Among the fascinating adaptations to limiting oxygen conditions (hypoxia) is the suppression of food intake and weight loss. In humans, this phenomenon is called high‐altitude anorexia and is observed in people suffering from acute mountain syndrome. The high‐altitude anorexia appears to be conserved in evolution and has been seen in species across the animal kingdom. However, the mechanism underlying the recovery of eating behavior after hypoxia is still not known. Here, we show that the phosphatidylinositol transfer protein PITP‐1 is essential for the fast recovery of eating behavior after hypoxia in the nematode Caenorhabditis elegans. Unlike the neuroglobin GLB‐5 that accelerates the recovery of eating behavior through its function in the oxygen (O2)‐sensing neurons, PITP‐1 appears to act downstream, in neurons that express the mod‐1 serotonin receptor. Indeed, pitp‐1 mutants display wild‐type‐like O2‐evoked‐calcium responses in the URX O2‐sensing neuron. Intriguingly, loss‐of‐function of protein kinase C 1 (PKC‐1) rescues pitp‐1 mutants’ recovery after hypoxia. Increased diacylglycerol (DAG), which activates PKC‐1, attenuates the recovery of wild‐type worms. Together, these data suggest that PITP‐1 enables rapid recovery of eating behavior after hypoxia by limiting DAG’s availability, thereby limiting PKC activity in mod‐1‐expressing neurons.

中文翻译：

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磷脂酰肌醇转移蛋白 PITP-1 促进线虫秀丽隐杆线虫缺氧后进食行为的快速恢复

对限制氧气条件（缺氧）的迷人适应包括抑制食物摄入和体重减轻。在人类中，这种现象被称为高海拔厌食症，在患有急性高山综合症的人中观察到。高原厌食症似乎在进化过程中是保守的，并且已经在整个动物界的物种中看到。然而，缺氧后饮食行为恢复的机制尚不清楚。在这里，我们表明磷脂酰肌醇转移蛋白 PITP-1 对于线虫秀丽隐杆线虫缺氧后进食行为的快速恢复至关重要。与通过其在氧 (O2) 感应神经元中的功能加速进食行为恢复的神经红蛋白 GLB-5 不同，PITP-1 似乎在下游起作用，在表达 mod-1 血清素受体的神经元中。事实上，pitp-1 突变体在 URX O2 感应神经元中显示出类似野生型的 O2 诱发的钙反应。有趣的是，蛋白激酶 C 1 (PKC-1) 的功能丧失可以挽救 pitp-1 突变体在缺氧后的恢复。激活 PKC-1 的二酰基甘油 (DAG) 的增加减弱了野生型蠕虫的恢复。总之，这些数据表明 PITP-1 通过限制 DAG 的可用性使缺氧后的进食行为能够快速恢复，从而限制表达 mod-1 的神经元中的 PKC 活性。减弱野生型蠕虫的恢复。总之，这些数据表明 PITP-1 通过限制 DAG 的可用性使缺氧后的进食行为能够快速恢复，从而限制表达 mod-1 的神经元中的 PKC 活性。减弱野生型蠕虫的恢复。总之，这些数据表明 PITP-1 通过限制 DAG 的可用性使缺氧后的进食行为能够快速恢复，从而限制表达 mod-1 的神经元中的 PKC 活性。