期刊文献+

真胰岛素测定对胰岛β细胞功能和胰岛素抵抗的评价 被引量:2

Study of true insulin determinations in evaluating β cell function and insulin resistance
下载PDF
导出
摘要 目的 探讨血清真胰岛素 (TI)与免疫反应性胰岛素 (IRI)在反映胰岛 β细胞功能和胰岛素抵抗 (IR)方面的不同。 方法 测定正常糖耐量 (NGT)组 (75例 )、糖耐量减低 (IGT)组 (43例 )和 2型糖尿病 (T2DM )组 (54例 )的TI(ELISA法 )和IRI(RIA法 )水平 ,计算胰岛 β细胞功能指数 (HOMA β)和IR指数 (HOMA IR)。 结果  (1 )HOMA βTI在IGT非肥胖组低于NGT非肥胖组 (P <0 0 5) ,T2DM非肥胖组低于NGT和IGT非肥胖组 (均P <0 0 1 ) ;在IGT和T2DM肥胖组低于NGT肥胖组 (均P <0 0 1 )。HOMA βIRI在IGT和T2DM非肥胖组低于NGT非肥胖组 (均P <0 0 5) ;在NGT、IGT和T2DM肥胖组之间无显著差异。(2 )HOMA IRTI和HOMA IRIRI在非肥胖组和肥胖组均显示T2DM有明显IR。结论 在反映胰岛 β细胞功能方面TI优于IRI,在反映IR方面TI与IRI有着相似的意义。 Objective To study the difference between true insulin (TI) and immunoreactive insulin (IRI) in evaluating β cell function and insulin resistance (IR).Methods The levels of serum TI and IRI were determined in 54 cases with type 2 diabetes mellitus (Group T2DM), 43 cases with impaired glucose tolerance (Group IGT) and 75 cases with normal glucose tolerance (Group NGT) with ELISA and RIA methods respectively. The insulin resistance index (HOMA-IR) and pancreatic β cell function index ( HOMA-β) were analyzed preliminarily.Results 1. HOMA-β TI in non-obese subgroup with IGT was lower than that in non-obese subgroup with NGT (P<0.05), and the HOMA-β TI in non-obese subgroup with T2DM was lower than that in non-obese subgroups with NGT and IGT (P<0.01). HOMA-β TI of obese subgroups with IGT and T2DM was lower than that in obese subgroup with NGT (P<0.01). HOMA-β IRI in non-obese subgroups with IGT and T2DM was lower than that in non-obese subgroup with NGT (P<0.05). There was not significant difference of HOMA-β IRI in obese subgroups of NGT, IGT and T2DM. 2. HOMA-β TI and HOMA-β IRI show that there was obvious IR in T2DM group no matter in non-obese subgroup or obese subgroup. Conclusions TI is better than IRI in evaluating β-cell function. TI is similar to IRI in evaluating insulin resistance.
出处 《中国老年学杂志》 CAS CSCD 北大核心 2004年第10期883-885,共3页 Chinese Journal of Gerontology
关键词 NGT IGT 肥胖 T2DM 胰岛Β细胞功能 真胰岛素 胰岛素抵抗 IRI 结论 TI True insulin (TI) β-cell function Insulin resistance
  • 相关文献

参考文献8

  • 1Haffner SM, Miettinen H, Stern MP. The homeostasis model in the San Antonio heart study[J]. Diabetes Care, 1997;20(7):1087-92.
  • 2Rachman J, Levy JC, Barrow BA, et al.Relative hyperproinsulinemia of NIDDM persists despite the reduction of hyperglycemia with insulin or sulfonylurea therapy[J].Diabetes, 1997;46(10):1557-62.
  • 3Kahn SE, Halban PA. Release of incompletely processed proinsulin is the cause of the disproportionate proinsulinemia of NIDDM[J].Diabetes, 1997;46(11): 1725-32.
  • 4Saad MF, Kahn SE, Nelson RG. et al .Disproportionately elevated proinsulin in Pima Indians with noninsulin-dependent diabetes mellitus[J]. J Clin Endocrinol Metab,1990;70(5):1247-53.
  • 5Coifman R, Dalbosco IS, Russo EMK,et al .Specific insulin and proinsulin in normal glucose tolerant first-degree relatives of NIDDM patients[J].Braz J Med Biol Res, 1999;32(1):67-72.
  • 6Haffner SM, Gonzalez C, Mykkanen L,et al.Total immunoreactive proinsulin, immunoreactive insulin and specific insulin in relation to conversion to NIDDM:The Mexico City Diabetes Study[J]. Diabetologia, 1997;40(7): 830-7.
  • 7杨建梅,高妍,马红,惠岩,陈澜.肥胖症患者和新诊断的2型糖尿病患者真胰岛素和前胰岛素的改变[J].中国糖尿病杂志,2000,8(5):285-288. 被引量:6
  • 8邓尚平,李双庆,熊中云.血中胰岛β细胞激素测定的新进展[J].中国糖尿病杂志,1995,3(1):54-58. 被引量:17

二级参考文献1

共引文献19

同被引文献33

  • 1王秀明,姜雪梅,王玲玲,吕淑云.胰岛素原转换酶1、2和羧基肽酶H与2型糖尿病的关系[J].华中医学杂志,2005,29(5):396-397. 被引量:1
  • 2BENZINOU M, WALLEY A J, MEYRE D, et al. Common nonsynonymous variants in PCSK1 confer risk of obesity[J]. Nature Genetics, 2008, 40(8): 943-945.
  • 3STEINER D F. The proprotein convertases[J]. Current Opinion in Chemical Biology, 1998, 2(1): 31-39.
  • 4LLOYD D J, BOHAN S, GEKAKIS N. Obesity, hyperphagia and increased metabolic efficiency in PCI mutant mice [J]. Human Molecular Genetics, 2006, 15(11): 1884-1893.
  • 5LU H F, YANG Y, ALLISTER E M, et al. The identification of potential factors associated with the development of Type 2 Dia- betes[J]. Molecullar & Cellular Proteomics, 2008, 7(8): 1434- 1451.
  • 6WANG J, XU J, FINNERTY J, et al. The prohormone conver- tase enzyme 2 (PC2) is essential for processing pro-islet amy- loid polypeptide at the NH2-terminal cleavage site[J]. Diabetes, 2001, 50(3): 534-539.
  • 7MARZBAN L, TRIGO-GONZALEZ G, VERCHERE C B. Role of,β-cell prohormone convertase (PC)1/3 in processing of pro- islet amyloid polypeptide[J]. Diabetes, 2004, 53 (1): 141 - 148.
  • 8FAROOQI I S, VOLDERS K, STANHOPE R, et al. Hyperpha- gia and early-onset obesity due to a novel homozygous mis- sense mutation in prohormone convertase 1/3 [J]. Endocrine Society, 2007, 92(9): 3369-3373.
  • 9ZHU X, ZHOU A, DEY A, et al. Disruption of PC1/3 expres- sion in mice causes dwarfism and multiple neuroendoerine peptide processing defects[J]. Proceedings of the National A- cademy of Science of the United States of America, 2002, 99 (16): 10293-10298.
  • 10WEN J H, CHEN Y Y, SONG S J, et al. Paired box 6 (PAX6) regulates glucose metabolism via proinsulin proceeding medi- ated by prohonnone convertase 1/3 (PC1/3)[J]. Diabetologia, 2009, 52(3): 504-513.

引证文献2

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部