TY - JOUR
T1 - Training down-regulates fatty acid synthase and body fat in obese Zucker rats
AU - Fiebig, Russell G.
AU - Hollander, John M.
AU - Ney, Denise
AU - Boileau, Richard
AU - Jeffery, Elizabeth
AU - Li Ji, Li
PY - 2002/1/1
Y1 - 2002/1/1
N2 - Introduction: The purpose of this study was to investigate whether chronic exercise training attenuates fatty acid synthase, the rate-limiting enzyme for hepatic lipogenesis, and the accumulation of body fat by using obese Zucker rats (OZR) as a model. Methods: Female obese Zucker (fa/fa) rats (O, N = 16) and their lean litter mates (L, N = 16) were randomly divided into a trained (T) and untrained (U) group. T was performed on a treadmill for 2 h·d-1, 5 d·wk-1], 10 wk with running speed and grade adjusted to elicit similar workloads. All rats were meal-fed a high-cornstarch diet for 4 h·d-1 and killed 8 h after the initiation of the last meal and 27 h after the last T session, in the resting state. Results: O rats exhibited twofold higher FAS activity and sixfold higher FAS mRNA abundance in the liver than L rats (P < 0.05), accompanied by a severe hyperinsulinemia (P < 0.05) but normal glucagon and glucose levels. FAS activity, but not mRNA level, was decreased by 18% with T in O rats (P < 0.05). T decreased percent body fat in both O and L rats (P < 0.05), and increased lean body mass in O rats (P < 0.05). Hepatic fatty acid profile showed higher 16:0, 16:1, and 18:1 concentrations in O rats, whereas 18:0, 18:2, and 20:4 were lower (P < 0.05). Training increased 20:4 in both O and L rats (P < 0.08). Nuclear protein binding to the insulin response sequence (IRS/A) and carbohydrate response element (ChoRE) on FAS gene promoter was decreased, whereas inverted CAATT box element (ICE) binding was increased in O versus L rats (P < 0.05). Training did not affect the binding of these gene sequences. Conclusion: De novo lipogenesis was greatly enhanced in OZR. Endurance training decreased body fat, which is partly explained by a decreased FAS activity. However, FAS down-regulation was not due to altered nuclear protein binding to FAS gene.
AB - Introduction: The purpose of this study was to investigate whether chronic exercise training attenuates fatty acid synthase, the rate-limiting enzyme for hepatic lipogenesis, and the accumulation of body fat by using obese Zucker rats (OZR) as a model. Methods: Female obese Zucker (fa/fa) rats (O, N = 16) and their lean litter mates (L, N = 16) were randomly divided into a trained (T) and untrained (U) group. T was performed on a treadmill for 2 h·d-1, 5 d·wk-1], 10 wk with running speed and grade adjusted to elicit similar workloads. All rats were meal-fed a high-cornstarch diet for 4 h·d-1 and killed 8 h after the initiation of the last meal and 27 h after the last T session, in the resting state. Results: O rats exhibited twofold higher FAS activity and sixfold higher FAS mRNA abundance in the liver than L rats (P < 0.05), accompanied by a severe hyperinsulinemia (P < 0.05) but normal glucagon and glucose levels. FAS activity, but not mRNA level, was decreased by 18% with T in O rats (P < 0.05). T decreased percent body fat in both O and L rats (P < 0.05), and increased lean body mass in O rats (P < 0.05). Hepatic fatty acid profile showed higher 16:0, 16:1, and 18:1 concentrations in O rats, whereas 18:0, 18:2, and 20:4 were lower (P < 0.05). Training increased 20:4 in both O and L rats (P < 0.08). Nuclear protein binding to the insulin response sequence (IRS/A) and carbohydrate response element (ChoRE) on FAS gene promoter was decreased, whereas inverted CAATT box element (ICE) binding was increased in O versus L rats (P < 0.05). Training did not affect the binding of these gene sequences. Conclusion: De novo lipogenesis was greatly enhanced in OZR. Endurance training decreased body fat, which is partly explained by a decreased FAS activity. However, FAS down-regulation was not due to altered nuclear protein binding to FAS gene.
KW - Exercise training
KW - Fatty acid synthase
KW - Lipogenesis
KW - Nuclear protein binding
KW - Obesity
UR - http://www.scopus.com/inward/record.url?scp=0036301844&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036301844&partnerID=8YFLogxK
U2 - 10.1097/00005768-200207000-00009
DO - 10.1097/00005768-200207000-00009
M3 - Article
C2 - 12131249
AN - SCOPUS:0036301844
SN - 0195-9131
VL - 34
SP - 1106
EP - 1114
JO - Medicine and science in sports and exercise
JF - Medicine and science in sports and exercise
IS - 7
ER -