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14-3-3ζ mediates an alternative non-thermogenic mechanism in male mice to reduce heat loss and improve cold tolerance

机译:14-3-3ζ在雄性小鼠中介导替代非热化机制以减少热量损失提高耐寒性

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摘要

Adaptive thermogenesis, which is partly mediated by sympathetic input on brown adipose tissue (BAT), is a mechanism of heat production that confers protection against prolonged cold exposure. Various endogenous stimuli, for example, norepinephrine and FGF-21, can also promote the conversion of inguinal white adipocytes to beige adipocytes, which may represent a secondary cell type that contributes to adaptive thermogenesis. We previously identified an essential role of the molecular scaffold 14-3-3ζ in adipogenesis, but one of the earliest, identified functions of 14-3-3ζ is its regulatory effects on the activity of tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of norepinephrine. Herein, we examined whether 14-3-3ζ could influence adaptive thermogenesis via actions on BAT activation or the beiging of white adipocytes.
机译:适应性热生成,其部分地通过对棕色脂肪组织(BAT)的交感神经输入介导的,是一种热量生产的机制,赋予延长冷寒冷暴露的保护。各种内源性刺激,例如去甲肾上腺素和FGF-21,也可以促进膨胀性白色脂肪细胞的转化为米色adipocytes,其可以代表有助于适应性热生成的二次细胞类型。我们以前鉴定了分子支架14-3-3-在脂肪发生中的基本作用,但最早鉴定的函数中的一个是其对酪氨酸羟化酶的活性的调节作用,其速率限制酶脱甲肾上腺素的合成。在此,我们检查了14-3-3ζ是否可以通过对BAT活化的作用或白色脂肪细胞的抗凸出来影响适应性的热生成。

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