Published January 8, 2008; doi:10. 0193-1849/08 $8.Versions of this Article: 294/3/E607 _most recent_ Services Google Scholar PubMed INSULIN-RESISTANT MUSCLE IS EXERCISE RESISTANT: EVIDENCE FOR REDUCED RESPONSE OF NUCLEAR-ENCODED MITOCHONDRIAL GENES TO EXERCISE ELENA DE FILIPPIS,1 GUY ALVAREZ,2 RACHELE BERRIA,2 KENNETH CUSI,2 SARAH EVERMAN,1 CHRISTIAN MEYER,3 AND LAWRENCE J._ 1Center for Metabolic Biology, Arizona State University, Tempe, Arizona; 2University of Texas Health Science Center at San Antonio, San Antonio, Texas; and 3Carl T.Veterans Affairs Medical Center, Phoenix, Arizona _ Submitted 19 November 2007 ; accepted in final form 4 January 2008 Mitochondrial dysfunction, associated with insulin resistance, is characterized by low expression of peroxisome proliferator-activated receptor-_ coactivator-1 (PGC-1) and nuclear-encoded mitochondrial genes.Deficit could be due to decreased physical activity or a decreased response of gene expression to exercise.Objective of this study was to investigate whether a bout of exercise induces the same increase in nuclear-encoded mitochondrial gene expression in insulin-sensitive and insulin-resistant subjects matched for exercise capacity.Lean and nine obese subjects took part.Sensitivity was assessed by an 80 mUm-2min-1 euglycemic clamp.Matched for aerobic capacity and underwent a single bout of exercise at 70 and 90% of maximum heart rate with muscle biopsies at 30 and 300 min postexercise.And immunoblot analyses were used to determine the effect of exercise on gene expression and protein abundance and phosphorylation.The postexercise period, lean subjects immediately increased PGC-1 mRNA level (reaching an eightfold increase by 300 min postexercise) and protein abundance and AMP-dependent protein kinase phosphorylation.PGC-1 was followed by increase of nuclear respiratory factor-1 and cytochrome c_ oxidase (subunit VIc).Insulin-resistant subjects, there was a delayed and reduced response in PGC-1 mRNA and protein, and phosphorylation of AMP-dependent protein kinase was transient.Of the genes downstream of PGC-1 was increased after exercise in insulin resistance.Subjects have a reduced response of nuclear-encoded mitochondrial genes to exercise, and this could contribute to the origin and maintenance of mitochondrial dysfunction.Resistance; mitochondrial function; exercise; peroxisome proliferator-activated receptor- coactivator-1; AMP-dependent protein kinase Address for reprint requests and other correspondence: L.Read more Half of patients undergoing cerebrovascular stent placement do not respond well to clopidogrel
Get more Diphenhydramine, benadryl
