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Resistance training modulates the expression of genes involved in glucose transport and oxidative reactions in skeletal muscle in type 2 diabetes
Author(s) -
CastanedaSceppa Carmen,
Castaneda Francisco
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1105.19
Subject(s) - insulin resistance , glucose transporter , skeletal muscle , type 2 diabetes , glycemic , medicine , endocrinology , gene expression , biology , oxidative stress , oxidative phosphorylation , glucose homeostasis , endurance training , glucose uptake , gene , glut4 , diabetes mellitus , insulin , biochemistry
We have shown a relationship between the expression of sodium‐dependent glucose co‐transporter system (SGLT3) and resistance training (RT) in older adults with uncontrolled type 2 diabetes (poor glycemic control and sustained hyperglycemia). In this study we examined the effect of RT on gene expression patterns using Affymetrix GeneChip Human Genome U133 plus 2.0 Array. Vastus lateralis muscle samples were obtained before and after 16 weeks. Total RNA was extracted and biotinylated cRNA prepared. Gene expression profile between groups 1 (RT) and 2 (control, no RT) were assessed by one‐step Tukey's biweight method. We found 23 (13 up and 10 down) genes regulated (p<0.01). Gene ontology analysis of up‐regulated genes demonstrated their involvement in glucose homeostasis [i.e. glucose transport (SLC2A4 regulator and SLC5A4) and glucose phosphorylation (HK2)], which corroborates the relationship between RT and glucose transport by SGLT3 in skeletal muscle. The down‐regulated genes observed have been involved in oxidative reactions (CYP4B1 and ADH1), suggesting an involvement of RT in reducing glucose toxicity due to oxidative stress. The novel findings of this study provide preliminary information of an insulin‐independent glucose transport in type 2 diabetes induced by resistance training. Support: Brookdale Foundation, Max Planck Institute, Dortmund, Germany, NIH‐ RR000054 , USDA‐ARS‐58‐1950‐9‐001.