| First Author | Scheja L | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 407 |
| Issue | 2 | Pages | 288-94 |
| PubMed ID | 21371440 | Mgi Jnum | J:171942 |
| Mgi Id | MGI:5002424 | Doi | 10.1016/j.bbrc.2011.02.137 |
| Citation | Scheja L, et al. (2011) Beneficial effects of IKKepsilon-deficiency on body weight and insulin sensitivity are lost in high fat diet-induced obesity in mice. Biochem Biophys Res Commun 407(2):288-94 |
| abstractText | Activation of the classical IkappaB kinases (IKKalpha and IKKbeta) was previously shown to contribute to obesity-induced inflammation and insulin resistance. Using knockout mice, we investigated whether the related isoform IKKepsilon plays a similar metabolic role. IKKepsilon(-/-) mice had reduced body weight, leptin levels, as well as higher insulin sensitivity when kept on chow diet. However, inflammatory parameters, measured in liver, adipose tissue and plasma, were either unaltered or showed a trend toward up-regulation (liver NF-kappaB activity, TNFalpha and IL-1beta expression). Chronic feeding of a high fat diet induced equal obesity and insulin resistance, and similarly induced inflammatory markers, in IKKepsilon(-/-) and wild-type mice, indicating that under high caloric conditions the inflammatory and metabolic effects of IKKepsilon deficiency were overridden. Taken together, our data indicate that IKKepsilon does not have general pro-inflammatory properties in liver and adipose tissue, and suggest that reduced adiposity is the primary mechanism for improved insulin sensitivity in IKKepsilon(-/-) mice on chow diet. |
