内分泌
词汇介绍
拓展阅读
解析
hyperuricemic
释 义 n. 血（内）尿酸过多的；高尿酸血症的
例 句 AIM: To clarify the relationship of serum uric acid and insulin resistance with first-phase islet secretion in hyperuricemic patients, and the factors that influence them. 目的：明确发生高尿酸血症患者胰岛素抵抗和胰岛第一分泌时相及其影响因素。
概述
概述
高尿酸血症是指血液中存在异常高水平的尿酸。在体液的pH值条件下，尿酸主要以离子形式存在。体内尿酸盐的含量取决于食物中嘌呤的量，体内合成的尿酸盐量与排出的尿酸盐量之间是平衡的。在人类中，女性正常范围的上限为360 μmol/L（6mg/dL），男性为400 μmol/L（6.8 mg/dL）。许多因素导致高尿酸血症，包括遗传，胰岛素抵抗，铁超负荷，高血压，甲状腺机能减退，慢性肾病，肥胖，饮食，使用利尿剂（例如噻嗪类，袢利尿剂）和摄入过量的酒精饮料。其中，饮酒是最主要的原因。
病理机制
高尿酸血症的原因可分为三种功能类型：尿酸生成增加，尿酸排泄减少，混合型。产量增加的原因包括饮食中高水平的嘌呤和增加的嘌呤代谢。排泄减少的原因包括肾病，某些药物以及尿酸和其他分子之间排泄的竞争。混合的原因包括饮食中高水平的酒精和/或果糖，以及饥饿。
尿酸生成增加
富含嘌呤的饮食是高尿酸血症常见但轻微的原因。单独饮食原因通常不足以引起高尿酸血症。食物的嘌呤含量各不相同，富含嘌呤腺嘌呤和次黄嘌呤的食物在加剧高尿酸血症方面可能更显著。这种类型的高尿酸血症是实体器官移植的常见并发症。除了正常变异（具有遗传成分），肿瘤溶解综合征产生极端水平的尿酸，最主要的是可导致肾衰竭。
尿酸排泄减少
一些药物可通过减少排泄导致高尿酸血症，包括利尿剂，水杨酸盐，吡嗪酰胺，乙胺丁醇，烟酸，环孢素，2-乙基氨基-1,3,4-噻二唑和细胞毒性剂。生酮饮食会损害肾排泄尿酸，血压升高与肾功能受损和高尿酸血症（尽管这些相关性之间的因果关系还不知道）显著相关。
诊断方法
可以使用血液和尿液测试检测高尿酸血症。
治疗方法
已知尿酸晶体的沉淀和相反的溶解取决于溶液中的尿酸浓度，pH，钠浓度和温度。
复制标题软骨素对氧酸钾诱导的高尿酸血症小鼠的影响: 黄嘌呤氧化酶和尿酸转运蛋白1的下调
发表时间：2019-01-08
影响指数：2.5
作者： Dool-Ri Oh
期刊：BMC Complement Altern Med
In the present study, we demonstrated that ChondroT, a new complex herbal medication reduced serum UA in hyperuricemic mice by downregulating XOD activity and renal mURAT1. Because XOD and URAT1 are important targets to regulate hyperuricemia and gout, potassium oxonate-induced hyperuricemic mice were used as appropriate experimental models for investigating the mechanism underlying hyperuricemia. XOD plays an important role in the catabolism of purines. The XOD enzyme catalyzes the oxidation of hypoxanthine to xanthine and can further catalyze the oxidation of xanthine to UA. AP, an XOD inhibitor has been used as an anti-hyperuricemia agent and anti-gout In addition, febuxostat is a novel orally administered antihyperuricemic drug that reduces the production of UA in the body by XOD inhibition. We demonstrated that ChondroT inhibited XOD activity in vitro (Table 3). PO-treated mice can serve as a useful animal model for investigating hyperuricemia pathology. The intraperitoneal administration of 300 mg/kg PO for 7 days to mice increased the serum UA, decreased the urinary UA, and elevated the serum and liver XOD activity (Figs. 1 and 2). ChondroT significantly reduced the serum UA level, whereas it increased the urinary UA level in hyperuricemic mice (Fig. 1). Moreover, the ChondroT-treated mice showed a significant decreased in serum and liver XOD activity compared with that of the hyperuricemic mice (Fig. 2). Thus, the in vivo enzyme inhibitory activity of ChondroT is the net inhibitory activity of both XOD and xanthine dehydrogenase (XDH). Hyperuricemia is frequently observed in patients with chronic kidney disease and can be accompanied by an increase in serum Cr and BUN. Previous other studies reported that AP significantly blocked renal functional changes in PO-induced hyperuricemic rats and lowered Cr levels as well as UA in patients. We demonstrated that ChondroT significantly reduced the serum Cr and BUN levels in hyperuricemic mice (Table 4). Furthermore, liver dysfunction, poor blood flow in the liver and raised uric acid may cause hyperuricemia. In this study, PO-induced hyperuricemic mice increased liver damages by increasing the levels of two markers for liver damages, GOT, and GPT, which was attenuated by ChondroT and AP.
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