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Article(id=1198558170164593420, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1198558165093675863, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.1536.2024.0612, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1701360000000, receivedDateStr=2023-12-01, revisedDate=null, revisedDateStr=null, acceptedDate=1713888000000, acceptedDateStr=2024-04-24, onlineDate=1763688135901, onlineDateStr=2025-11-21, pubDate=1724774400000, pubDateStr=2024-08-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1763688135901, onlineIssueDateStr=2025-11-21, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1763688135901, creator=13701087609, updateTime=1763688135901, updator=13701087609, issue=Issue{id=1198558165093675863, tenantId=1146029695717560320, journalId=1189873630562394117, year='2024', volume='49', issue='8', pageStart='855', pageEnd='976', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1763688134691, creator=13701087609, updateTime=1763689174168, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1198562525043327039, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1198558165093675863, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1198562525043327040, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1198558165093675863, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=939, endPage=945, ext={EN=ArticleExt(id=1198558170412057368, articleId=1198558170164593420, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress on the relationship between abnormal uric acid metabolism and type 2 diabetes mellitus, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Uric acid, the end product of purine metabolism in human body, can lead to uric acid metabolism abnormality when its production and excretion are out of balance. This abnormality has emerged as one of the important risk factors for metabolic diseases, including diabetes, obesity, hypertension and metabolic syndrome. Recent studies have found that abnormal uric acid metabolism increases the risk of occurrence and development of type 2 diabetes mellitus (T2DM) and its complications, suggesting that uric acid metabolism could be a novel approach for intervening in T2DM. This review summarizes the research progress on how uric acid metabolism abnormality influences the occurrence, development and pathogenesis of T2DM, the beneficial effects of uric acid-lowering therapy, and the selection of hypoglycemic drugs on T2DM, which provide evidence for the early prevention and treatment of T2DM and its complications.

, correspAuthors=Zhen-Cheng Yan, authorNote=null, correspAuthorsNote=
E-mail:
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尿酸是人体内嘌呤代谢的终产物，当尿酸生成与排泄失衡时可发生尿酸代谢异常。尿酸代谢异常目前已成为代谢性疾病(如糖尿病、肥胖、高血压、代谢综合征)的重要危险因素之一。近年来研究发现，尿酸代谢异常增加了2型糖尿病(T2DM)及其并发症的发生风险，改善尿酸代谢可能是干预T2DM的新手段。本文主要从尿酸代谢异常对T2DM发生发展的影响及其机制、降尿酸疗法对T2DM的获益效果以及降糖药物的选择等方面阐述了尿酸代谢异常与T2DM关系的研究进展，以期为T2DM及其并发症的早期防治提供参考。

, correspAuthors=闫振成, authorNote=null, correspAuthorsNote=
闫振成，E-mail：
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杨若梅，硕士研究生，主治医师，主要从事内分泌与代谢性疾病的基础与临床研究

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杨若梅，硕士研究生，主治医师，主要从事内分泌与代谢性疾病的基础与临床研究

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杨若梅，硕士研究生，主治医师，主要从事内分泌与代谢性疾病的基础与临床研究

