| First Author | Collier JJ | Year | 2020 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 318 |
| Issue | 1 | Pages | E11-E21 |
| PubMed ID | 31661298 | Mgi Jnum | J:286270 |
| Mgi Id | MGI:6400840 | Doi | 10.1152/ajpendo.00309.2019 |
| Citation | Collier JJ, et al. (2020) Hepatic IKKepsilon expression is dispensable for high-fat feeding-induced increases in liver lipid content and alterations in glucose tolerance. Am J Physiol Endocrinol Metab 318(1):E11-E21 |
| abstractText | There are endocrine and immunological changes that occur during onset and progression of the overweight and obese states. The inhibitor of nuclear factor-kappaB kinase-epsilon (IKKepsilon) was originally described as an inducible protein kinase; whole body gene deletion or systemic pharmaceutical targeting of this kinase improved insulin sensitivity and glucose tolerance in mice. To investigate the primary sites of action associated with IKKepsilon during weight gain, we describe the first mouse line with conditional elimination of IKKepsilon in the liver (IKKepsilon(Alb-/-)). IKKepsilon(Alb-/-) mice and littermate controls gain weight, show similar changes in body composition, and do not display any improvements in insulin sensitivity or whole body glucose tolerance. These studies were conducted using breeder chow diets and matched low- vs. high-fat diets. While glycogen accumulation in the liver is reduced in IKKepsilon(Alb-/-) mice, lipid storage in liver is similar in IKKepsilon(Alb-/-) mice and littermate controls. Our results using IKKepsilon(Alb-/-) mice suggest that the primary action of this kinase to impact insulin sensitivity during weight gain lies predominantly within extrahepatic tissues. |
