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This research investigates the mechanisms regulating IRS-2 expression in pancreatic beta-cells and its role in apoptosis.

Insulin Receptor Substrate-2 Proteasomal Degradation Mediated by a Mammalian Target of Rapamycin (mTOR)-induced Negative Feedback Down-regulates Protein Kinase B-mediated Signaling Pathway in β-Cells

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This research investigates the mechanisms regulating IRS-2 expression in pancreatic beta-cells and its role in apoptosis.
Chronic exposure of INS-1 cells to glucose and IGF-1 for over 8 hours
Use of lactacystin and rapamycin to assess proteasomal degradation
Adenoviral expression of active and inactive mTOR forms
Chronic exposure to glucose and IGF-1 increased Ser/Thr phosphorylation of IRS-2, leading to reduced IRS-2 levels.
mTOR inhibition by rapamycin prevented the decrease in IRS-2 levels caused by glucose/IGF-1.
Increased mTOR activity correlated with higher beta-cell apoptosis and decreased PKB activation.

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Randomized trial demonstrates mTOR's role in IRS-2 degradation in beta-cells, indicating a link to apoptosis.

Briaud et al. (2004) studied this question.

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