• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

那格列奈对一名患有复合杂合子ABCC8突变的儿童的反应性低血糖糖尿病有效。

Nateglinide is Effective for Diabetes Mellitus with Reactive Hypoglycemia in a Child with a Compound Heterozygous ABCC8 Mutation.

作者信息

Saito-Hakoda Akiko, Yorifuji Tohru, Kanno Junko, Kure Shigeo, Fujiwara Ikuma

机构信息

Department of Pediatrics, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Clin Pediatr Endocrinol. 2012 Jul;21(3):45-52. doi: 10.1297/cpe.21.45. Epub 2012 Jul 25.

DOI:10.1297/cpe.21.45
PMID:23926410
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3687649/
Abstract

ABCC8 encodes the sulfonylurea receptor 1 (SUR1) subunits of the beta-cell ATP-sensitive potassium (K-ATP) channel playing a critical role in the regulation of insulin secretion, and inactivating mutations in ABCC8 cause congenital hyperinsulinism. Recently, ABCC8 inactivating mutations were reported to be involved in the development of diabetes mellitus later in life. We report a girl who was born macrosomic with transient hypoglycemia and thereafter developed diabetes mellitus accompanied by severe reactive hypoglycemia at the age of 11 yr. An OGTT (oral glucose tolerance test) revealed hyperglycemia due to poor early insulin response and subsequent hypoglycemia due to delayed prolonged insulin secretion. Hypoglycemia was improved by the combination of nateglinide, which stimulates early insulin secretion, and an alpha-glucosidase inhibitor, voglibose. Sequencing of the ABCC8 identified a compound heterozygous mutation (R1420H/F591fs604X), suggesting that this mutation may alter regulation of insulin secretion with advancing age, leading to diabetes mellitus with reactive hypoglycemia from hyperinsulinism. Therefore, long-term follow-up and periodic OGTTs are important for early detection of insulin dysregulation in congenital hyperinsulinism patients carrying the ABCC8 mutation, even though hypoglycemia resolves spontaneously during infancy. Furthermore, nateglinide may be useful therapeutically in the treatment of not only diabetes mellitus but also reactive hypoglycemia.

摘要

ABCC8基因编码β细胞ATP敏感性钾(K-ATP)通道的磺脲类受体1(SUR1)亚基,该通道在胰岛素分泌调节中起关键作用,ABCC8基因的失活突变会导致先天性高胰岛素血症。最近,有报道称ABCC8基因失活突变与晚年糖尿病的发生有关。我们报告了一名出生时巨大儿且有短暂低血糖的女孩,此后在11岁时患糖尿病并伴有严重的反应性低血糖。口服葡萄糖耐量试验(OGTT)显示,早期胰岛素反应不佳导致血糖升高,随后胰岛素分泌延迟延长导致低血糖。刺激早期胰岛素分泌的那格列奈与α-葡萄糖苷酶抑制剂伏格列波糖联合使用可改善低血糖症状。对ABCC8基因进行测序发现了一个复合杂合突变(R1420H/F591fs604X),这表明该突变可能随着年龄增长改变胰岛素分泌调节,导致因高胰岛素血症引起的反应性低血糖的糖尿病。因此,对于携带ABCC8基因突变的先天性高胰岛素血症患者,即使低血糖在婴儿期自发缓解,长期随访和定期进行OGTT对于早期发现胰岛素调节异常也很重要。此外,那格列奈不仅在治疗糖尿病方面可能有用,在治疗反应性低血糖方面也可能有效。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b5a/3687649/c67ed424c195/cpe-21-045-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b5a/3687649/5fcc6d1b10ec/cpe-21-045-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b5a/3687649/c67ed424c195/cpe-21-045-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b5a/3687649/5fcc6d1b10ec/cpe-21-045-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b5a/3687649/c67ed424c195/cpe-21-045-g002.jpg

