Key result
Inhibition of kcnma1 expression or treatment with a BK channel blocker attenuated insulin-induced Akt phosphorylation in mature adipocytes.
KCNMA1 contributes to the regulation of insulin signalling in mature adipocytes, highlighting a potential mechanism in metabolic dysfunction.
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May link BK channel loss to adipocyte insulin resistance; leaves open therapeutic targeting in obesity.
channels, referred to as BK channels, which play key roles in various physiological functions. However, the role of KCNMA1 in mature adipocytes remains unclear. In this study, we reveal that kcnma1 expression is downregulated in white adipose tissue of mice fed a high-fat diet and in hypertrophied adipocytes. Furthermore, inhibition of kcnma1 expression or treatment with a BK channel blocker attenuated insulin-induced Akt phosphorylation in mature adipocytes. These results strongly indicate that KCNMA1 contributes to the regulation of insulin signalling in mature adipocytes.
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Nishizuka et al. (2016) studied Insulin signalling in mature adipocytes. Inhibition of kcnma1 expression or BK channel blocker was evaluated on Insulin-induced Akt phosphorylation. Inhibition of kcnma1 expression or treatment with a BK channel blocker attenuated insulin-induced Akt phosphorylation in mature adipocytes.
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