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华西医学  2011 

胰岛素强化治疗对2型糖尿病患者血清脂联素的影响

, PP. 823-827

Keywords: 2型糖尿病,脂联素,胰岛素强化治疗

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Abstract:

【】 目的 探讨胰岛素强化治疗对2型糖尿病(type2diabetesmellitus,T2DM)患者血清脂联素(adiponectin,APN)的影响。 方法 2007年7―12月,研究纳入连续使用胰岛素治疗至少3个月但血糖控制欠佳6.5%≤糖化血红蛋白(hemoglobinA1c,HbA1c)≤11.0%的T2DM患者40例,其中男18例,女22例;年龄29~〖JP2〗69岁;平均诊断T2DM病史11年。治疗方案为进行16周的胰岛素强化治疗,血糖控制目标为空腹血糖≤7mmol/L,〖JP〗餐后2h血糖≤8mmol/L。分别于强化治疗前、强化治疗4周后及强化治疗16周后测定HbA1c以及血清APN水平。 结果 与强化治疗前相比,胰岛素治疗4周后空腹及三餐后2h血糖明显下降(P0.05);强化16周后,HbA1c水平明显低于治疗前和治疗4周后且差异具有统计学意义(P0.05).After16weeksoftreatment,thelevelofHbA1cwassignificantlylowerthanthoseatbaselineand4weeksaftertreatment(P<0.05),andserumAPNconcentrationincreasedsignificantly(P<0.05),comparedwiththosetwotimepoints.However,anevidentincreaseofbodymassindex(BMI)wasfoundwhilecomparedwithBMIatbaselineand4weeksaftertreatment(P<0.05).ThelinearregressionanalysisindicatedthatAPNwasnegativelyassociatedwithfastingbloodglucose(b=-0.225,P=0.013)andbloodglucoselevel2hoursafterbreakfast(b=-0.229,P=0.012). Conclusion Intensiveinsulintherapycanimproveserumadiponectinlevelintype-2diabeticpatients.

References

[1]   The Diabetes Control and Complications Trial Research Group. The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the diabetes control and complications trial[J]. Diabetes, 1995, 44(8): 968-983.
[2]   UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34)[J]. Lancet, 1998, 352(9131): 854-865.
[3]   ADVANCE Collaborative Group, Patel A, MacMahon S, et al. Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes[J]. N Engl J Med, 2008, 358(24): 2560-2572.
[4]   Duckworth W, Abraira C, Moritz T, et al. Glucose control and vascular complications in veterans with type 2 diabetes[J]. N Engl J Med, 2009, 360(2): 129-139.
[5]   ACCORD Study Group, Gerstein HC, Miller ME, et al. Long-term effects of intensive glucose lowering on cardiovascular outcomes[J]. N Engl J Med, 2011, 364(9): 818-828.
[6]   Ziegler D. Type 2 diabetes as an inflammatory cardiovascular disorder[J]. Curr Mol Med, 2005, 5(3): 309-322.
[7]   Weyer C, Funahashi T, Tanaka S, et al. Hypoadiponectinemia in obesity and type 2 diabetes: close association with insulin resistance and hyperinsulinemia[J]. J Clin Endocrinol Metab, 2001, 86(5): 1930-1935.
[8]   Daimon M, Oizumi T, Saitoh T, et al. Decreased serum levels of adiponectin are a risk factor for the progression to type 2 diabetes in the Japanese Population: the Funagata study[J]. Diabetes Care, 2003, 26(7): 2015-2020.
[9]   Lindsay RS, Funahashi T, Hanson RL, et al. Adiponectin and development of type 2 diabetes in the Pima Indian population[J]. Lancet, 2002, 360(9326): 57-58.
[10]   Spranger J, Kroke A, M?hlig M, et al. Adiponectin and protection against type 2 diabetes mellitus[J]. Lancet, 2003, 361(9353): 226-228.
[11]   张春秀, 张喜凤, 石红蕾, 等. 胰岛素强化治疗对2型糖尿病儿童血清脂联素与胰岛素抵抗的影响[J]. 实用儿科临床杂志, 2009, 24(20): 1620-1621.
[12]   郭红霞, 任巧华, 王战建, 等. 胰岛素泵强化治疗对初诊2型糖尿病血清内脂素、脂联素的影响[J]. 临床荟萃, 2009, 24(20): 1816-1818.
[13]   Knobler H, Benderly M, Boyko V, et al. Adiponectin and the development of diabetes in patients with coronary artery disease and impaired fasting glucose[J]. Eur J Endocrinol, 2006, 154(1): 87-92.
[14]   Berg AH, Scherer PE. Adipose tissue, inflammation, and cardiovascular disease[J]. Circ Res, 2005, 96(9): 939-949.
[15]   Combs TP, Berg AH, Obici S, et al. Endogenous glucose production is inhibited by the adipose-derived protein Acrp30[J]. J Clin Invest, 2001, 108(12): 1875-1881.
[16]   Kurzer E, Leveillee R, Bird V. Obesity as a risk factor for complications during laparoscopic surgery for renal cancer: Multivariate analysis[J]. J Endourol, 2006, 20(10): 794-799.
[17]   Takahashi M, Arita Y, Yamagata K, et al. Genomic structure and mutations in adiposespecic gene, adiponectin[J]. Int J Obes Relat Metab Disord, 2000, 24(7): 861-868.
[18]   Kissebah AH, Sonnenberg GE, Myklebust J, et al. Quantitative trait loci on chromosomes 3 and 17 influence phenotypes of the metabolic syndrome[J]. Proc Natl Acad Sci USA, 2000, 97(26): 14478-14483.
[19]   Stumvoll M, Tschritter O, Fritsche A, et al. Association of the T-G polymorphism in adiponectin (exon 2) with obesity and insulin sensitivity: interaction with family history of type 2 diabetes[J]. Diabetes, 2002, 51(1): 37-41.
[20]   Stefan N, Vozarova B, Funahashi T, et al. Plasma adiponectin concentration is associated with skeletal muscle insulin receptor tyrosine phosphorylation, and low plasma concentration precedes a decrease in whole-body insulin sensitivity in humans[J]. Diabetes, 2002, 51(6): 1884-1888.
[21]   Ouchi N, Kihara S, Arita Y, et al. Adipocyte-derived plasma protein, adiponectin, suppresses lipid accumulation and class A scavenger receptor expression in human monocyte-derived macrophages[J]. Circulation, 2001, 103(8): 1057-1063.
[22]   Yamauchi T, Kamon J, Waki H, et al. The fat-derived hormone adiponectin reverses insulin resistance associated with both lipoatrophy and obesity[J]. Nat Med, 2001, 7(8): 941-946.
[23]   Hernandez-Morante JJ, Milagro FI, Lujan JA, et al. Insulin effect on adipose tissue (AT) adiponectin expression is regulated by the insulin resistance status of the patients[J]. Clin Endocrinol (Oxf), 2008, 69(3): 412-417.
[24]   Festa A, D’Agostino R Jr, Tracy RP, et al. Elevated levels of acute phase proteins and plasminogen activeat or inhibitor-1 predict the development of type 2 diabetes: the insulin resistance atherosclerosis study[J]. Diabetes, 2002, 51(4): 1131-1137.
[25]   Dandona P, Aljada A, Mohanty P, et al. Insulin inhibits intranuclear nuclear factor kappa B and stimulates Ikappa B in mononuclear calls in obse subjects: evidence for an anti-inflammatory effect[J]. J Clin Endocrinol Metab, 2001, 86(7): 3257-3265.

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