相似文献

1
Nateglinide is Effective for Diabetes Mellitus with Reactive Hypoglycemia in a Child with a Compound Heterozygous ABCC8 Mutation.那格列奈对一名患有复合杂合子ABCC8突变的儿童的反应性低血糖糖尿病有效。
Clin Pediatr Endocrinol. 2012 Jul;21(3):45-52. doi: 10.1297/cpe.21.45. Epub 2012 Jul 25.
2
ABCC8 (SUR1) and KCNJ11 (KIR6.2) mutations in persistent hyperinsulinemic hypoglycemia of infancy and evaluation of different therapeutic measures.ABCC8(SUR1)和KCNJ11(KIR6.2)突变与婴儿持续性高胰岛素血症性低血糖症及不同治疗措施的评估
J Pediatr Endocrinol Metab. 2002 Jul-Aug;15(7):993-1000. doi: 10.1515/jpem.2002.15.7.993.
3
Novel de novo mutation in sulfonylurea receptor 1 presenting as hyperinsulinism in infancy followed by overt diabetes in early adolescence.磺脲类受体1的新型新发突变,表现为婴儿期高胰岛素血症,随后在青春期早期发展为显性糖尿病。
Diabetes. 2008 Jul;57(7):1935-40. doi: 10.2337/db08-0159. Epub 2008 Apr 4.
4
Genetics and Natural History of Non-pancreatectomized Patients With Congenital Hyperinsulinism Due to Variants in ABCC8.ABCC8 基因突变致先天性高胰岛素血症未行胰腺切除术患者的遗传学和自然史
J Clin Endocrinol Metab. 2023 Oct 18;108(11):e1316-e1328. doi: 10.1210/clinem/dgad280.
5
Hyperinsulinemic hypoglycemia evolving to gestational diabetes and diabetes mellitus in a family carrying the inactivating ABCC8 E1506K mutation.一个携带 ABCC8 E1506K 失活突变的家族中出现高胰岛素血症性低血糖症发展为妊娠期糖尿病和糖尿病。
Pediatr Diabetes. 2010 Nov;11(7):505-8. doi: 10.1111/j.1399-5448.2009.00626.x.
6
Diabetes and hypoglycaemia in young children and mutations in the Kir6.2 subunit of the potassium channel: therapeutic consequences.幼儿糖尿病与低血糖以及钾通道Kir6.2亚基突变:治疗后果
Diabetes Metab. 2006 Dec;32(6):569-80. doi: 10.1016/S1262-3636(07)70311-7.
7
Identification of a compound heterozygous inactivating ABCC8 gene mutation responsible for young-onset diabetes with exome sequencing.外显子组测序鉴定致早发糖尿病的 ABCC8 基因复合杂合失活突变
J Diabetes Investig. 2020 Mar;11(2):333-336. doi: 10.1111/jdi.13138. Epub 2019 Sep 19.
8
Clinical characteristics and biochemical mechanisms of congenital hyperinsulinism associated with dominant KATP channel mutations.与显性KATP通道突变相关的先天性高胰岛素血症的临床特征及生化机制
J Clin Invest. 2008 Aug;118(8):2877-86. doi: 10.1172/JCI35414.
9
Congenital Hyperinsulinism and Evolution to Sulfonylurearesponsive Diabetes Later in Life due to a Novel Homozygous p.L171F Mutation.先天性高胰岛素血症及因新型纯合子p.L171F突变在生命后期演变为磺脲类药物反应性糖尿病。
J Clin Res Pediatr Endocrinol. 2019 Feb 20;11(1):82-87. doi: 10.4274/jcrpe.galenos.2018.2018.0077. Epub 2018 Mar 29.
10
A new subtype of autosomal dominant diabetes attributable to a mutation in the gene for sulfonylurea receptor 1.一种常染色体显性糖尿病的新亚型,由磺脲类受体1基因的突变所致。
Lancet. 2003 Jan 25;361(9354):301-7. doi: 10.1016/S0140-6736(03)12325-2.

引用本文的文献

1
Targeted gene panel analysis of Japanese patients with maturity-onset diabetes of the young-like diabetes mellitus: Roles of inactivating variants in the ABCC8 and insulin resistance genes.日本年轻起病型糖尿病样糖尿病患者的靶向基因panel 分析:ABCC8 和胰岛素抵抗基因失活变异的作用。
J Diabetes Investig. 2023 Mar;14(3):387-403. doi: 10.1111/jdi.13957. Epub 2022 Dec 12.
2
Variable phenotypes of individual and family monogenic cases with hyperinsulinism and diabetes: a systematic review.高胰岛素血症和糖尿病的个体及家族单基因病例的可变表型:一项系统综述
Rev Endocr Metab Disord. 2022 Oct;23(5):1063-1078. doi: 10.1007/s11154-022-09749-2. Epub 2022 Aug 23.
3