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Saudi J Biol Sci, 2019, 26(2): 421-426., articleTitle=Effects of sodium glucose cotransporter-2 inhibitors on serum uric acid in type 2 diabetes mellitus: a systematic review with an indirect comparison meta-analysis, refAbstract=null), Reference(id=1198558181321441492, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1198558170164593420, doi=null, pmid=null, pmcid=null, year=2021, volume=25, issue=14, pageStart=6733, pageEnd=6745, url=null, language=null, rfNumber=[47], rfOrder=46, authorNames=Jiao Z, Chen Y, Xie Y, journalName=J Cell Mol Med, refType=null, unstructuredReference=Jiao Z, Chen Y, Xie Y, et al. Metformin protects against insulin resistance induced by high uric acid in cardiomyocytes via AMPK signalling pathways in vitro and in vivo[J]. 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Diabetes Res Clin Pract, 2019, 153: 14-22., articleTitle=Exenatide twice-daily does not affect renal function or albuminuria compared to titrated insulin glargine in patients with type 2 diabetes mellitus: a post-hoc analysis of a 52-week randomised trial, refAbstract=null), Reference(id=1198558181489213659, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1198558170164593420, doi=null, pmid=null, pmcid=null, year=2020, volume=70, issue=4, pageStart=131, pageEnd=136, url=null, language=null, rfNumber=[49], rfOrder=48, authorNames=Kusunoki M, Sato D, Sakazaki T, journalName=Drug Res (Stuttg), refType=null, unstructuredReference=Kusunoki M, Sato D, Sakazaki T, et al. Effects of additional administration of a selective inhibitor of sodium glucose co-transporter-2 inhibitor on the glycemic control in Japanese type 2 diabetes mellitus patients receiving treatment with a dipeptidyl peptidase-4 inhibitor[J]. Drug Res (Stuttg), 2020, 70(4): 131-136., articleTitle=Effects of additional administration of a selective inhibitor of sodium glucose co-transporter-2 inhibitor on the glycemic control in Japanese type 2 diabetes mellitus patients receiving treatment with a dipeptidyl peptidase-4 inhibitor, refAbstract=null), Reference(id=1198558182172885213, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1198558170164593420, doi=null, pmid=null, pmcid=null, year=2022, volume=88, issue=8, pageStart=3627, pageEnd=3637, url=null, language=null, rfNumber=[50], rfOrder=49, authorNames=Najafi S, Bahrami M, Butler AE, journalName=Br J Clin Pharmacol, refType=null, unstructuredReference=Najafi S, Bahrami M, Butler AE, et al. The effect of glucagon-like peptide-1 receptor agonists on serum uric acid concentration: a systematic review and meta-analysis[J]. Br J Clin Pharmacol, 2022, 88(8): 3627-3637., articleTitle=The effect of glucagon-like peptide-1 receptor agonists on serum uric acid concentration: a systematic review and meta-analysis, refAbstract=null), Reference(id=1198558182361628898, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1198558170164593420, doi=null, pmid=null, pmcid=null, year=2015, volume=44, issue=5, pageStart=592, pageEnd=596, url=null, language=null, rfNumber=[51], rfOrder=50, authorNames=MacFarlane LA, Liu CC, Solomon DH, journalName=Semin Arthritis Rheum, refType=null, unstructuredReference=MacFarlane LA, Liu CC, Solomon DH. The effect of initiating pharmacologic insulin on serum uric acid levels in patients with diabetes: a matched cohort analysis[J]. 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PEP. 磷酸烯醇式丙酮酸；PEPCK. 磷酸烯醇式丙酮酸羧激酶；G-6-Pase. 葡萄糖-6-磷酸酶；AMPK. AMP活化蛋白激酶；NF-κB. 核因子-κB；PPAR-γ. 过氧化物酶体增殖物激活受体-γ；MCP-1. 单核细胞趋化蛋白-1；CXCL-1. 趋化因子C-X-C基序配体1；IL-6. 白细胞介素-6；ENPP1. 外核苷酸焦磷酸酶/磷酸二酯酶1；NO. 一氧化氮；ROS. 活性氧；ERK. 细胞外信号调节激酶；T2DM. 2型糖尿病

, figureFileSmall=8ouznfaXzD3hxnJmVSZ9lw==, figureFileBig=Pz6eMGcbRRtayT3X39f9uw==, tableContent=null), ArticleFig(id=1198558175025791974, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1198558170164593420, language=EN, label=Tab.1, caption=

Hypoglycemic drugs choice for T2DM with uric acid metabolism abnormality

, figureFileSmall=null, figureFileBig=null, tableContent=
降糖药物种类 代表药物 对血尿酸的影响 推荐建议 参考文献
SGLT-2抑制剂 达格列净、恩格列净、卡格列净 降低 推荐 [44-46,50]
二甲双胍 二甲双胍 降低 推荐 [47,50]
GLP-1RA 利拉鲁肽、度拉糖肽 降低 不推荐 [48,50]
DDP4抑制剂 利格列汀、西格列汀、阿格列汀 不明确 不推荐 [49,50]
胰岛素 胰岛素 升高 不推荐 [5,51]
), ArticleFig(id=1198558175130649579, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1198558170164593420, language=CN, label=表1, caption=

