Inflammation has been widely reported to regulate adipocyte functions in adipose tissue. Our early study suggests that NFkB signaling pathway is activated by inflammation and involved in inhibition of insulin sensitivity in adipocytes. NFkB was found to inhibit PPARg function through several possible mechanisms in 3T3-L1 adipocytes. To test this possibility in vivo, we increased the NFkB activity in adipocytes in transgenic mice by expression of NFkB p65 subunit under the aP2 gene promoter.
The phenotype study shows that the food intake, physical activity and development are similar in the two groups. The reproductivity was not different in the two groups. However, the body weight gain and fat content increment are apparently less in the Tg mice, which was associated with a significant increase in energy expenditure and a defect in adipogenesis. Chronic inflammation was observed in the adipose tissue of Tg mice with macrophage infiltration and secretion of inflammatory cytokines. The data suggest that NFkB p65 inhibits PPARg function in adipose tissue, and prevents adulthood and diet-induced obesity. However, it does not provide benefit to the protection of systemic insulin sensitivity.
| Identifer | oai:union.ndltd.org:LSU/oai:etd.lsu.edu:etd-04152009-094001 |
| Date | 21 April 2009 |
| Creators | Tang, Tianyi |
| Contributors | Michael Keenan, Roy J Martin, Jianping Ye |
| Publisher | LSU |
| Source Sets | Louisiana State University |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.lsu.edu/docs/available/etd-04152009-094001/ |
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