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The findings regarding trace element concentrations in patients diagnosed with type 2 diabetes and healthy controls are inconsistent, and therefore, we determined to gather them in the form of a review to further indicate the need for more advanced knowledge development. In our study, we reviewed articles and studies that involved the topics of micronutrient and metal associations with the occurrence and development of type 2 diabetes. We mainly included works regarding human-based studies, but with limited research results, animal-based research was also taken into account. With some newer studies, we reached for initial assumptions of previous statements. The results indicated that higher serum levels of lead, cadmium, arsenic, bromine, barium, strontium, nickel, aluminum, calcium, copper, and ferritin are positively associated with diabetic prevalence. Both too-low and too-high levels of zinc, selenium, and magnesium may be connected to the development of diabetes. Chromium has the capability of insulin response modulation, with enhanced insulin-cell binding, and thus, lower serum levels of chromium can be found in diabetic patients. There are contradictory discoveries regarding manganese. Its supplementation can possibly cease the development of insulin resistance and type 2 diabetes. On the contrary, other studies reported that there is no such connection. Our work indicates that, as micronutrients play a significant role in the pathogenesis of metabolic disorders, more research regarding their bodily homeostasis and type 2 diabetes should be conducted. [ABSTRACT FROM AUTHOR]

Changes in trace element concentrations are being wildly considered when it comes to neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. This study aims to present the role that trace elements play in the central nervous system. Moreover, we reviewed the mechanisms involved in their neurotoxicity. Low zinc concentrations, as well as high levels of copper, manganese, and iron, activate the signalling pathways of the inflammatory, oxidative and nitrosative stress response. Neurodegeneration occurs due to the association between metals and proteins, which is then followed by aggregate formation, mitochondrial disorder, and, ultimately, cell death. In Alzheimer's disease, low Zn levels suppress the neurotoxicity induced by β-amyloid through the selective precipitation of aggregation intermediates. High concentrations of copper, iron and manganese cause the aggregation of intracellular α-synuclein, which results in synaptic dysfunction and axonal transport disruption. Parkinson's disease is caused by the accumulation of Fe in the midbrain dopaminergic nucleus, and the pathogenesis of multiple sclerosis derives from Zn deficiency, leading to an imbalance between T cell functions. Aluminium disturbs the homeostasis of other metals through a rise in the production of oxygen reactive forms, which then leads to cellular death. Selenium, in association with iron, plays a distinct role in the process of ferroptosis. Outlining the influence that metals have on oxidoreduction processes is crucial to recognising the pathophysiology of neurodegenerative diseases and may provide possible new methods for both their avoidance and therapy. [ABSTRACT FROM AUTHOR]

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Copyright of Social Dissertations / Rozpraw Społecznych is the property of Pope John Paul II State School of Higher Education in Biala Podlaska and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)