| First Author | Bai X | Year | 2019 |
| Journal | Prostaglandins Other Lipid Mediat | Volume | 142 |
| Pages | 53-58 | PubMed ID | 30953718 |
| Mgi Jnum | J:293593 | Mgi Id | MGI:6443017 |
| Doi | 10.1016/j.prostaglandins.2019.04.001 | Citation | Bai X, et al. (2019) Regulation of nicotinic acetylcholine receptor alpha3 subtype in adipose tissue dysfunction. Prostaglandins Other Lipid Mediat 142:53-58 |
| abstractText | Nicotinic acetylcholine receptor alpha3 subtype (alpha3-nAChR) plays a pivotal role in regulating inflammatory responses. Inflammation leads to the adipose tissue dysfunction and further increases the risk of metabolic and cardiovascular diseases. Therefore, we hypothesize that alpha3-nAChR could regulate the disorder of adipose functions. Adipocytokines and inflammatory cytokines were evaluated in apolipoprotein E knockout (ApoE(-/-)) mice after alpha3-nAChR was antagonized and in adipocytes after alpha3-nAChR gene was silenced. Results showed that in high fat diet-fed ApoE(-/-) mice with alpha3-nAChR blocked and in IL-6-stimulated adipocytes with alpha3-nAChR gene silenced the productions of leptin, resistin, triglyceride, cholesterol and low density lipoprotein were significantly increased but the generations of adiponectin and high density lipoprotein were markedly deceased. Meanwhile, the release of inflammatory cytokines was notably augmented. Moreover, the activation of JAK2/STAT3 was involved in the alpha3-nAChR-dependent signaling pathways in the regulation of adipose tissue dysfunction. A way may be paved for further investigations for the regulatory role of alpha3-nAChR in inflammatory and metabolic diseases. |
