Nicotinic Acetylcholine Receptor Signaling Activates Beige Adipocytes and Mediates Systemic Metabolism.

Shanshan Liu, Kezhou Zhu, Wenwen Zhang, Tong Pan, Martin O'Brien, Ichitaro Abe, Lily Dale, Justin Piejak, Nadia Houssein, Biyang Zhang, Matthew Fein, Shingo Kajimura, Raymond Yung, X Z Shawn Xu, Jun Wu

Life Sciences Institute, University of Michigan, Ann Arbor, MI. · pubmed

Paper

Abstract

Beige-adipocyte activity, mediated by CHRNA2, significantly influences adipose function and systemic metabolism. The CHRNB2 subunit forms a functional receptor with CHRNA2 and is essential for the response to nicotinic acetylcholine receptor agonists in beige adipocytes. Deletion of Chrnb2 in mice compromises the adaptive response to cold in subcutaneous adipose tissue and renders exacerbated metabolic dysfunction due to diet-induced obesity. This cholinergic signaling within subcutaneous adipose tissue declines with aging. CHRNB2 partial agonists, a family of drugs clinically used for smoking cessation, activate both murine and human beige adipocytes.

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Research summary

The paper claims that nicotinic acetylcholine receptor signaling activates beige adipocytes, influencing systemic metabolism and potentially addressing metabolic dysfunction associated with aging. The research is relevant as it explores mechanisms that could impact metabolic health and aging, particularly through the modulation of adipose tissue function.

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