T2DM合并尿酸代谢异常患者降糖药物的选择

, figureFileSmall=null, figureFileBig=null, tableContent=
降糖药物种类 代表药物 对血尿酸的影响 推荐建议 参考文献
SGLT-2抑制剂 达格列净、恩格列净、卡格列净 降低 推荐 [44-46,50]
二甲双胍 二甲双胍 降低 推荐 [47,50]
GLP-1RA 利拉鲁肽、度拉糖肽 降低 不推荐 [48,50]
DDP4抑制剂 利格列汀、西格列汀、阿格列汀 不明确 不推荐 [49,50]
胰岛素 胰岛素 升高 不推荐 [5,51]
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尿酸代谢异常与2型糖尿病关系的研究进展
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杨若梅 , 闫振成 *
解放军医学杂志 | 综述 2024,49(8): 939-945
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解放军医学杂志 | 综述 2024, 49(8): 939-945
尿酸代谢异常与2型糖尿病关系的研究进展
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杨若梅, 闫振成*
作者信息
  • 陆军军医大学陆军特色医学中心高血压内分泌科，重庆 400042

    • 杨若梅，硕士研究生，主治医师，主要从事内分泌与代谢性疾病的基础与临床研究

通讯作者:

闫振成，E-mail：
Research progress on the relationship between abnormal uric acid metabolism and type 2 diabetes mellitus
Ruo-Mei Yang, Zhen-Cheng Yan*
Affiliations
  • Department of Hypertension and Endocrinology, Army Medical Center, Army Medical University, Chongqing 400042, China
出版时间: 2024-08-28 doi: 10.11855/j.issn.0577-7402.1536.2024.0612
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摘要
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尿酸是人体内嘌呤代谢的终产物，当尿酸生成与排泄失衡时可发生尿酸代谢异常。尿酸代谢异常目前已成为代谢性疾病(如糖尿病、肥胖、高血压、代谢综合征)的重要危险因素之一。近年来研究发现，尿酸代谢异常增加了2型糖尿病(T2DM)及其并发症的发生风险，改善尿酸代谢可能是干预T2DM的新手段。本文主要从尿酸代谢异常对T2DM发生发展的影响及其机制、降尿酸疗法对T2DM的获益效果以及降糖药物的选择等方面阐述了尿酸代谢异常与T2DM关系的研究进展，以期为T2DM及其并发症的早期防治提供参考。

尿酸  /  糖尿病，2型  /  代谢  /  嘌呤

Uric acid, the end product of purine metabolism in human body, can lead to uric acid metabolism abnormality when its production and excretion are out of balance. This abnormality has emerged as one of the important risk factors for metabolic diseases, including diabetes, obesity, hypertension and metabolic syndrome. Recent studies have found that abnormal uric acid metabolism increases the risk of occurrence and development of type 2 diabetes mellitus (T2DM) and its complications, suggesting that uric acid metabolism could be a novel approach for intervening in T2DM. This review summarizes the research progress on how uric acid metabolism abnormality influences the occurrence, development and pathogenesis of T2DM, the beneficial effects of uric acid-lowering therapy, and the selection of hypoglycemic drugs on T2DM, which provide evidence for the early prevention and treatment of T2DM and its complications.

