| First Author | Vandanmagsar B | Year | 2016 |
| Journal | Cell Rep | Volume | 15 |
| Issue | 8 | Pages | 1686-99 |
| PubMed ID | 27184848 | Mgi Jnum | J:235755 |
| Mgi Id | MGI:5800627 | Doi | 10.1016/j.celrep.2016.04.057 |
| Citation | Vandanmagsar B, et al. (2016) Impaired Mitochondrial Fat Oxidation Induces FGF21 in Muscle. Cell Rep 15(8):1686-99 |
| abstractText | Fatty acids are the primary fuel source for skeletal muscle during most of our daily activities, and impaired fatty acid oxidation (FAO) is associated with insulin resistance. We have developed a mouse model of impaired FAO by deleting carnitine palmitoyltransferase-1b specifically in skeletal muscle (Cpt1b(m-/-)). Cpt1b(m-/-) mice have increased glucose utilization and are resistant to diet-induced obesity. Here, we show that inhibition of mitochondrial FAO induces FGF21 expression specifically in skeletal muscle. The induction of FGF21 in Cpt1b-deficient muscle is dependent on AMPK and Akt1 signaling but independent of the stress signaling pathways. FGF21 appears to act in a paracrine manner to increase glucose uptake under low insulin conditions, but it does not contribute to the resistance to diet-induced obesity. |
