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Tungstate promotes β-cell survival in Irs2-/- mice
Joana Moitinho Oliveira1, Sandra A Rebuffat, Rosa Gasa
1Diabetes and Obesity Research Laboratory, Institut d'Investigations Biomediques August Pi i Sunyer, Barcelona, Spain;
American Journal of Physiology. Endocrinology and Metabolism
|November 21, 2013
Summary
Tungstate treatment improved glucose tolerance and increased pancreatic beta-cell survival in mice lacking insulin receptor substrate-2 (IRS-2). This suggests therapies targeting beta-cell mass decline can prevent type 2 diabetes progression.
Area of Science:
- Endocrinology
- Molecular Biology
- Diabetes Research
Background:
- Pancreatic beta-cell dysfunction and apoptosis are central to type 2 diabetes (T2D) pathogenesis.
- Insulin receptor substrate-2 (IRS-2) is crucial for beta-cell survival and compensation.
- Tungstate shows promise in promoting beta-cell recovery in diabetic models.
Purpose of the Study:
- To investigate if tungstate can prevent diabetes onset in IRS-2 deficient mice with significant beta-cell loss.
- To explore tungstate's effects on beta-cell mass, apoptosis, and related signaling pathways.
Main Methods:
- Treatment of IRS-2 deficient (Irs2(-/-)) mice with tungstate for three weeks.
- Assessment of glucose tolerance, beta-cell mass, apoptosis rates, and beta-cell replication.
- Analysis of phosphorylated Erk1/2 levels and gene expression related to apoptosis in islets.
Main Results:
- Tungstate normalized glucose tolerance in Irs2(-/-) mice.
- Treated mice showed increased beta-cell mass, enhanced replication, and a threefold reduction in apoptosis.
- Tungstate upregulated phosphorylated Erk1/2 and repressed apoptosis-related genes in islets.
Conclusions:
- Beta-cell death can be inhibited even in the absence of IRS-2.
- Tungstate demonstrates a protective effect on beta-cells, suggesting its therapeutic potential.
- Strategies to reverse beta-cell mass decline are viable for preventing T2D progression.
