الفهرس | Only 14 pages are availabe for public view |
Abstract Diabetes mellitus (diabetes) is a complex metabolic disorder Characterized by abnormal levels of glucose (fasting glucose >7 μmol/l) in the blood. During the fed state, the pancreas Releases insulin to induce glucose uptake by the recipient cells, thus reducing the high blood glucose levels. However, during low Sugar levels, it secretes glucagon to induce liver cells to release the stored glucose, thus increasing the blood glucose concentration. Hence, blood glucose homeostasis is maintained by balancing the pancreatic endocrine hormones, insulin and glucagon production. Diabetes is characterized by two subtypes: Type 1 diabetes (T1D), which is insulin dependent, and Type 2 diabetes (T2D), which is insulin independent. In T1D, the β-cells in the pancreas produce little or no insulin, resulting in the build-up of glucose. Type 1 diabetes mellitus (T1DM) is characterized by autoimmune destruction of pancreatic beta-cells by T lymphocytes and macrophages The disease is usually diagnosed when over 80–90% of beta-cells have been destructed by the infiltrating immune system. T1DM development is slow, providing a potentially long window of time in which it is possible to identify and theoretically treat individuals at risk. The first sign of autoimmunity against beta-cells, frequently detectable a few months/years before the appearance of clinical symptoms, is the occurrence of antibodies against beta-cell antigens. These autoantibodies are used as biomarkers of T1DM risk and are directed against insulin, glutamic acid decarboxylase, zinc cation efflux transporter and tyrosine phosphatases-2 and -2β |