uric acid  /  diabetes mellitus, type 2  /  metabolism  /  purine
杨若梅, 闫振成. 尿酸代谢异常与2型糖尿病关系的研究进展. 解放军医学杂志, 2024 , 49 (8) : 939 -945 . DOI: 10.11855/j.issn.0577-7402.1536.2024.0612
Ruo-Mei Yang, Zhen-Cheng Yan. Research progress on the relationship between abnormal uric acid metabolism and type 2 diabetes mellitus[J]. Medical Journal of Chinese People’s Liberation Army, 2024 , 49 (8) : 939 -945 . DOI: 10.11855/j.issn.0577-7402.1536.2024.0612
正文
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人体嘌呤代谢的终产物是尿酸[1]。嘌呤代谢障碍可引起血尿酸水平异常升高[2]，进而导致高尿酸血症和痛风[3]。近年来，随着生活方式及饮食结构的改变，我国高尿酸血症的患病率逐渐升高，且呈年轻化的趋势[4]，已成为仅次于糖尿病的第二大代谢性疾病，严重威胁民众健康[5]。既往研究发现，肥胖、高血压、血脂异常和缺血性脑卒中等疾病均可合并尿酸代谢异常[5-6]。近年的研究也发现，尿酸代谢异常还与2型糖尿病(type 2 diabetes mellitus，T2DM)及其并发症的发生发展有关，改善尿酸代谢可能是干预T2DM的新手段[7]。本文主要从尿酸代谢异常对T2DM发生发展的影响及其机制、降尿酸疗法对T2DM的获益效果以及降糖药物的选择等方面阐述尿酸代谢异常与T2DM关系的研究进展，旨在为T2DM及其并发症的早期防治提供参考。
1 尿酸代谢过程
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血尿酸水平取决于尿酸生成与排泄之间的平衡[8]。人体内的尿酸约20%由饮食摄入，80%由核苷酸分解代谢产生[5]。黄嘌呤氧化还原酶(xanthine oxidoreductase，XOR)是嘌呤代谢途径最后两个步骤中的限速酶，可将次黄嘌呤转化为黄嘌呤，并将黄嘌呤转化为尿酸[9]。XOR底物增多或酶活性增强均可导致血尿酸水平升高，进而引起高尿酸血症和痛风[9]。因此，XOR被认为是治疗高尿酸血症和痛风的有效靶点，多种XOR抑制剂药物(如别嘌呤醇、非布司他)已在临床广泛应用[10]。
血尿酸经肾小球全部滤过，再由肾近端小管重吸收-分泌-二次重吸收后，约占肾滤过总量10%的尿酸经尿液排出体外。经肾脏排泄的尿酸占全部尿酸排泄量的2/3，其余1/3的尿酸分泌至肠道中，由消化道进行排泄[11]。尿酸不能自由通过细胞膜，尿酸的重吸收和分泌依赖于尿酸离子通道蛋白或转运体。在尿酸的重吸收和分泌过程中，尿酸盐转运蛋白1(urate transporter 1，URAT1)、葡萄糖转运蛋白9(glucose transporter member 9，GLUT9)和有机阴离子转运体10(organic anion transporter 10，OAT10)等尿酸转运蛋白主要参与尿酸的重吸收，而OAT1、OAT3、钠依赖性磷酸转运蛋白1(sodium-dependent phosphate cotransporter type 1，NPT1)和NPT4等主要参与尿酸的分泌过程[11-12]。临床上常规使用的降尿酸药物苯溴马隆就是通过抑制URAT1，抑制肾小管对尿酸的重吸收，增加尿酸排泄，从而降低血尿酸水平[5]。
