The hyperstimulated β cell: prelude to diabetes?

Type 2 diabetes (T2D) is most often initiated by diminished sensitivity of insulin target tissues, which is normally compensated for by increased secretory activity of cells and by expansion of the functional -cell mass. However, with worsening of the disease mainly caused by mitochondrial dysfunction, oxidative and endoplasmic reticulum stress, and glucolipotoxicity, this adaptive mechanism fails to compensate for the increased insulin needs, leading to insufficient hormone supply and postprandial hyperglycemia. Indeed, hyperstimulation of  cells may lead to -cell failure and the progressive deterioration of insulin secretion accompanied by a loss of -cell mass in predisposed subjects. Insufficient functional -cell mass is also the underlying cause of type 1 diabetes, underscoring the importance of understanding -cell dynamics. Knowledge of how insulin gene expression and insulin secretion are regulated and how the  cell develops defenses against metabolic stress or after injury can help to better define normal and abnormal pancreatic -cell function. During the XIIIth symposium of the International Group on Insulin Secretion (IGIS), supported by an unrestricted educational grant from Servier, the most recent research findings from the foremost international specialists in the field of the hyperstimulated  cell and diabetes were presented. Below is a summary of the main points addressed.

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The hyperstimulated β cell: prelude to diabetes?
I- What is the role of epigenetics in insulin gene expression and insulin secretion and action
II- Impact of insulin resistance on β-cell function
III- Intrinsic hyperstimulation of β-cells
IV- Modulation of β-cell function by secretory products
V- Conclusion
Lectures during IGIS meeting
References