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SIRT1 activation attenuates palmitate induced apoptosis in C2C12 muscle cells
Gholamreza Taheripak1,2, Niusha Sabeti2,3, Naba Najar1,2
1Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Background:
Type 2 diabetes is characterized by insulin resistance, which manifests mainly in skeletal muscles. SIRT1 has been found to play a role in the insulin signaling pathway. However, the molecular underpinnings of SIRT1's function in palmitate fatty acid-induced apoptosis still need to be better understood.
Methods:
In this research, skeletal muscle cells are treated with palmitate to be insulin resistant. It is approached that SIRT1 is downregulated in C2C12 muscle cells during palmitate-induced apoptosis and that activating SIRT1 mitigates this effect.
Results:
Based on these findings, palmitate-induced apoptosis suppressed mitochondrial biogenesis by lowering PGC-1 expression, while SIRT1 overexpression boosted. The SIRT1 inhibitor sirtinol, on the other hand, decreased mitochondrial biogenesis under the same conditions. This research also shows that ROS levels rise in the conditions necessary for apoptosis induction by palmitate, and ROS inhibitors can mitigate this effect. This work demonstrated that lowering ROS levels by boosting SIRT1 expression inhibited apoptotic induction in skeletal muscle cells.
Conclusion:
This study's findings suggested that SIRT1 can improve insulin resistance in type 2 diabetes by slowing the rate of lipo-apoptosis and boosting mitochondrial biogenesis, among other benefits.
Insights
Activating SIRT1 combats palmitate-induced apoptosis in skeletal muscle cells, improving mitochondrial biogenesis and insulin resistance in type 2 diabetes. This research highlights SIRT1
Area of Science:
- Cell Biology
- Metabolic Diseases
- Molecular Biology
Background:
- Type 2 diabetes involves insulin resistance, primarily in skeletal muscles.
- Sirtuin 1 (SIRT1) is implicated in insulin signaling pathways.
- The precise role of SIRT1 in palmitate-induced apoptosis requires further elucidation.
Purpose of the Study:
- To investigate the role of SIRT1 in palmitate-induced apoptosis in skeletal muscle cells.
- To determine if activating SIRT1 can mitigate palmitate-induced insulin resistance and apoptosis.
Main Methods:
- C2C12 skeletal muscle cells were treated with palmitate to induce insulin resistance.
- SIRT1 expression levels were monitored during palmitate-induced apoptosis.
- The effects of SIRT1 activation and inhibition on apoptosis, mitochondrial biogenesis, and reactive oxygen species (ROS) were assessed.
Main Results:
- Palmitate-induced apoptosis downregulated SIRT1 and suppressed mitochondrial biogenesis via PGC-1 reduction.
- SIRT1 overexpression enhanced mitochondrial biogenesis, while the SIRT1 inhibitor sirtinol decreased it.
- Palmitate treatment increased ROS levels, which were mitigated by ROS inhibitors and by boosting SIRT1 expression, thereby inhibiting apoptosis.
Conclusions:
- SIRT1 activation can improve insulin resistance in type 2 diabetes.
- SIRT1 mitigates lipo-apoptosis and enhances mitochondrial biogenesis in skeletal muscle cells.
- Targeting SIRT1 may offer a therapeutic strategy for type 2 diabetes.
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