الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Diabetes Mellitus is a worldwide health problem that affects 4 to 5% of the global population. It results from insulin availability that is insufficient to meet tissue insulin demand. Decreased β-cell function is not only a prerequisite for the development of hyperglycemia and type-2 diabetes, but its progressive character also determines the course of the disease. There is considered to be a gradual deterioration of the β-cell function during the course of the disease. The β-cell function is to secrete the appropriate amounts of bioactive insulin in response to nutrients, hormones and nervous stimuli, to maintain the plasma glucose levels in a tight physiological range for optimal functioning of all tissues in the body. The β-cell plasticity is the ability to adapt the cell mass to variations in insulin demand, to ensure optimal control of glucose homeostasis. The β-cell mass is constantly renewed through a balance between the mechanisms of expansion and involution. During growth and development, islet neogenesis and β-cell replication are key mechanisms in β-cell mass expansion. Changes in insulin sensitivity induce changes in insulin secretion to keep glucose concentrations within a tight physiological range. Net changes in β-cell mass are reflective of the amount of growth (i.e., the sum of β-cell replication, neogenesis and size) minus the degree of β-cell death (i.e., the sum of β-cell apoptosis, necrosis and autophagic cell death). When the workload on the β-cell increases by factors such as obesity, aging, insulin resistance or low-grade inflammation, healthy β-cell can adapt by augmenting insulin secretion to meet this increased demand. In T2DM, the ability of β-cell to adequately meet the need for insulin to maintain glucose homeostasis is compromised resulting in hyperglycaemia. Both increased apoptosis and decreased proliferation may contribute to β-cell loss in type-2 diabetic patients. The β-cell exposed to chronic hyperglycaemia generates excess levels of reactive oxygen species, leading to oxidative stress and The β-cell dysfunction. According to the glucolipotoxicity hypothesis, the deleterious effects of fatty acids on the β-cell may only occur in the presence of elevated glucose levels. Many new strategies for β-cell preservation are promising, and when aided with the in vivo assessment of the beta cell, would be more promising, specifically, good diet and a healthy life style would help prevent diabetes or delay its onset. In conclusion, preservation of a functional β-cell mass is a life without diabetes, so new strategies should be aimed at preserving a functionalβ-cell mass making diabetes a preventable disease.