الفهرس 
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Abstract
The link between T2D and dyslipidemia may be considered a Janus-faced relation. While the impact of diabetes on abnormalities in lipid metabolism is well-established, recent data provide evidence for a reverse direction, assigning a key role for hypercholesterolemia and low HDL-C levels in the development of beta-cell dysfunction.
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.
Summary
117
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.
Steatosis is the storage of fat in non-physiological sites such as the liver, skeletal muscle, heart, and pancreas. It is the greatest determinant of all metabolic complications of obesity as it interferes with cellular and organ functions.
Summary
118
Pancreatic steatosis is the best description of fat accumulation in the pancreatic gland without fat replacement, this excessive pancreatic lipid content may enter a continuous vicious cycle of hydrolysis and fatty acid re-esterification thereby generating toxic intermediates, which may induce β-cell dysfunction and apoptosis. Several studies were made to study whether these fat depositions are harmful or inert.
It will be important to understand how lipid disorders can be metabolically dangerous for beta-cells to define the optimal therapy.