene expression in icv-STZ injection in rats.