Upregulation of uncoupling protein homologues in skeletal muscle but not adipose tissue in posttraumatic insulin resistance

被引:11
|
作者
Strommer, L
El-Ella, GA
Kamel, A
Marcus, C
Hager, P
Adrian, TE
Permert, J
机构
[1] Huddinge Univ Hosp, Karolinska Inst, Arvid Wretlinds Lab Metab & Nutr Res, Stockholm, Sweden
[2] Huddinge Univ Hosp, Karolinska Inst, Dept Pediat, Endocrine Res Unit, Stockholm, Sweden
[3] Creighton Univ, Dept Biomed Sci, Omaha, NE 68178 USA
基金
英国医学研究理事会;
关键词
surgical trauma; glucose transport; lipogenesis; lipolysis; uncoupling proteins;
D O I
10.1006/bbrc.2001.4360
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Metabolic alterations after surgical stress include peripheral insulin resistance and increased utilization of fat as a fuel substrate. An up-regulation of skeletal muscle uncoupling proteins (UCPs) has been associated with physiologic states of insulin resistance and enhanced fat metabolism in rodents. We examined whether posttraumatic insulin resistance induced the UCPs in gastrocnemius and soleus muscle and white adipose tissue in an experimental model of surgical trauma. Insulin sensitivity was significantly reduced in isolated soleus muscles but unchanged in adipocytes after trauma. In traumatized rats, mRNA and protein contents of UCP2 and UCP3 and were significantly increased in both muscle types. UCP2 protein content in adipose tissue was unaltered by surgical stress, Circulating NEFAs and glycerol were reduced after surgical trauma, We hypothesize that the changes in UCP2 and UCP3 gene and protein expression are involved in the regulation of substrate utilization in posttraumatic insulin resistance. (C) 2001 Academic Press.
引用
收藏
页码:334 / 340
页数:7
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