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Effects of exercise on expression of skeletal muscle acyl‐CoA synthetase isoform gene expression in obese African‐American and Caucasian women
Author(s) -
Woodlief Tracey Leigh,
Sweazey Melanie A.,
File Courtney,
Hickner Robert C.,
Neufer P. Darrell,
Cortright Ronald N.
Publication year - 2008
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.22.1_supplement.958.8
Subject(s) - medicine , endocrinology , gene isoform , skeletal muscle , endurance training , biology , gene , biochemistry
Reduced skeletal muscle (SKM) mitochondrial fatty acid oxidation (FAO) in African‐American women (AAW) may be due to reduced activity of Acyl‐CoA Synthetase‐long form (ACSL). However, endurance exercise training (EET) has been shown to increase SKM FAO in both AAW and Caucasian women (CW). The purpose was to determine the metabolic flexibility of SKM to expand the activity of ACSL in response to EET in obese (BMI 35–40 kg/m 2 ) AAW and CW women. Following a 12 hr fast, biopsies from AAW and CW were obtained from either the rectus abdominus or vastus lateralis before and 4 h after acute exercise in the sedentary and trained (10 d and 8 wk of cycle ergometry) condition. Assays for total ACSL activity, protein content, and gene expression of ACSL 1, 3, 4, 5, and 6 isoforms were assessed. In rectus abdominus, lower (P<0.05) ACSL‐5 protein content was observed in obese AAW vs. CW. Prior to EET, total ACSL activity in vastus lateralis was lower in both obese groups compared to leans, although activity was lower in obese AAW. 10 days of EET did not result in elevated ACSL activity in either obese AAW or CW. However, following 8 wk of EET, both groups demonstrated increased enzyme activity. In response to acute exercise, ACSL‐1 and ‐3 isoform gene expression rose solely in CW. In the trained, rested state, ACSL‐1 and ‐3 isoform expression was elevated in obese CW only (P < 0.05). Results support ACSL as a potential molecular mechanism to explain reduced SKM mitochondrial oxidative capacity in AAW although the increase in FAO in AAW after EET can not be explained by ACSL isoform gene expression. Supported by NIH DK065183 ‐01 and DK075880 ‐01