Other
15 Authors
- Patrikeev I,
- Cheng H,
- Wei J,
- Cheng X,
- Hu Y,
- Chen J,
- Lao DH,
- Motamedi M,
- Mei FC,
- Dineley KT,
- Hao D,
- Yan J,
- Stutz SJ,
- Cunningham KA,
- Hommel JD
| First Author | Yan J | Year | 2013 |
| Journal | Mol Cell Biol | Volume | 33 |
| Issue | 5 | Pages | 918-26 |
| PubMed ID | 23263987 | Mgi Jnum | J:207599 |
| Mgi Id | MGI:5559195 | Doi | 10.1128/MCB.01227-12 |
| Citation | Yan J, et al. (2013) Enhanced leptin sensitivity, reduced adiposity, and improved glucose homeostasis in mice lacking exchange protein directly activated by cyclic AMP isoform 1. Mol Cell Biol 33(5):918-26 |
| abstractText | The prototypic second messenger cyclic AMP (cAMP) is essential for controlling cellular metabolism, including glucose and lipid homeostasis. In mammals, the majority of cAMP functions are mediated by cAMP-dependent protein kinase (PKA) and exchange proteins directly activated by cAMP (Epacs). To explore the physiological functions of Epac1, we generated Epac1 knockout mice. Here we report that Epac1 null mutants have reduced white adipose tissue and reduced plasma leptin levels but display heightened leptin sensitivity. Epac1-deficient mice are more resistant to high-fat diet-induced obesity, hyperleptinemia, and glucose intolerance. Furthermore, pharmacological inhibition of Epac by use of an Epac-specific inhibitor reduces plasma leptin levels in vivo and enhances leptin signaling in organotypic hypothalamic slices. Taken together, our results demonstrate that Epac1 plays an important role in regulating adiposity and energy balance. |
