Effects of acute inflammation on plasma retinol, retinol-binding protein, and its mRNA in the liver and kidneys of vitamin A-sufficient rats.
Effects of acute inflammation on plasma retinol, retinol-binding protein, and its mRNA in the liver and kidneys of vitamin A-sufficient rats.
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发表时间：
1996-05
影响因子：
6.5
通讯作者：
Francisco;Rosales;S. J. Ritter;R. Zolfaghari;E. Smith;A. Rossl
中科院分区：
文献类型：
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作者：
Francisco;Rosales;S. J. Ritter;R. Zolfaghari;E. Smith;A. Rossl
对组织损伤和感染的急性炎症反应与低浓度的血浆视黄醇及其特异性转运蛋白、视黄醇结合蛋白（RBP）和甲状腺素运载蛋白（TTR）有关。为了研究低视网膜血症的动力学和机制，我们用脂多糖（LPS，来自铜绿假单胞菌）在维生素A储备充足的大鼠中诱导急性炎症。在用LPS（每100 g体重腹腔注射50微克）或盐水和食物戒断治疗后24小时，5只LPS治疗的大鼠的血浆视黄醇等于0.72 +/- 0.06 mumol/L（平均值+/- SEM），而5只盐水治疗的大鼠的血浆视黄醇等于1.35 +/- 0.1 mumol/L（P < 0.01）。血浆、肝脏和肾脏RBP和TTR浓度也显著降低，但治疗组之间肝脏和肾脏视黄醇浓度无差异。肝脏中RBP mRNA的相对丰度（LPS处理与盐水处理相比）早在12 h就降低（0.44 +/- 0.15，n = 4对，P < 0.02），并在24 h继续降低（0.57 +/- 0.12，n = 5对，P < 0.02）。在肾脏中，由于LPS处理，该比率没有显著变化。细胞视黄醇结合蛋白（CRBP）mRNA在肝脏和肾脏的相对丰度也不受LPS治疗。我们从这些数据中推断，炎症诱导的低视网膜血症的结果，在肝脏合成的RBP和分泌的视黄醇-RBP复合物的减少。此外，结果表明，血浆视黄醇浓度是炎症期间维生素A状态的不良指标。
The acute inflammatory response to tissue injury and infection is associated with low concentrations of plasma retinol and its specific transport proteins, retinol-binding protein (RBP) and transthyretin (TTR). To examine the kinetics and mechanism of hyporetinemia, we have induced acute inflammation with lipopolysaccharide (LPS, from Pseudomonas aeruginosa) in rats with adequate stores of vitamin A. Twenty-four h after treatment with LPS (50 micrograms i.p. per 100 g body weight) or saline and food withdrawal, plasma retinol equalled 0.72 +/- 0.06 mumol/L (mean +/- SEM) in five LPS-treated rats versus 1.35 +/- 0.1 mumol/L in five saline-treated rats (P < 0.01). Plasma, liver, and kidney RBP and TTR concentrations were also significantly reduced, but liver and kidney retinol concentrations did not differ between treatment groups. The relative abundance of RBP mRNA in liver (LPS treatment compared to saline treatment) was reduced as early as 12 h (0.44 +/- 0.15, n = 4 pairs, P < 0.02), and continued to be reduced at 24 h (0.57 +/- 0.12, n = 5 pairs, P < 0.02). In the kidney this ratio did not change significantly due to LPS treatment. The relative abundance of cellular retinol-binding protein (CRBP) mRNA in liver and kidney also was not affected by LPS treatment. We infer from these data that inflammation-induced hyporetinemia results from a reduction in the hepatic synthesis of RBP and secretion of the retinol-RBP complex. Moreover, the results imply that plasma retinol concentration is a poor indicator of vitamin A status during inflammation.