Cerium Oxide Nanoparticles Regulate Insulin Sensitivity and Oxidative Markers in 3T3-L1 Adipocytes and C2C12 Myotubes.
Amaya López-PascualAndoni Urrutia-SarrateaSilvia Lorente-CebriánJosé Alfredo Martínez HernándezPedro González-MuniesaPublished in: Oxidative medicine and cellular longevity (2019)
Insulin resistance is associated with oxidative stress, mitochondrial dysfunction, and a chronic low-grade inflammatory status. In this sense, cerium oxide nanoparticles (CeO2 NPs) are promising nanomaterials with antioxidant and anti-inflammatory properties. Thus, we aimed to evaluate the effect of CeO2 NPs in mouse 3T3-L1 adipocytes, RAW 264.7 macrophages, and C2C12 myotubes under control or proinflammatory conditions. Macrophages were treated with LPS, and both adipocytes and myotubes with conditioned medium (25% LPS-activated macrophages medium) to promote inflammation. CeO2 NPs showed a mean size of ≤25.3 nm (96.7%) and a zeta potential of 30.57 ± 0.58 mV, suitable for cell internalization. CeO2 NPs reduced extracellular reactive oxygen species (ROS) in adipocytes with inflammation while increased in myotubes with control medium. The CeO2 NPs increased mitochondrial content was observed in adipocytes under proinflammatory conditions. Furthermore, the expression of Adipoq and Il10 increased in adipocytes treated with CeO2 NPs. In myotubes, both Il1b and Adipoq were downregulated while Irs1 was upregulated. Overall, our results suggest that CeO2 NPs could potentially have an insulin-sensitizing effect specifically on adipose tissue and skeletal muscle. However, further research is needed to confirm these findings.
Keyphrases
- oxide nanoparticles
- adipose tissue
- oxidative stress
- insulin resistance
- anti inflammatory
- low grade
- high fat diet
- high fat diet induced
- reactive oxygen species
- skeletal muscle
- dna damage
- type diabetes
- inflammatory response
- high grade
- diabetic rats
- ischemia reperfusion injury
- poor prognosis
- polycystic ovary syndrome
- photodynamic therapy
- metabolic syndrome
- cell death
- stem cells
- single cell
- newly diagnosed
- heat shock
- signaling pathway
- risk assessment
- human health
- climate change