Abstract
Diabetes mellitus (DM) is a group of metabolic disorders characterized by hyperglycemia. In particular, type 2 diabetes (T2D) represents one of the main causes of death in the world, and those suffering from it have a lower quality of life. Although there are multiple hypotheses about the pathophysiological mechanisms that lead to the development of T2D, the effects of this pathology on pancreatic β-cells are often ignored. We now know that in addition to genetic defects, β-cell organellar dysfunction participates in the earliest stages of the disease; other factors also contribute to this dysfunction, such as excessive production of reactive oxygen species and a decrease in cellular volume and mass. These features usually result from increased apoptosis, which is not adequately compensated for by the characteristic regeneration mechanisms of these cells. In this study, we specifically examine the genetic, epigenetic and metabolic defects that contribute to β-cell dysfunction and lead to the establishment of T2D, particularly the dysregulated insulin synthesis and secretion in these cells.
Keywords: Type 2 diabetes, genetic defects, hyperglycemia, insulin, organellar dysfunction, pancreatic β-cells.
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