Document Detail

NF-κB activity in muscle from obese and type 2 diabetic subjects under basal and exercise-stimulated conditions.
MedLine Citation:
PMID:  20739506     Owner:  NLM     Status:  MEDLINE    
NF-κB is a transcription factor that controls the gene expression of several proinflammatory proteins. Cell culture and animal studies have implicated increased NF-κB activity in the pathogenesis of insulin resistance and muscle atrophy. However, it is unclear whether insulin-resistant human subjects have abnormal NF-κB activity in muscle. The effect that exercise has on NF-κB activity/signaling also is not clear. We measured NF-κB DNA-binding activity and the mRNA level of putative NF-κB-regulated myokines interleukin (IL)-6 and monocyte chemotactic protein-1 (MCP-1) in muscle samples from T2DM, obese, and lean subjects immediately before, during (40 min), and after (210 min) a bout of moderate-intensity cycle exercise. At baseline, NF-κB activity was elevated 2.1- and 2.7-fold in obese nondiabetic and T2DM subjects, respectively. NF-κB activity was increased significantly at 210 min following exercise in lean (1.9-fold) and obese (2.6-fold) subjects, but NF-κB activity did not change in T2DM. Exercise increased MCP-1 mRNA levels significantly in the three groups, whereas IL-6 gene expression increased significantly only in lean and obese subjects. MCP-1 and IL-6 gene expression peaked at the 40-min exercise time point. We conclude that insulin-resistant subjects have increased basal NF-κB activity in muscle. Acute exercise stimulates NF-κB in muscle from nondiabetic subjects. In T2DM subjects, exercise had no effect on NF-κB activity, which could be explained by the already elevated NF-κB activity at baseline. Exercise-induced MCP-1 and IL-6 gene expression precedes increases in NF-κB activity, suggesting that other factors promote gene expression of these cytokines during exercise.
Puntip Tantiwong; Karthigayan Shanmugasundaram; Adriana Monroy; Sangeeta Ghosh; Mengyao Li; Ralph A DeFronzo; Eugenio Cersosimo; Apiradee Sriwijitkamol; Sumathy Mohan; Nicolas Musi
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-08-24
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  299     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-27     Completed Date:  2010-11-16     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E794-801     Citation Subset:  IM    
Texas Diabetes Institute, University of Texas Health Science Center at San Antonio, USA.
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MeSH Terms
Blood Glucose / metabolism
Blotting, Western
Caspase 8 / biosynthesis,  genetics
Chemokine CCL2 / biosynthesis,  genetics
Diabetes Mellitus, Type 2 / metabolism*
Exercise / physiology*
Fatty Acids, Nonesterified / blood
Insulin / blood
Interleukin-6 / biosynthesis,  genetics
Middle Aged
Muscle, Skeletal / metabolism*
NF-kappa B / metabolism*
Obesity / metabolism*
Oxygen Consumption
RNA, Messenger / chemistry,  genetics
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction
Grant Support
Reg. No./Substance:
0/Blood Glucose; 0/CCL2 protein, human; 0/Chemokine CCL2; 0/Fatty Acids, Nonesterified; 0/Insulin; 0/Interleukin-6; 0/NF-kappa B; 0/RNA, Messenger; EC 3.4.22.-/CASP8 protein, human; EC 3.4.22.-/Caspase 8

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