Regulation of nicotinic acetylcholine receptor α3 subtype in adipose tissue dysfunction

• Published in: Prostaglandins & other lipid mediators Vol. 142; pp. 53 - 58
• Main Authors: Bai, Xiaoqing, Ju, Haibing, Gao, Li, Xiong, Yong, Dai, Rong, Huang, Xiangzhong, Yang, Cui
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.06.2019
• Subjects: 3T3-L1 Cells; Adipokines - metabolism; Adipose Tissue - metabolism; Adipose Tissue - pathology; Adipose tissue function; Animals; Cytokines - metabolism; Inflammation; Male; Mice; Nicotinic acetylcholine receptors α3 subtype; Receptors, Nicotinic - metabolism; Signal Transduction; α3-nAChR; Nicotinic acetylcholine receptors α3 subtype; HFD; Inflammation; CHO; WAT; PVDF; siRNAs; nAChRs; DMEM; HDL; TG; TNF-α; LDL; Adipose tissue function; ApoE
• ISSN: 1098-8823
• DOI: 10.1016/j.prostaglandins.2019.04.001

•The mechanisms triggering the adipose tissue dysfunction is still under debate.•There is a close relationship between α3-nAChR and inflammation.•The inhibition of α3-nAChR influences adipokines and inflammatory cytokines production and serum lipids release.•α3-nAChR may act as a novel therapeutical target to cardiometabolic diseases. Nicotinic acetylcholine receptor α3 subtype (α3-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 α3-nAChR could regulate the disorder of adipose functions. Adipocytokines and inflammatory cytokines were evaluated in apolipoprotein E knockout (ApoE−/−) mice after α3-nAChR was antagonized and in adipocytes after α3-nAChR gene was silenced. Results showed that in high fat diet-fed ApoE−/− mice with α3-nAChR blocked and in IL-6-stimulated adipocytes with α3-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 α3-nAChR-dependent signaling pathways in the regulation of adipose tissue dysfunction. A way may be paved for further investigations for the regulatory role of α3-nAChR in inflammatory and metabolic diseases.