| First Author | Hotamisligil GS | Year | 1996 |
| Journal | Science | Volume | 274 |
| Issue | 5291 | Pages | 1377-9 |
| PubMed ID | 8910278 | Mgi Jnum | J:37027 |
| Mgi Id | MGI:84433 | Doi | 10.1126/science.274.5291.1377 |
| Citation | Hotamisligil GS, et al. (1996) Uncoupling of obesity from insulin resistance through a targeted mutation in aP2, the adipocyte fatty acid binding protein. Science 274(5291):1377-9 |
| abstractText | Fatty acid binding proteins (FABPs) are small cytoplasmic proteins that are expressed in a highly tissue-specific manner and bind to fatty acids such as oleic and retinoic acid. Mice with a null mutation in aP2, the gene encoding the adipocyte FABP, were developmentally and metabolically normal. The aP2-deficient mice developed dietary obesity but, unlike control mice, they did not develop insulin resistance or diabetes. Also unlike their obese wild-type counterparts, obese aP2-/- animals failed to express in adipose tissue tumor necrosis factor-alpha (TNF-alpha), a molecule implicated in obesity-related insulin resistance. These results indicate that aP2 is central to the pathway that links obesity to insulin resistance, possibly by linking fatty acid metabolism to expression of TNF-alpha. |
