Inflammation causes tissue-specific depletion of vitamin B6.

Inflammation causes tissue-specific depletion of vitamin B6.
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炎症会导致维生素B6的组织特异性耗竭。

DOI:
10.1186/ar1821
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发表时间:
2005
影响因子:
4.9
通讯作者:
Roubenoff R
Roubenoff R
中科院分区:
医学2区
文献类型:
--
作者:
Chiang EP;Smith DE;Selhub J;Dallal G;Wang YC;Roubenoff R

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以前,我们观察到维生素B6状态与类风湿关节炎患者的几个炎症指标之间存在强烈且一致的相关性。临床指标,包括残疾评分,晨僵时间和疼痛程度,以及生化标志物,包括红细胞沉降率和C反应蛋白水平,被发现与循环维生素B6水平呈负相关。这种强烈的关联意味着这些患者的维生素B6状态受损是由炎症引起的。在本研究中,我们研究了炎症是否直接改变体内维生素B6组织含量及其排泄。一项横断面病例对照人体临床试验与炎症动物模型中的实验平行进行。比较了患者和健康受试者的血浆和红细胞及吡哆醛5 '-磷酸盐浓度、尿4-吡哆酸排泄量和红细胞天冬氨酸转氨酶活性系数。在大鼠中诱导佐剂性关节炎,以研究急性和慢性炎症期间肝脏和肌肉的含量以及维生素B6的尿排泄。与健康对照组相比,类风湿性关节炎患者血浆5 '-磷酸吡哆醛水平较低,但红细胞5'-磷酸吡哆醛和尿4-吡哆酸排泄正常。大鼠佐剂关节炎不影响4-吡哆酸排泄或5 '-磷酸吡哆醛的肌肉储存,但它导致炎症期间循环和肝脏中5'-磷酸吡哆醛水平显着降低。炎症诱导了维生素B6的组织特异性消耗。在炎症中观察到的低血浆5 '-磷酸吡哆醛水平不太可能是由于摄入不足或过量的维生素B6排泄。维生素B6水平下降的可能原因进行了讨论。
Previously we observed strong and consistent associations between vitamin B6 status and several indicators of inflammation in patients with rheumatoid arthritis. Clinical indicators, including the disability score, the length of morning stiffness, and the degree of pain, and biochemical markers, including the erythrocyte sedimentation rate and C-reactive protein levels, were found to be inversely correlated with circulating vitamin B6 levels. Such strong associations imply that impaired vitamin B6 status in these patients results from inflammation. In the present study we examined whether inflammation directly alters vitamin B6 tissue contents and its excretion in vivo. A cross-sectional case-controlled human clinical trial was performed in parallel with experiments in an animal model of inflammation. Plasma and erythrocyte and pyridoxal 5'-phosphate concentrations, urinary 4-pyridoxic acid excretion, and the activity coefficient of erythrocyte aspartate aminotransferase were compared between patients and healthy subjects. Adjuvant arthritis was induced in rats for investigating hepatic and muscle contents as well as the urinary excretion of vitamin B6 during acute and chronic inflammation. Patients with rheumatoid arthritis had low plasma pyridoxal 5'-phosphate compared with healthy control subjects, but normal erythrocyte pyridoxal 5'-phosphate and urinary 4-pyridoxic acid excretion. Adjuvant arthritis in rats did not affect 4-pyridoxic acid excretion or muscle storage of pyridoxal 5'-phosphate, but it resulted in significantly lower pyridoxal 5'-phosphate levels in circulation and in liver during inflammation. Inflammation induced a tissue-specific depletion of vitamin B6. The low plasma pyridoxal 5'-phosphate levels seen in inflammation are unlikely to be due to insufficient intake or excessive vitamin B6 excretion. Possible causes of decreased levels of vitamin B6 are discussed.
DOI: 10.1016/s0021-9150(03)00161-8
发表时间: 2003-07-01
期刊: ATHEROSCLEROSIS
影响因子: 5.3
作者:
Folsom, AR;Desvarieux, M;Chambless, LE
通讯作者: Chambless, LE
DOI: 10.1093/ajcn/4.4.318
发表时间: 1956-01-01
影响因子: 7.1
作者:
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通讯作者: GREENBERG, LD
DOI: 10.1093/jn/121.3.318
发表时间: 1991-03-01
影响因子: 4.2
作者:
BODE, W;MOCKING, JAJ;VANDENBERG, H
通讯作者: VANDENBERG, H
DOI: 10.1017/s0007114599000380
发表时间: 1999-03-01
影响因子: 3.6
作者:
Bates, CJ;Pentieva, KD;Finch, S
通讯作者: Finch, S
DOI: 10.1093/ajcn/32.4.879
发表时间: 1979-01-01
影响因子: 7.1
作者:
GREGORY, JF;KIRK, JR
通讯作者: KIRK, JR