| First Author | Hu ZJ | Year | 2018 |
| Journal | Neurosci Bull | Volume | 34 |
| Issue | 2 | Pages | 321-329 |
| PubMed ID | 29204732 | Mgi Jnum | J:327530 |
| Mgi Id | MGI:6884252 | Doi | 10.1007/s12264-017-0194-2 |
| Citation | Hu ZJ, et al. (2018) Peripheral Leptin Signaling Mediates Formalin-Induced Nociception. Neurosci Bull 34(2):321-329 |
| abstractText | Accumulating evidence suggests that obesity is associated with chronic pain. However, whether obesity is associated with acute inflammatory pain is unknown. Using a well-established obese mouse model induced by a high-fat diet, we found that: (1) the acute thermal pain sensory threshold did not change in obese mice; (2) the model obese mice had fewer nociceptive responses in formalin-induced inflammatory pain tests; restoring the obese mice to a chow diet for three weeks partly recovered their pain sensation; (3) leptin injection induced significant phosphorylation of STAT3 in control mice but not in obese mice, indicating the dysmodulation of topical leptin-leptin receptor signaling in these mice; and (4) leptin-leptin receptor signaling-deficient mice (ob/ob and db/db) or leptin-leptin receptor pathway blockade with a leptin receptor antagonist and the JAK2 inhibitor AG 490 in wild-type mice reduced their nociceptive responses in formalin tests. These results indicate that leptin plays a role in nociception induced by acute inflammation and that interference in the leptin-leptin receptor pathway could be a peripheral target against acute inflammatory pain. |
