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.