正常情况下，体内尿酸的生成与排泄保持平衡。凡是导致尿酸生成过多或排泄不足的因素均可引起血尿酸水平异常升高或高尿酸血症，其中肾功能不全导致尿酸排泄减少是尿酸代谢异常的重要病因。人体血液中尿酸的饱和浓度为420 μmol/L。当血尿酸的浓度超过这一饱和浓度时，尿酸盐晶体析出可直接黏附、沉积于关节及周围软组织、肾组织和血管等部位，导致这些部位组织的炎症和损害，如痛风性关节炎、尿酸盐肾病等[11]。在大多数哺乳动物体内，嘌呤代谢产生的尿酸被尿酸氧化酶进一步降解为尿囊素，但在人体内尿酸氧化酶基因发生突变，嘌呤不能被转化为尿囊素，而最终转化为尿酸，因此人体内的尿酸水平远高于其他哺乳动物[13-14]。尿酸氧化酶类似物是催化尿酸向尿囊素转化的生物制剂，可减少血尿酸、尿酸结晶沉积，并促进痛风石溶解，此类药物包括普瑞凯希、拉布立酶等[15]。
2 尿酸代谢异常与T2DM及其并发症
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2.1 增高T2DM的发生风险
血尿酸水平升高是T2DM发生的独立危险因素[5,16]。目前研究发现，基线血尿酸水平可用来预测胰岛素抵抗和T2DM的发生[17-18]。我国一项追踪9471例受试者的前瞻性临床研究发现，与健康受试者相比，高尿酸血症受试者1年后患糖尿病的风险增加1.20倍[17]。该研究还发现，与1年内血尿酸水平稳定(±10%)的受试者相比，血尿酸水平增加≥30%的人群患糖尿病的风险增加了30%(95%CI 1.01~1.79)，血尿酸水平减少≥10%的人群患糖尿病的风险降低了21%(95%CI 0.62~0.99)[17]。另一项针对5012名美国年轻人(18~30岁)随访15年的临床研究发现，基线血尿酸水平升高的人群患糖尿病和胰岛素抵抗的风险较未升高的人群分别增加了87%(95%CI 1.33~2.62)和36%(95%CI 1.23~1.51)[18]。以上研究表明，基线血尿酸水平与T2DM的患病风险呈正相关，可能是预测T2DM发生风险的新型血清标志物。
2.2 促进T2DM的并发症
血尿酸水平与T2DM患者的大血管病变存在相关性。血尿酸水平升高可增加T2DM患者发生冠心病、缺血性或出血性脑卒中、下肢动脉病变等疾病的发生风险[19]。Mannarino等[20]发现，与第2个四分位数(Q2)血尿酸水平(295~366 μmol/L)组相比，Q4组(>385 μmol/L)人群发生冠状动脉血管病变、脑血管病变、外周血管病变的比例均增高(分别为4.23% vs. 2.28%、2.71% vs. 0.87%、3.47% vs. 1.41%)，同时Q1组(<295 μmol/L)人群发生冠状动脉血管病变、脑血管病变、外周血管病变的比例也增高(分别为3.04% vs. 2.28%、2.06% vs. 0.87%、2.39% vs. 1.41%)，提示血尿酸水平降低也预示着T2DM患者的预后不良，这可能与尿酸的抗氧化能力降低有关[21]。
血尿酸水平也与T2DM患者的微血管病变密切相关。血尿酸水平较高的T2DM患者糖尿病肾病患病率明显增高，蛋白尿更严重，肾功能更差；此外，随着糖尿病肾病逐渐加重，血尿酸水平逐渐升高，即与肾功能正常和伴有微量白蛋白尿的糖尿病患者相比，伴有大量白蛋白尿的T2DM患者血尿酸水平更高[22]。但血尿酸与T2DM视网膜病变的关系仍不明确。Chen等[23]发现，与无视网膜病变的T2DM患者相比，T2DM视网膜病变患者的血尿酸水平明显升高；相较于非增殖性糖尿病视网膜病变(non-proliferative diabetic retinopathy，NPDR)患者，增殖性糖尿病视网膜病变(proliferative diabetic retinopathy，PDR)患者的血尿酸水平升高；多因素logistic回归分析显示，高尿酸水平与更严重的糖尿病视网膜病变相关。但另一项纳入2961例T2DM患者的横断面研究显示，尿酸水平与视网膜病变的严重程度相关不明显[22]。而一项荟萃分析显示，T2DM视网膜病变患者的血尿酸水平明显高于T2DM无视网膜病变患者，但NPDR与无视网膜病变的T2DM患者血尿酸水平差异不明显，提示血尿酸水平可能是反映T2DM视网膜病变严重程度的潜在生物标志物，但不能预测T2DM视网膜病变的发生[24]。然而，该结论尚需要更多的前瞻性临床研究来证实。血尿酸水平也是反映T2DM周围神经病变的潜在标志物。一项多中心横断面研究结果显示，血尿酸水平升高的T2DM患者周围神经病变的患病率明显增高[25]。Zhang等[26]发现，T2DM并发周围神经病变患者的血尿酸水平降低，较低的血尿酸水平可造成糖尿病周围神经病变，尤其是影响胫神经的传导速度，提示将血尿酸升高到一定水平可能会减轻T2DM周围神经病变的病情。而另一项基于我国25个省份人群的横断面研究发现，T2DM合并疼痛性神经病变的患者比例较高(57.2%)，尿酸水平过高(≥420 μmol/L)和过低(<150 μmol/L)均可导致周围神经病变的进展[27]。
