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J Physiol Volume 586, Number 17, 4241-4249, September 1, 2008 DOI: 10.1113/jphysiol.2008.156745
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ALIMENTARY

Cessation of daily exercise dramatically alters precursors of hepatic steatosis in Otsuka Long-Evans Tokushima Fatty (OLETF) rats

 R. Scott Rector1, John P. Thyfault1,2,3, Matthew J. Laye4, R. Tyler Morris4, Sarah J. Borengasser3, Grace M. Uptergrove1, Manu V. Chakravarthy5, Frank W. Booth4,6,7 and Jamal A. Ibdah1,2,4

1 Division of Gastroenterology and Hepatology
2 Harry S. Truman Memorial Veterans Medical Center, Departments of
3 Nutritional Sciences
4 Medical Pharmacology and Physiology
6 Biomedical Sciences
7 Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65212, USA
5 Endocrinology, Metabolism, and Lipid Research, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA

The purpose of this study was to delineate potential mechanisms initiating the onset of hepatic steatosis following the cessation of daily physical activity. Four-week-old, hyperphagic/obese Otsuka Long-Evans Tokushima Fatty rats were given access to voluntary running wheels for 16 weeks to prevent the development of hepatic steatosis. The animals were then suddenly transitioned to a sedentary condition as wheels were locked (wheel lock; WL) for 5 h (WL5), 53 h (WL53) or 173 h (WL173). Importantly after the cessation of daily exercise (5–173 h), no changes occurred in body weight, fat pad mass (omental and retroperitoneal), food intake, serum insulin, hepatic triglycerides or in the exercise-suppressed hepatic stearoyl-CoA desaturase-1 and peroxisome proliferator-activated receptor-{gamma} protein content. However, complete hepatic fatty acid oxidation and mitochondrial enzyme activities were highest at WL5 and WL53 and dropped significantly to SED levels by WL173. In addition, cessation of daily exercise quickly increased the hepatic protein contents of fatty acid synthase and acetyl-coenzyme A carboxylase (ACC), reduced ACC phosphorylation status, and dramatically increased hepatic malonyl-CoA concentration. This study is the first to show that the sudden cessation of daily exercise in a hyperphagic/obese model activates a subgroup of precursors and processes known to initiate hepatic steatosis, including decreased hepatic mitochondrial oxidative capacity, increased hepatic expression of de novo lipogenesis proteins, and increased hepatic malonyl CoA levels; each probably increasing the susceptibility to non-alcoholic fatty liver disease.

(Received 12 May 2008; accepted after revision 8 July 2008; first published online 10 July 2008)
Corresponding author J. A. Ibdah: Division of Gastroenterology and Hepatology, 5 Hospital Drive, CE405 Clinical Support & Education Building, University of Missouri-Columbia, Columbia, MO 65212, USA. Email: ibdahj{at}health.missouri.edu






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