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BK Ca channel participates in insulin‐induced lipid deposition in adipocytes by increasing intracellular calcium
Author(s) -
Ren Jie,
Cheng Yuan,
Wen Xinxin,
Liu Ping,
Zhao Feng,
Xin Fang,
Wang Meili,
Huang Haixia,
Wang Wei
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30266
Subject(s) - adipose tissue , medicine , endocrinology , protein kinase b , chemistry , calcium in biology , intracellular , adipocyte , insulin , extracellular , calcium , pi3k/akt/mtor pathway , microbiology and biotechnology , phosphorylation , signal transduction , biology , biochemistry
Storing energy in the form of triglyceride (TG) is one of the basic functions of adipose tissue. Large‐conductance calcium‐activated potassium channels (BK Ca channels) are expressed in adipose tissue and adipocyte‐specific BK Ca deficiency resists obesity in mice, but the role of BK Ca channels in lipid deposition and the underlying mechanisms have not been elucidated. In the present study, we generated BK Ca knockout (KO) rats and performed a transcriptome analysis of adipose tissue. We found that the phosphoinositide 3‐kinase (PI3K)–protein kinase B (Akt) signaling pathway, which is important for lipid deposition, exhibited the most notable reduction among various signaling pathways in BK Ca KO rats compared to wild‐type rats. Insulin‐induced TG deposition, glucose uptake, and Akt (Ser473) phosphorylation were significantly reduced in cultured adipocytes differentiated from adipose‐derived stem cells of BK Ca KO rats. Furthermore, we found that the insulin‐induced increase of intracellular calcium resulting from extracellular calcium influx was significantly impaired in BK Ca KO adipocytes. Finally, insulin activated BK Ca currents through PI3K, which was independent of Akt and intracellular calcium. The results of this study suggested that BK Ca channels participate in the insulin signaling pathway and promote TG deposition by increasing extracellular calcium influx in adipocytes.