الفهرس 
Aim of the WorkOnly 14 pages are availabe for public view
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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