留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

甘油激酶在移植后糖尿病中的潜在调节作用

明英姿 RichardM.Kream GeorgeB.Stefano 庄权 郁孟

明英姿, RichardM.Kream, GeorgeB.Stefano, 等. 甘油激酶在移植后糖尿病中的潜在调节作用[J]. 器官移植, 2019, 10(3): 336-338. doi: 10.3969/j.issn.1674-7445.2019.03.020
引用本文: 明英姿, RichardM.Kream, GeorgeB.Stefano, 等. 甘油激酶在移植后糖尿病中的潜在调节作用[J]. 器官移植, 2019, 10(3): 336-338. doi: 10.3969/j.issn.1674-7445.2019.03.020
Ming Yingzi, Richard M. Kream, George B. Stefano, et al. Potential regulation of glycerol kinase in post transplantation diabetes mellitus[J]. ORGAN TRANSPLANTATION, 2019, 10(3): 336-338. doi: 10.3969/j.issn.1674-7445.2019.03.020
Citation: Ming Yingzi, Richard M. Kream, George B. Stefano, et al. Potential regulation of glycerol kinase in post transplantation diabetes mellitus[J]. ORGAN TRANSPLANTATION, 2019, 10(3): 336-338. doi: 10.3969/j.issn.1674-7445.2019.03.020

甘油激酶在移植后糖尿病中的潜在调节作用

doi: 10.3969/j.issn.1674-7445.2019.03.020
基金项目: 

国家自然科学基金 81700658

国家自然科学基金 81771722

详细信息
    通讯作者:

    明英姿,女,博士,教授,研究方向为器官移植与移植免疫,Email:myz_china@aliyun.com

  • 中图分类号: R617

Potential regulation of glycerol kinase in post transplantation diabetes mellitus

  • 摘要: 肝移植术后受体易出现高血糖,进而可能导致移植后糖尿病(PTDM)。PTDM受体脂肪组织中正常糖酵解途径会受到显著的抑制,致使3磷酸甘油(G3P)只能由称为甘油新生的逆向糖酵途径生成。G3P生成不足可导致游离脂肪酸过多进入血液循环进而促进糖尿病(如胰岛素抵抗)的发生和发展。本文从供肝脂肪性肝病与PTDM的关系、甘油激酶(GK)在PTDM中的作用及其临床应用前景进行综述。

     