因此，血尿酸水平与T2DM并发症发生风险之间存在着“U”形关系。血尿酸水平增高至高尿酸血症时可增加糖尿病并发症的发生风险，但血尿酸水平降低至低尿酸血症时同样也预示着糖尿病并发症的不良结局。对于尿酸代谢异常的高风险人群，检测血尿酸水平有助于及早实施分层管理。
3 尿酸代谢异常导致T2DM的机制
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3.1 内皮细胞功能障碍
血管内皮细胞可分泌多种血管活性物质，包括血管扩张剂(NO、前列腺素Ⅰ2、内皮衍生因子等)和血管收缩剂(内皮素-1、凝血酶A2、血管紧张素Ⅱ等)。目前认为，胰岛素能够增加一氧化氮合酶的表达，并增加NO的释放，对于维持血管内皮的正常功能至关重要[28-29]。反过来，血管内皮细胞的功能状态可影响胰岛素的作用，从而参与糖代谢的调节。因此，血管内皮功能改变是糖尿病和血管并发症发病的重要因素，主要是导致胰岛素抵抗。内皮细胞影响糖代谢的过程主要跟两个因素有关：胰岛素跨内皮细胞转运和内皮细胞的调节。内皮细胞对胰岛素的转运直接决定了到达细胞中的胰岛素含量，且内皮细胞分泌的血管活性物质也会影响胰岛素敏感性，如内皮素-1可降低胰岛素的敏感性[29]。
在XOR催化尿酸生成的过程中，还伴有NADH、活性氧(reactive oxygen species，ROS)等生物分子产生[30]。体内的自由基与抗氧化剂失衡，导致ROS水平过高被定义为氧化应激[1]。氧化应激被认为是细胞损伤和疾病预后不良的重要原因之一。高水平尿酸一方面可直接与细胞内NO结合，导致NO生物利用度降低，另一方面可激活肾素-血管紧张素系统(renin-angiotensin system，RAS)，使血管紧张素Ⅱ水平升高[31]，刺激血管内皮细胞产生ROS，导致氧化应激和慢性低度炎症反应，直接影响β细胞的功能，也可导致胰岛素抵抗，进而导致糖尿病的发生[28]。
3.2 胰岛素抵抗
一项纳入354例T2DM高危患者(有≥2个危险因素)进行口服葡萄糖耐量试验(oral glucose tolerance test，OGTT)的研究显示，血尿酸水平与受试者胰岛素抵抗稳态模型评估(homeostasis model assessment of insulin resistance，HOMA-IR)指数呈正相关，该研究结果支持“血尿酸通过诱导胰岛素抵抗导致T2DM发生”的假说[32]。该假说分子机制层面的证据包括：(1)尿酸抑制脂肪细胞过氧化物酶体增殖物激活受体-γ(peroxisome proliferator activated receptor-γ，PPAR-γ)的活化，抑制脂联素(一种胰岛素增敏激素)的生成，诱发脂肪细胞内促炎因子如单核细胞趋化蛋白-1(monocyte chemotactic protein-1，MCP-1)的生成，进而导致胰岛素抵抗。在代谢综合征小鼠中，别嘌呤醇在降尿酸的同时可增加脂联素的生成，抑制MCP-1的表达，从而减轻脂肪组织中的胰岛素抵抗，提示高尿酸血症可能是脂肪组织胰岛素抵抗的重要因素[33]。(2)尿酸能够将外核苷酸焦磷酸酶/磷酸二酯酶1(ectonucleotide pyrophosphatase/phosphodiesterase 1，ENPP1)募集到胰岛素受体上，直接干扰胰岛素信号通路，导致胰岛素信号转导受损及胰岛素抵抗[34]。
3.3 炎症、胰腺β细胞死亡
