AI Article Synopsis
- Neuronatin (NNAT) is essential for regulating ion channels and maintaining nervous system structure, and it was found to be overexpressed in obese rodents.
- The study aimed to explore NNAT's function in adipose tissue amid obesity-related inflammation, revealing that its expression actually decreased after lipopolysaccharide (LPS) treatment in C57BL/6 mice.
- Further experiments with 3T3-L1 cells showed that overexpressing NNAT reduced inflammation markers, suggesting NNAT has an anti-inflammatory role in adipose tissue.
Article Abstract
Neuronatin (NNAT) is known to regulate ion channels during brain development and plays a role in maintaining the structure of the nervous system. A previous in silico analysis showed that was overexpressed in the adipose tissue of an obese rodent model relative to the wild type. Therefore, the aim of the present study was to investigate the function of in the adipose tissue. Because obesity is known to systemically induce low-grade inflammation, the expression level was examined in the adipose tissue obtained from C57BL/6 mice administered lipopolysaccharide (LPS). Unexpectedly, the expression level decreased in the white adipose tissue after LPS administration. To determine the role of NNAT in inflammation, 3T3-L1 cells overexpressing were treated with LPS. The level of the p65 subunit of nuclear factor-kappa B (NF-κB) and the activity of NF-κB luciferase decreased following LPS treatment. These results indicate that NNAT plays an anti-inflammatory role in the adipose tissue.
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| http://dx.doi.org/10.4014/jmb.1702.02049 | DOI Listing |
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