  • [1] WISSING KM, ABRAMOWICZ D, WEEKERS L, et al. Prospective randomized study of conversion from tacrolimus to cyclosporine A to improve glucose metabolism in patients with posttransplant diabetes mellitus after renal transplantation[J]. Am J Transplant, 2018, 18(7):1726-1734. DOI: 10.1111/ajt.14665.
    [2] GUPTA S, POLLACK T, FULKERSON C, et al. Hyperglycemia in the posttransplant period: NODAT vs posttransplant diabetes mellitus[J]. J Endocr Soc, 2018, 2(11):1314-1319. DOI: 10.1210/js.2018-00227.
    [3] ZELADA H, VANWAGNER LB, POLLACK T, et al. Development of a predictive model for hyperglycemia in nondiabetic recipients after liver transplantation[J]. Transplant Direct, 2018, 4(10):e393. DOI: 10.1097/TXD.0000000000000830.
    [4] KE QH, HUANG HT, LING Q, et al. New-onset hyperglycemia immediately after liver transplantation: a national survey from China Liver Transplant Registry[J]. Hepatobiliary Pancreat Dis Int, 2018, 17(4):310-315. DOI: 10.1016/j.hbpd.2018.08.005.
    [5] LIU FC, LIN JR, CHEN HP, et al. Prevalence, predictive factors, and survival outcome of new-onset diabetes after liver transplantation: a population-based cohort study[J]. Medicine (Baltimore), 2016, 95(25):e3829. DOI: 10.1097/MD.0000000000003829.
    [6] ANDRADE AR, BITTENCOURT PL, CODES L, et al. New onset diabetes and non-alcoholic fatty liver disease after liver transplantation[J]. Ann Hepatol, 2017, 16(6):932-940. DOI: 10.5604/01.3001.0010.5285.
    [7] TINIAKOS DG, VOS MB, BRUNT EM. Nonalcoholic fatty liver disease: pathology and pathogenesis[J]. Annu Rev Pathol, 2010, 5:145-171. DOI: 10.1146/annurev-pathol-121808-102132.
    [8] GOLABI P, BUSH H, STEPANOVA M, et al. Liver transplantation (LT) for cryptogenic cirrhosis (CC) and nonalcoholic steatohepatitis (NASH) cirrhosis: data from the Scientific Registry of Transplant Recipients (SRTR): 1994 to 2016[J]. Medicine (Baltimore), 2018, 97(31):e11518. DOI: 10.1097/MD.0000000000011518.
    [9] MIKOLASEVIC I, FILIPEC-KANIZAJ T, MIJIC M, et al. Nonalcoholic fatty liver disease and liver transplantation - where do we stand?[J]. World J Gastroenterol, 2018, 24(14):1491-1506. DOI: 10.3748/wjg.v24.i14.1491.
    [10] RAHIB L, SRIRAM G, HARADA MK, et al. Transcriptomic and network component analysis of glycerol kinase in skeletal muscle using a mouse model of glycerol kinase deficiency[J]. Mol Genet Metab, 2009, 96(3):106-112. DOI: 10.1016/j.ymgme.2008.11.163.
    [11] CADOUDAL T, BLOUIN JM, COLLINET M, et al. Acute and selective regulation of glyceroneogenesis and cytosolic phosphoenolpyruvate carboxykinase in adipose tissue by thiazolidinediones in type 2 diabetes[J]. Diabetologia, 2007, 50(3):666-675. doi: 10.1007/s00125-006-0560-5
    [12] CADOUDAL T, FOUQUE F, BENELLI C, et al. Glyceroneogenesis and PEPCK-C: pharmacological targets in type 2 diabetes[J]. Med Sci (Paris), 2008, 24(4):407-413. DOI: 10.1051/medsci/2008244407.
    [13] CADOUDAL T, LEROYER S, REIS AF, et al. Proposed involvement of adipocyte glyceroneogenesis and phosphoenolpyruvate carboxykinase in the metabolic syndrome[J]. Biochimie, 2005, 87(1):27-32. doi: 10.1016/j.biochi.2004.12.005
    [14] HANSON RW, RESHEF L. Glyceroneogenesis revisited[J]. Biochimie, 2003, 85(12):1199-1205. doi: 10.1016/j.biochi.2003.10.022
    [15] BEALE EG, HAMMER RE, ANTOINE B, et al. Disregulated glyceroneogenesis: PCK1 as a candidate diabetes and obesity gene[J]. Trends Endocrinol Metab, 2004, 15(3):129-135. doi: 10.1016/j.tem.2004.02.006
    [16] BAJAJ M, SURAAMORNKUL S, ROMANELLI A, et al. Effect of a sustained reduction in plasma free fatty acid concentration on intramuscular long-chain fatty acyl-CoAs and insulin action in type 2 diabetic patients[J]. Diabetes, 2005, 54(11):3148-3153. doi: 10.2337/diabetes.54.11.3148
    [17] HAMMOND LE, NESCHEN S, ROMANELLI AJ, et al. Mitochondrial glycerol-3-phosphate acyltransferase-1 is essential in liver for the metabolism of excess acyl-CoAs[J]. J Biol Chem, 2005, 280(27):25629-25636. doi: 10.1074/jbc.M503181200
    [18] WENDEL AA, LEWIN TM, COLEMAN RA. Glycerol-3-phosphate acyltransferases: rate limiting enzymes of triacylglycerol biosynthesis[J]. Biochim Biophys Acta, 2009, 1791(6):501-506. DOI: 10.1016/j.bbalip.2008.10.010.
    [19] STEFANO GB, FINE R, KREAM RM. Microbiome and health: ramifications of intelligent deception[J]. Med Sci Monit, 2018, 24:2060-2062. doi: 10.12659/MSM.910248
    [20] STEFANO GB, PILONIS N, PTACEK R, et al. Gut, microbiome, and brain regulatory axis: relevance to neurodegenerative and psychiatric disorders[J]. Bioc Cell Mol Neurobiol, 2018, 38(6):1197-1206. DOI: 10.1007/s10571-018-0589-2.
    [21] MILLER C, WANG L, OSTERGAARD E, et al. The interplay between SUCLA2, SUCLG2, and mitochondrial DNA depletion[J]. Biochim Biophys Acta, 2011, 1812(5):625-629. DOI: 10.1016/j.bbadis.2011.01.013.
    [22] CAPUTI V, MARSILIO I, FILPA V, et al. Antibiotic-induced dysbiosis of the microbiota impairs gut neuromuscular function in juvenile mice[J]. Br J Pharmacol, 2017, 174(20):3623-3639. DOI: 10.1111/bph.13965.
    [23] MING Y, STEFANO GB, KREAM RM, et al. Anti-diabetogenic properties of mineralocorticoid receptor antagonists: implications for enhanced safety and efficacy of post-transplantation pharmacotherapies [J]. Med Sci Monit, 2019, 25:1102-1104. doi: 10.12659/MSM.914340
    [24] 罗招凡, 李芳萍, 程桦.抵抗素介导AMPK信号通路对HepG2细胞脂质代谢的影响[J].实用医学杂志, 2017, 33(11):1743-1747. DOI: 10.3969/j.issn.1006-5725.2017.11.007.

    LUO ZF, LI FP, CHENG Y. The effect of the recombinant human resistin on lipid metabolism by AMPK pathway in HepG2 cells[J]. J Prac Med, 2017, 33(11):1743-1747. DOI: 10.3969/j.issn.1006-5725.2017.11.007.
    [25] JAHANSOUZ C, STALEY C, KIZY S, et al. Antibiotic-induced disruption of intestinal microbiota contributes to failure of vertical sleeve gastrectomy[J]. Ann Surg, 2018. DOI: 10.1097/SLA.0000000000002729 [Epubahead of print].
  • 加载中
计量
  • 文章访问数:  132
  • HTML全文浏览量:  49
  • PDF下载量:  10
  • 被引次数: 0
出版历程
  • 收稿日期:  2019-01-05
  • 网络出版日期:  2021-01-19
  • 刊出日期:  2019-05-15

目录

    /

    返回文章
    返回