本文引用的文献

1
Molecular and clinical analysis of Japanese patients with persistent congenital hyperinsulinism: predominance of paternally inherited monoallelic mutations in the KATP channel genes.日本持续性先天性胰岛素分泌过多症患者的分子和临床分析:KATP 通道基因的父系单等位基因突变为主。
J Clin Endocrinol Metab. 2011 Jan;96(1):E141-5. doi: 10.1210/jc.2010-1281. Epub 2010 Oct 13.
2
Hyperinsulinemic hypoglycemia evolving to gestational diabetes and diabetes mellitus in a family carrying the inactivating ABCC8 E1506K mutation.一个携带 ABCC8 E1506K 失活突变的家族中出现高胰岛素血症性低血糖症发展为妊娠期糖尿病和糖尿病。
Pediatr Diabetes. 2010 Nov;11(7):505-8. doi: 10.1111/j.1399-5448.2009.00626.x.
3
A case report of Maturity-onset diabetes of the young 12: large fragment deletion in gene with literature review.
青少年发病的成年型糖尿病12型病例报告:基因大片段缺失并文献复习
Ann Transl Med. 2022 Mar;10(6):378. doi: 10.21037/atm-22-807.
4
Clinical and Genetic Characteristics of Nonneonatal Diabetes Mellitus: A Systematic Review.非新生儿糖尿病的临床和遗传特征:系统综述。
J Diabetes Res. 2021 Sep 30;2021:9479268. doi: 10.1155/2021/9479268. eCollection 2021.
5
Congenital Hyperinsulinism and Evolution to Sulfonylurearesponsive Diabetes Later in Life due to a Novel Homozygous p.L171F Mutation.先天性高胰岛素血症及因新型纯合子p.L171F突变在生命后期演变为磺脲类药物反应性糖尿病。
J Clin Res Pediatr Endocrinol. 2019 Feb 20;11(1):82-87. doi: 10.4274/jcrpe.galenos.2018.2018.0077. Epub 2018 Mar 29.
6
ABCC8 R1420H Loss-of-Function Variant in a Southwest American Indian Community: Association With Increased Birth Weight and Doubled Risk of Type 2 Diabetes.美国西南部印第安社区中ABCC8基因R1420H功能缺失变异:与出生体重增加及2型糖尿病风险翻倍相关
Diabetes. 2015 Dec;64(12):4322-32. doi: 10.2337/db15-0459. Epub 2015 Aug 5.
Update of mutations in the genes encoding the pancreatic beta-cell K(ATP) channel subunits Kir6.2 (KCNJ11) and sulfonylurea receptor 1 (ABCC8) in diabetes mellitus and hyperinsulinism.
糖尿病和高胰岛素血症中编码胰腺β细胞K(ATP)通道亚基Kir6.2(KCNJ11)和磺脲类受体1(ABCC8)的基因突变的更新
Hum Mutat. 2009 Feb;30(2):170-80. doi: 10.1002/humu.20838.
4
Novel de novo mutation in sulfonylurea receptor 1 presenting as hyperinsulinism in infancy followed by overt diabetes in early adolescence.磺脲类受体1的新型新发突变,表现为婴儿期高胰岛素血症,随后在青春期早期发展为显性糖尿病。
Diabetes. 2008 Jul;57(7):1935-40. doi: 10.2337/db08-0159. Epub 2008 Apr 4.
5
Glucose intolerance and diabetes are observed in the long-term follow-up of nonpancreatectomized patients with persistent hyperinsulinemic hypoglycemia of infancy due to mutations in the ABCC8 gene.在因ABCC8基因突变导致婴儿持续性高胰岛素血症性低血糖症的非胰腺切除患者的长期随访中,观察到葡萄糖耐量异常和糖尿病。
Diabetes Care. 2008 Jun;31(6):1257-9. doi: 10.2337/dc07-2059. Epub 2008 Mar 13.
6
beta-cell hyperexcitability: from hyperinsulinism to diabetes.β细胞过度兴奋:从高胰岛素血症到糖尿病
Diabetes Obes Metab. 2007 Nov;9 Suppl 2:81-8. doi: 10.1111/j.1463-1326.2007.00778.x.
7
[Postprandial hypoglycemia].[餐后低血糖症]
Nihon Rinsho. 2006 Sep 28;Suppl 3:224-9.
8
Postprandial reactive hypoglycemia in an oldest-old patient effectively treated with low-dose acarbose.老年患者餐后反应性低血糖经小剂量阿卡波糖有效治疗
Endocr J. 2006 Dec;53(6):767-71. doi: 10.1507/endocrj.k05-140. Epub 2006 Sep 12.
9
Hyperinsulinism in mice with heterozygous loss of K(ATP) channels.K(ATP)通道杂合缺失小鼠中的高胰岛素血症
Diabetologia. 2006 Oct;49(10):2368-78. doi: 10.1007/s00125-006-0367-4. Epub 2006 Aug 19.
10
ATP-sensitive potassium channelopathies: focus on insulin secretion.ATP敏感性钾通道病:聚焦于胰岛素分泌
J Clin Invest. 2005 Aug;115(8):2047-58. doi: 10.1172/JCI25495.