Gout and Metabolic Syndrome: a Tangled Web
Gout and Metabolic Syndrome: a Tangled Web
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DOI：
10.1007/s11926-017-0688-y
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发表时间：
2017-10-01
影响因子：
5
通讯作者：
Pillinger, Michael H.
中科院分区：
文献类型：
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作者：
Thottam, Gabrielle E.;Krasnokutsky, Svetlana;Pillinger, Michael H.
回顾的目的痛风的复杂性继续解开每一个新的调查。痛风位于多个内在复杂过程的交叉点，其患病率，对医疗保健成本的影响以及与重要并发症的关联使其越来越相关。痛风与2型糖尿病、高血压、高脂血症、心血管疾病、肾脏疾病和肥胖之间的相关性表明，痛风或其必要的前体高尿酸血症可能在代谢综合征的表现中起重要作用。在这篇综述中，我们分析了痛风和代谢综合征之间复杂的相互联系，通过回顾痛风的生理和流行病学与其主要的并发症的关系。最近的研究结果越来越多的证据支持痛风与代谢综合征的关联。更具体地说，人类研究和动物模型都表明，高尿酸血症可能在促进炎症、高血压和心血管疾病、脂肪生成和脂肪生成、胰岛素和葡萄糖失调以及肝脏疾病中起作用。果糖摄入与高血压、体重增加、葡萄糖耐量受损和血脂异常的发生率增加相关，并且是尿酸盐生物合成的关键驱动因素。AMP激酶（AMPK）是倾向于减轻代谢综合征的过程的中心调节剂。在肝细胞、白细胞和其他细胞内，果糖/尿酸盐代谢环驱动AMPK的关键抑制剂，包括AMP脱氨酶和果糖激酶，这可能使平衡向代谢综合征进展倾斜。初步证据表明，阻断细胞内尿酸盐合成的药物可以恢复AMPK活性，帮助维持代谢稳态。概述痛风既是一种炎症性疾病，也是一种代谢性疾病。随着对尿酸盐作用的进一步研究，适当的痛风管理是否可能减轻代谢综合征是一个不断发展的重要问题。
Purpose of review The complexity of gout continues to unravel with each new investigation. Gout sits at the intersection of multiple intrinsically complex processes, and its prevalence, impact on healthcare costs, and association with important co-morbidities make it increasingly relevant. The association between gout and type 2 diabetes, hypertension, hyperlipidemia, cardiovascular disease, renal disease, and obesity suggest that either gout, or its necessary precursor hyperuricemia, may play an important role in the manifestations of the metabolic syndrome. In this review, we analyze the complex interconnections between gout and metabolic syndrome, by reviewing gout's physiologic and epidemiologic relationships with its major co-morbidities.Recent findings Increasing evidence supports gout's association with metabolic syndrome. More specifically, both human studies and animal models suggest that hyperuricemia may play a role in promoting inflammation, hypertension and cardiovascular disease, adipogenesis and lipogenesis, insulin and glucose dysregulation, and liver disease. Fructose ingestion is associated with increased rates of hypertension, weight gain, impaired glucose tolerance, and dyslipidemia and is a key driver of urate biosynthesis. AMP kinase (AMPK) is a central regulator of processes that tend to mitigate against the metabolic syndrome. Within hepatocytes, leukocytes, and other cells, a fructose/urate metabolic loop drives key inhibitors of AMPK, including AMP deaminase and fructokinase, that may tilt the balance toward metabolic syndrome progression. Preliminary evidence suggests that agents that block the intracellular synthesis of urate may restore AMPK activity and help maintain metabolic homeostasis.Summary Gout is both an inflammatory and a metabolic disease. With further investigation of urate's role, the possibility of proper gout management additionally mitigating metabolic syndrome is an evolving and important question.