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.
Keywords: Adipose tissue function; Inflammation; Nicotinic acetylcholine receptors α3 subtype.
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