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Blockade of the Renin‐Angiotensin System Increases Skeletal Muscle Total IRS‐1 in Burn Injury
Author(s) -
Conway Sarah Elaine,
Ziga Taylor Michelle,
Schertzer Megan Danielle,
Erdei Timothy Ryan,
Kasper Sherry Oden,
Daley Brian J,
Enderson Blaine L,
Karlstad Michael D
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.1095.6
Subject(s) - losartan , glut4 , endocrinology , medicine , renin–angiotensin system , blockade , chemistry , angiotensin ii , valsartan , burn injury , angiotensin ii receptor type 1 , total body surface area , skeletal muscle , insulin resistance , receptor , insulin , surgery , blood pressure
We have shown a correlation between burn injury and insulin resistance as a result of modification of the insulin receptor pathway. More specifically, the effects of total IRS‐1 were studied by inhibiting the renin‐angiotensin (RAS) with losartan, an AT 1 receptor blocker. Male Sprague Dawley rats were subjected to a 30% total body surface area burn in 90°C water for 15 seconds while sham rats were immersed in 23°C water. Losartan (30 mg/kg/day) was administered by gavage three days consecutively post‐burn. Total IRS‐1 was determined in rectus abdominus muscle by Western blotting. There was a significant increase in total IRS‐1 (p<0.05, n=7) in muscle from burned rats treated with losartan as compared with sham and burned rats treated with placebo (water). We have observed a similar pattern later in the pathway among the plasma membrane GLUT4 transporter and IRS‐1 associated PI3‐kinase levels. These findings show a significant increase in total IRS‐1 as a result of losartan treatment and suggests a potential role of RAS in regulating total IRS‐1 in skeletal muscle.