Changes in adipose tissue gene expression and plasma levels of adipokines and acute-phase proteins in patients with critical illness

被引:43
作者
Jernas, Margareta [1 ]
Olsson, Bob [1 ]
Sjoholm, Kajsa [1 ]
Sjogren, Anders [3 ]
Rudemo, Mats
Nellgard, Bengt [2 ]
Carlsson, Lena M. S. [1 ]
Sjostrom, C. David [2 ]
机构
[1] Univ Gothenburg, Sahlgrenska Acad, Dept Mol & Clin Med, SE-41345 Gothenburg, Sweden
[2] Univ Gothenburg, Sahlgrenska Acad, Dept Anaesthesiol & Intens Care, SE-41345 Gothenburg, Sweden
[3] Chalmers, Dept Math Stat, SE-41296 Gothenburg, Sweden
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2009年 / 58卷 / 01期
基金
瑞典研究理事会;
关键词
LIPID MOBILIZING FACTOR; C-REACTIVE PROTEIN; SERUM AMYLOID-A; METABOLIC SYNDROME; INSULIN-RESISTANCE; OBESE SUBJECTS; ILL PATIENTS; ADIPOCYTES; RETINOL-BINDING-PROTEIN-4; PHOSPHOLIPASE-A2;
D O I
10.1016/j.metabol.2008.08.012
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Insulin resistance develops rapidly during critical illness. The release of adipokines from adipose tissue is thought to play a key role ill the development Of insulin resistance, as are elevated levels of acute-phase proteins. The aim Of this Study was to identify changes in adipose tissue gene expression and plasma levels of adipokines and acute-phase proteins during critical illness. From 8 patients with subarachnoidal hemorrhage, consecutive blood samples and adipose tissue biopsies were obtained at 3 time points, twice during intensive care (1-2 days [ICI] and 7-9 days after subarachnoidal hemorrhagge) and once after 8 months (recovery). The patients received a continuous insulin infusion to maintain normal glucose levels reflecting insulin resistance. The DNA microarray analysis showed increased zink-alpha2 glycoprotein (ZAG) and phospholipase A2, group IIA messenger RNA levels during intensive care compared with recovery (P <.05). Real-time polymerase chain reaction confirmed the increased expression of ZAG and phospholipase A2, group IIA. Plasma levels of ZAG, serum amyloid A, and C-reactive protein were higher at 7 to 9 days after subarachnoidal hemorrhage compared with either ICI or recovery (P=.0001); and plasma levels of retinol-binding protein 4 and adiponectin were lower at ICI compared with recovery (P =.05). The described changes in adipose tissue gene expression and plasma levels of adipokines and acute-phase proteins may influence the development of insulin resistance during critical illness. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:102 / 108
页数:7
相关论文
共 37 条
[1]   Molecular aspects of insulin therapy in critically ill patients [J].
Andreelli, F ;
Jacquier, D ;
Troy, S .
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE, 2006, 9 (02) :124-130
[2]   Zinc-α2-glycoprotein, a lipid mobilizing factor, and is expressed and secreted by human (SGBS) adipocytes [J].
Bao, Y ;
Bing, C ;
Hunter, L ;
Jenkins, JR ;
Wabitsch, M ;
Trayhurn, P .
FEBS LETTERS, 2005, 579 (01) :41-47
[3]   Dissociation between adipose tissue expression and serum levels of adiponectin during and after diet-induced weight loss in obese subjects with and without the metabolic syndrome [J].
Behre, Carl Johan ;
Gummesson, Anders ;
Jernas, Margareta ;
Lystig, Theodore C. ;
Fagerberg, Bjorn ;
Carlsson, Bjorn ;
Carlsson, Lena M. S. .
METABOLISM-CLINICAL AND EXPERIMENTAL, 2007, 56 (08) :1022-1028
[4]  
Bernard C., 1878, LECONS PHENOMENES CO
[5]   Zinc-α2-glycoprotein, a lipid mobilizing factor, is expressed in adipocytes and is up-regulated in mice with cancer cachexia [J].
Bing, C ;
Bao, Y ;
Jenkins, J ;
Sanders, P ;
Manieri, M ;
Cinti, S ;
Tisdale, MJ ;
Trayhurn, P .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (08) :2500-2505
[6]   RETINOL-BINDING PROTEIN - THE SERUM TRANSPORT PROTEIN FOR VITAMIN-A [J].
BLANER, WS .
ENDOCRINE REVIEWS, 1989, 10 (03) :308-316
[7]   Minimum information about a microarray experiment (MIAME) - toward standards for microarray data [J].
Brazma, A ;
Hingamp, P ;
Quackenbush, J ;
Sherlock, G ;
Spellman, P ;
Stoeckert, C ;
Aach, J ;
Ansorge, W ;
Ball, CA ;
Causton, HC ;
Gaasterland, T ;
Glenisson, P ;
Holstege, FCP ;
Kim, IF ;
Markowitz, V ;
Matese, JC ;
Parkinson, H ;
Robinson, A ;
Sarkans, U ;
Schulze-Kremer, S ;
Stewart, J ;
Taylor, R ;
Vilo, J ;
Vingron, M .
NATURE GENETICS, 2001, 29 (04) :365-371
[8]  
COPPACK SW, 1994, J LIPID RES, V35, P177
[9]  
CROWL RM, 1991, J BIOL CHEM, V266, P2647
[10]   The metabolic syndrome [J].
Eckel, RH ;
Grundy, SM ;
Zimmet, PZ .
LANCET, 2005, 365 (9468) :1415-1428