Escharectomy and Allografting During Shock Stage Reduces Insulin Resistance Induced by Major Burn

被引:5
作者
Chen, Xin-Long [1 ]
Xia, Zhao-Fan [2 ]
Wei, Hai-Feng [3 ]
机构
[1] Yangzhou Univ, Dept Burn, Taizhou Peoples Hosp, Coll Med, Taizhou 225300, Jiangsu Prov, Peoples R China
[2] Second Mil Med Univ, Changhai Hosp, Burn Ctr, Shanghai, Peoples R China
[3] Yangzhou Univ, Dept Spine Surg, Taizhou Peoples Hosp, Coll Med, Taizhou 225300, Jiangsu Prov, Peoples R China
关键词
NECROSIS-FACTOR-ALPHA; SKELETAL-MUSCLE; EARLY EXCISION; RECEPTOR SUBSTRATE-1; ENERGY-EXPENDITURE; 3T3-L1; ADIPOCYTES; WOUND EXCISION; TNF-ALPHA; PHOSPHORYLATION; INJURY;
D O I
10.1097/BCR.0b013e31820aaf96
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Hyperglycemia and insulin resistance have long been recognized in severe burn patients. Early excision and grafting reduces cytokines and insulin resistance in burned rats. The authors hypothesized that early wound excision and grafting in patients would also reduce insulin resistance induced by major burn. Thirty-five adult surviving major burn patients (>40% TBSA burn) were recruited. The removal of dead devitalized tissue and allografting in escharectomy group was performed within 72 hours and in control group about 7 days after burn injury. The concentrations of plasma insulin, glucose, and cytokines were measured at 2 and 5 days postburn. Euglycemic-hyperinsulinemic glucose clamps were performed at 5 days after burn. The levels of phosphotyrosine, phosphoserine(312) of insulin receptor substrate (IRS)-1, and phospho-jun N-terminal kinase (JNK) in muscle were analyzed with immunoprecipitation and Western blotting at 5 days postburn. Escharectomy and allografting during shock stage significantly reduced the levels of interleukin-6 and tumor necrosis factor-alpha, decreased the levels of phosphoserine(312) and phospho-JNK, increased the level of phosphotyrosine of IRS-1, and further reduced insulin resistance at 5 days after thermal injury compared with delayed excision group. Escharectomy and allografting during shock stage seemed to have an immunomodulatory effect on the inflammatory mediators and further to reduce insulin resistance induced by major burns in patients by decreasing the phosphorylation of IRS-1 serine(312) and JNK1/2. (J Burn Care Res 2011;32:e59-e66)
引用
收藏
页码:E59 / E66
页数:8
相关论文
共 39 条
[1]   The c-Jun NH2-terminal kinase promotes insulin resistance during association with insulin receptor substrate-1 and phosphorylation of Ser307 [J].
Aguirre, V ;
Uchida, T ;
Yenush, L ;
Davis, R ;
White, MF .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (12) :9047-9054
[2]   SiRNA-mediated reduction of inhibitor of nuclear factor-κB kinase prevents tumor necrosis factor-α-induced insulin resistance in human skeletal muscle [J].
Austin, Reginald L. ;
Rune, Anna ;
Bouzakri, Karim ;
Zierath, Juleen R. ;
Krook, Anna .
DIABETES, 2008, 57 (08) :2066-2073
[3]  
Bastard JP, 2006, EUR CYTOKINE NETW, V17, P4
[4]   MANAGEMENT OF BURN WOUNDS [J].
BAXTER, CR .
DERMATOLOGIC CLINICS, 1993, 11 (04) :709-714
[5]  
CARTER EA, 1998, PHYS REV LETT, V56, pS170
[6]  
Chai J, 2000, CHINESE MED J-PEKING, V113, P1142
[7]   Effects of early excision and grafting on cytokines and insulin resistance in burned rats [J].
Chen Xin-Long ;
Xia Zhao-Fan ;
Ben Dao-Feng ;
Duo Wei .
BURNS, 2010, 36 (07) :1122-1128
[8]   Insulin resistance following thermal injury: An animal study [J].
Chen, Xin-Lony ;
Xia, Zhao-Fan ;
Ben, Dao-Feng ;
Tian, Jian-Guang ;
Wei, Duo .
BURNS, 2007, 33 (04) :480-483
[9]   Role of fat metabolism in burn trauma-induced skeletal muscle insulin resistance [J].
Cree, Melanie G. ;
Aarsland, Asle ;
Herndon, David N. ;
Wolfe, Robert R. .
CRITICAL CARE MEDICINE, 2007, 35 (09) :S476-S483
[10]  
DEFRONZO RA, 1979, AM J PHYSIOL, V237, pE214