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首页> 外文期刊>American Journal of Physiology >Albumin turnover: FcRn-mediated recycling saves as much albumin from degradation as the liver produces.
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Albumin turnover: FcRn-mediated recycling saves as much albumin from degradation as the liver produces.

机译：白蛋白周转率：FcRn介导的回收与肝脏产生的白蛋白一样，可以避免降解。

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摘要

It is now understood that the nonclassical major histocompatibility complex-I molecule FcRn binds albumin and retrieves it from an intracellular degradative fate. Whether FcRn in the liver modulates albumin turnover through effects on biosynthesis and production is not known. Thus we quantified the appearance of biosynthetically labeled albumin in plasma after an intravenous bolus injection of [(3)H]leucine in FcRn-deficient mice. The production rates for both albumin (FcRn substrate) and transferrin (nonsubstrate) are increased by approximately 20% in FcRn-deficient mice compared with normal mice, likely compensating for the lowered plasma oncotic pressure caused by hypoalbuminemia in FcRn-deficient mice. Determining the magnitude of FcRn-mediated effects on albumin turnover, we then measured the steady-state plasma concentrations of biosynthetically labeled albumin and transferrin during [(3)H]leucine infusion. The concentration of albumin was approximately 40% lower in FcRn-deficient mice compared with normal mice. Furthermore, the approximately 40% lower plasma albumin concentration in FcRn-deficient mice along with the approximately 20% increase in albumin production indicate, by the mass-balance equation, that albumin degradation in FcRn-deficient mice is twice that of normal mice. These studies of biosynthetically labeled, and thus native, albumin support our previous finding that FcRn protects albumin from degradation. Permitting quantification of the magnitude of FcRn-mediated recycling, they further indicate that FcRn has extraordinary capacity: the amount of albumin saved from degradation by FcRn-mediated recycling is the same as that produced by the liver.
机译：现已理解，非经典的主要组织相容性复合物-I分子FcRn结合白蛋白并从细胞内降解的命运中回收白蛋白。肝脏中的FcRn是否通过影响生物合成和生产来调节白蛋白更新。因此，我们量化了在FcRn缺陷型小鼠中静脉推注[（3）H]亮氨酸后血浆中生物合成标记的白蛋白的出现。与正常小鼠相比，在FcRn缺陷小鼠中白蛋白（FcRn底物）和转铁蛋白（非底物）的生产率均增加了约20％，这可能弥补了FcRn缺陷小鼠中由低白蛋白血症引起的血浆渗透压降低。确定FcRn介导的对白蛋白更新的影响的大小，然后我们在[（3）H]亮氨酸输注过程中测量了生物合成标记的白蛋白和转铁蛋白的稳态血浆浓度。与正常小鼠相比，FcRn缺陷型小鼠的白蛋白浓度低约40％。此外，通过质量平衡方程，在FcRn缺陷型小鼠中血浆白蛋白浓度降低约40％，同时白蛋白产生量增加约20％，表明FcRn缺陷型小鼠中白蛋白降解是正常小鼠的两倍。这些对生物合成标记的，因此是天然白蛋白的研究支持了我们先前的发现，即FcRn保护白蛋白免于降解。他们允许对FcRn介导的再循环的数量进行量化，进一步表明FcRn具有非凡的能力：通过FcRn介导的再循环从降解中保存的白蛋白量与肝脏产生的量相同。

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