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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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    Öğe
    Relationship of Dietary Zinc Status with Pubertal Parameters and Cognitive Functions in Male Offspring of Pregnant Rats Fed a Zinc-Deficient Diet
    (Wiley, 2023) Unal, Omer; Baltaci, Saltuk Bugra; Mutlu, Elif Gulbahce; Unal, Nilufer Akgun; Mogulkoc, Rasim; Baltaci, Abdulkerim Kasim
    [Abstract No tAvailable]
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    The Effect of Dietary Zinc Status on ZEB1 Levels in Muscle and Bone Tissue in Maternal Zinc Deficiency Rats
    (Wiley, 2023) Alcay, Osman; Mutlu, Elif Gulbahce; Unal, Omer; Baltaci, Saltuk Bugra; Mogulkoc, Rasim; Baltaci, Abdulkerim Kasim
    [Abstract No tAvailable]
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    The Effects of Resveratrol and Melatonin on Cardiac Dysfunction in Diabetic Elderly Female Rats
    (Acad Sciences Czech Republic, Inst Physiology, 2023) Akgun-Unal, Nilufer; Ozyildirim, Serhan; Unal, Omer; Baltaci, Saltuk Bugra; Mogulkoc, Rasim; Baltaci, Abdulkerim Kasim
    We aimed to investigate the effects of melatonin and resveratrol on diabetes-related papillary muscle dysfunction and structural heart disorders. The protective effect of resveratrol and melatonin supplementation on cardiac functions was investigated in a diabetic elderly female rat model. 16-month-old rats (n=48) were allocated into 8 groups. Group1: Control, Group2: Resveratrol Control, Group3: Melatonin Control, Group4: Resveratrol and Melatonin Control, Group5: Diabetes, Group6: Diabetes Resveratrol, Group7: Diabetes Melatonin, Group8: Diabetes Resveratrol and Melatonin. Streptozotocin was injected intraperitoneally to the rats for experimental diabetes induction. Thereafter, resveratrol (intraperitoneal) and melatonin (subcutaneous) were administered for 4 weeks. Resveratrol and melatonin had a protective effect on the contractile parameters and structural properties of the papillary muscle, which was impaired by diabetes. it has been presented that diabetes impairs the contractile function of the papillary muscle for each stimulus frequency tested and the responses obtained as a result of Ca+2 uptake and release mechanisms from the Sarcoplasmic reticulum, and it has been observed that these effects are improved with resveratrol and melatonin injection. The decrease in myocardial papillary muscle strength in the diabetic elderly female rat can be reversed with the combination of resveratrol, melatonin and resveratrol+melatonin. Melatonin+resveratrol supplementation is no different from melatonin and/or resveratrol supplementation. Resveratrol and melatonin supplementation may have a protective effect on cardiac functions in a diabetic elderly female rat model.
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    The relationship between beta cell activation and SLC30A8/ZnT8 levels of the endocrine pancreas and maternal zinc deficiency in rats
    (Elsevier Gmbh, 2023) Goktepe, Emre; Baltaci, Saltuk Bugra; Unal, Omer; Unlukal, Nejat; Mogulkoc, Rasim; Baltaci, Abdulkerim Kasim
    Objectives: Zinc, which is found in high concentrations in the 13-cells of the pancreas, is also a critical component for the endocrine functions of the pancreas. SLC30A8/ZnT8 is the carrier protein responsible for the transport of zinc from the cytoplasm to the insulin granules. The aim of this study was to investigate how dietary zinc status affects pancreatic beta cell activation and ZnT8 levels in infant male rats born to zinc-deficient mothers.Methods: The study was performed on male pups born to mothers fed a zinc-deficient diet. A total of 40 male rats were divided into 4 equal groups. Group 1: In addition to maternal zinc deficiency, this group was fed a zinc -deficient diet. Group 2: In addition to maternal zinc deficiency, this group was fed a standard diet. Group 3: In addition to maternal zinc deficiency, this group was fed a standard diet and received additional zinc sup-plementation. Group 4: Control group. Pancreas ZnT8 levels were determined by ELISA method and insulin -positive cell ratios in 13-cells by immunohistochemistry.Results: The highest pancreatic ZnT8 levels and anti-insulin positive cell ratios in the current study were obtained in Group 3 and Group 4. In our study, the lowest pancreatic ZnT8 levels were obtained in Group 1 and Group 2, and the lowest pancreatic anti-insulin positive cell ratios were obtained in Group 1.Conclusion: The results of the present study; in rats fed a zinc-deficient diet after maternal zinc deficiency has been established shows that ZnT8 levels and anti-insulin positive cell ratios in pancreatic tissue, which is significantly suppressed, reach control values with intraperitoneal zinc supplementation.
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    Öğe
    The Relationship Between Dietary Zinc Status and Pubertal Parameters in Offspring Female Rats Born to Zinc-Deficient Diet-fed Mothers
    (Wiley, 2023) Turker, Buse Gunaydin; Unal, Nilufer Akgun; Mutlu, Elif Gulbahce; Baltaci, Saltuk Bugra; Unal, Omer; Mogulkoc, Rasim; Baltaci, Abdulkerim Kasim
    [Abstract No tAvailable]
  • Küçük Resim
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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.
  • Küçük Resim
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    Zinc Supplementation Improves ZIP14 (SLC39A14) Levels in Cerebral Cortex Suppressed by icv-STZ Injection
    (Turkish Neuropsychiatry Assoc-Turk Noropsikiyatri Dernegi, 2024) Baltaci, Saltuk Bugra; Gumus, Haluk; Unal, Omer; Acar, Gozde; Bayiroglu, Aysenur Feyza
    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.