尿酸除了诱导胰岛素抵抗外，还可引起胰腺细胞炎症损伤及β细胞死亡，从而导致T2DM的发生，其分子机制：(1)尿酸可激活核因子-κB(nuclear transcription factor-κB，NF-κB)炎症信号通路，促进NF-κB核转位及炎性介质如MCP-1、趋化因子C-X-C基序配体1(chemokine C-X-C motif ligand 1，CXCL-1)和白细胞介素-6(interleukin-6，IL-6)的生成，诱导胰腺低度炎症[35]；(2)尿酸可激活RAS，增加胰腺细胞内ROS水平，诱导胰腺细胞AMP活化蛋白激酶(AMP-activated protein kinase，AMPK)磷酸化，进而增强胰腺细胞外信号调节激酶(extracellular signal-regulated kinase，ERK)磷酸化，触发胰腺β细胞死亡和胰岛素分泌受损[35]；(3)尿酸可促进诱导型一氧化氮合酶合成NO，而过量NO也可抑制胰岛素分泌及促进β细胞凋亡[35]。
3.4 糖异生
尿酸也可刺激肝脏糖异生，使血糖升高。Cicerchi等[36]发现，尿酸可阻断肝脏AMPK活性，激活糖异生的关键限速酶(磷酸烯醇式丙酮酸羧激酶、葡萄糖-6-磷酸酶)基因的表达，增加肝脏糖异生。
因此，尿酸代谢异常可导致T2DM，其致病过程可能是多因素介导的。尿酸导致的内皮细胞功能障碍、胰岛素抵抗、胰岛素分泌受损和肝脏糖异生等可能协同参与了该发病过程(图1)。
4 降尿酸疗法对T2DM的获益效果
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4.1 对T2DM合并高尿酸血症的疗效
由于高水平尿酸是T2DM的致病因素，从理论上来说，降尿酸疗法可使合并高尿酸血症的T2DM患者获益。对糖尿病大鼠模型的研究发现，别嘌呤醇或非布司他可抑制糖尿病大鼠的异常XOR活性，改善糖尿病大鼠的血管内皮功能和肾功能[37]。在小鼠模型中，非布司他在改善葡萄糖耐量和胰岛素抵抗方面优于别嘌呤醇[38]。但是，在人体内通过降低血尿酸水平来预防或治疗T2DM及其并发症的证据仍十分有限。一项随机对照试验发现，别嘌呤醇可改善T2DM合并高尿酸血症患者的胰岛素抵抗，延缓动脉粥样硬化的发展[39]，提示对于T2DM合并高尿酸血症人群来说，降低血尿酸水平有助于延缓T2DM的进展。
4.2 对T2DM合并痛风的疗效
在痛风人群中，降尿酸疗法是否能改善T2DM结局的研究结果并不一致。我国台湾学者发现，接受磺吡酮和别嘌呤醇治疗的痛风患者发生T2DM的风险均明显低于未接受降尿酸治疗者[40]。但另一项台湾学者的研究发现，长时间或高剂量使用降尿酸药物的痛风患者T2DM的患病风险增加；相对于未使用降尿酸药物人群，使用别嘌呤醇和苯溴马隆人群T2DM的患病风险分别增高了17%(95%CI 1.07~1.28)和9%(95%CI 1.03~1.15)[41]。一项荟萃分析结果显示，痛风患者使用别嘌呤醇治疗与T2DM的发生风险相关不明显(HR=1.01，95%CI 0.55~1.84)[42]。笔者认为T2DM的致病因素是多样的，且可能存在异质性，痛风患者仅降低血尿酸水平而不改善其他危险因素(如缺乏运动、睡眠不足、肥胖)不足以预防和延缓T2DM的病情进展。
5 T2DM合并尿酸代谢异常的降糖药物选择
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T2DM合并尿酸代谢异常的患者在选择降糖药物时，推荐优先考虑具有明确降低尿酸证据的药物，并根据尿酸水平的变化适当调整药物剂量。钠-葡萄糖协同转运蛋白2(sodium-dependent glucose transporters 2，SGLT-2)抑制剂是一类已经应用于临床的新型降糖药物，可选择性抑制SGLT-2蛋白，从而抑制肾小管对葡萄糖的重吸收，增加尿糖排泄，在不依赖胰岛素降低血糖的同时也可降低尿蛋白，可能在糖尿病患者中具有潜在的肾脏保护作用[5,43]。近期研究发现，SGLT-2抑制剂可明显降低T2DM患者的血尿酸水平[44-46]。例如，达格列净(10 mg/d)治疗90 d后，血尿酸水平下降，尿液中的尿酸水平升高[44]。吕继宏等[45]发现，恩格列净和达格列净分别可使74%、68%的T2DM合并轻度高尿酸血症患者的血尿酸水平恢复正常(血尿酸控制在≤420 μmol/L)，两组的有效率均高于对照组(40%)。一项纳入13 650例患者的荟萃分析也显示，T2DM患者接受SGLT-2抑制剂治疗后，血清尿酸水平明显降低，其中卡格列净可使尿酸水平降低约37.02 μmol/L，达格列净可使尿酸水平降低约38.05 μmol/L，恩格列净可使尿酸水平降低约42.07 μmol/L[46]。还有研究发现，二甲双胍可增加细胞内的葡萄糖摄取并改善尿酸诱导的胰岛素抵抗，因而既可降低血糖，也可降低血尿酸水平[47]。
