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首页> 外文期刊>American Journal of Physiology >p38gamma MAPK regulation of glucose transporter expression and glucose uptake in L6 myotubes and mouse skeletal muscle.
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p38gamma MAPK regulation of glucose transporter expression and glucose uptake in L6 myotubes and mouse skeletal muscle.

机译：p38gamma MAPK调节L6肌管和小鼠骨骼肌中葡萄糖转运蛋白表达和葡萄糖摄取。

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Skeletal muscle expresses at least three p38 MAPKs (alpha, beta, gamma). However, no studies have examined the potential regulation of glucose uptake by p38gamma, the isoform predominantly expressed in skeletal muscle and highly regulated by exercise. L6 myotubes were transfected with empty vector (pCAGGS), activating MKK6 (MKK6CA), or p38gamma-specific siRNA. MKK6CA-transfected cells had higher rates of basal 2-deoxy-d-[3H]glucose (2-DG) uptake (P < 0.05) but lower rates of 2,4-dinitrophenol (DNP)-stimulated glucose uptake, an uncoupler of oxidative phosphorylation that operates through an insulin-independent mechanism (P < 0.05). These effects were reversed when MKK6CA cells were cotransfected with p38gamma-specific siRNA. To determine whether the p38gamma isoform is involved in the regulation of contraction-stimulated glucose uptake in adult skeletal muscle, the tibialis anterior muscles of mice were injected with pCAGGS or wild-type p38gamma (p38gammaWT) followed by intramuscular electroporation. Basal and contraction-stimulated 2-DG uptake in vivo was determined 14 days later. Overexpression of p38gammaWT resulted in higher basal rates of glucose uptake compared with pCAGGS (P < 0.05). Muscles overexpressing p38gammaWT showed a trend for lower in situ contraction-mediated glucose uptake (P = 0.08) and significantly lower total GLUT4 levels (P < 0.05). These data suggest that p38gamma increases basal glucose uptake and decreases DNP- and contraction-stimulated glucose uptake, partially by affecting levels of glucose transporter expression in skeletal muscle. These findings are consistent with the hypothesis that activation of stress kinases such as p38 are negative regulators of stimulated glucose uptake in peripheral tissues.
机译：骨骼肌表达至少三个p38 MAPK（α，β，γ）。但是，没有研究检查过p38gamma对葡萄糖摄取的潜在调节作用，p38gamma主要在骨骼肌中表达，并受运动高度调节。用空载体（pCAGGS），激活MKK6（MKK6CA）或p38γ特异性siRNA转染L6肌管。 MKK6CA转染的细胞具有较高的基础2-脱氧-d- [3H]葡萄糖（2-DG）摄取率（P <0.05），但是具有较低的2,4-二硝基苯酚（DNP）刺激的葡萄糖摄取率，这是一种非偶联剂通过胰岛素非依赖性机制起作用的氧化磷酸化作用（P <0.05）。当MKK6CA细胞与p38gamma特异性siRNA共转染时，这些作用被逆转。为了确定p38gamma同工型是否参与成年骨骼肌收缩刺激的葡萄糖摄取的调节，给小鼠胫骨前肌注射pCAGGS或野生型p38gamma（p38gammaWT），然后进行肌内电穿孔。 14天后确定体内基础和收缩刺激的2-DG摄取。与pCAGGS相比，p38gammaWT的过表达导致更高的基础葡萄糖摄取率（P <0.05）。过度表达p38gammaWT的肌肉表现出原位收缩介导的葡萄糖摄取降低的趋势（P = 0.08），总GLUT4水平显着降低（P <0.05）。这些数据表明，p38gamma可部分影响骨骼肌中葡萄糖转运蛋白的表达水平，从而增加基础葡萄糖的摄取并降低DNP和收缩刺激的葡萄糖摄取。这些发现与这样的假设相一致，即应激激酶（例如p38）的激活是周围组织刺激的葡萄糖摄取的负调节剂。

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