研究发现，胰高血糖素样肽-1受体激动剂(glucagon-like peptide-1 receptor agonist，GLP-1RA)治疗T2DM患者1年后，几乎不影响其肾功能和尿酸水平[48]。日本学者发现单纯采用二肽基肽酶4(dipeptidyl peptidase 4，DPP4)抑制剂(如利格列汀、西格列汀)治疗T2DM患者6个月后，其血尿酸水平有所升高，而联合使用达格列净、鲁格列净、恩格列净等SGLT-2抑制剂治疗后血尿酸水平才明显降低[49]。然而，利格列汀等DDP4抑制剂具有黄嘌呤样结构，可抑制XOR的活性，导致嘌呤代谢减弱、血尿酸水平降低[50]。因此，DDP4抑制剂对血尿酸水平的影响尚不明确。荟萃分析显示，SGLT-2抑制剂、二甲双胍较GLP-1RA和DDP4抑制剂更能有效地降低血尿酸水平[50]。此外，胰岛素可升高血尿酸水平并诱发痛风，通常发生在内源性高胰岛素血症患者(如肥胖)[5,51]。
总之，T2DM合并高尿酸血症或痛风患者可优先选用SGLT-2抑制剂和具有改善胰岛素抵抗作用的药物如二甲双胍(表1)。
6 总结与展望
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尿酸代谢异常不仅是糖尿病发病过程的始动因素，还可促进糖尿病相关并发症的发生发展。尽管有证据支持降尿酸治疗对T2DM有益，但尿酸代谢异常与糖尿病之间的因果关系尚未完全阐明。今后的前瞻性临床研究和随机对照试验应侧重于探索血尿酸与T2DM之间的因果关系，尿酸在糖尿病发病及并发症风险筛查中的效用，以及生活方式改变在血糖和尿酸管理中的作用等。未来的基础性或应用性研究需借助大数据、人工智能、代谢组学等现代技术，深入研究尿酸致糖尿病的机制及其在糖尿病个体化诊疗中的价值，挖掘在传统危险因素之上进行风险分层的有价值的生物学标志物等。在预防策略的制定上，可考虑将血尿酸作为胰岛素抵抗、T2DM进展的早期预警指标用于人群筛查，并尽早采取防治措施，如选用兼具降尿酸作用的降糖药物、选择低嘌呤食物等。
基金
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  • 国家自然科学基金面上项目(81870614)
文献
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doi: 10.11855/j.issn.0577-7402.1536.2024.0612
  • 接收时间：2023-12-01
  • 首发时间：2025-11-21
  • 出版时间：2024-08-28
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  • 收稿日期：2023-12-01
  • 录用日期：2024-04-24
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National Natural Science Foundation of China(81870614)
国家自然科学基金面上项目(81870614)
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    陆军军医大学陆军特色医学中心高血压内分泌科，重庆 400042

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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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