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Am J Physiol Endocrinol Metab 290: E207-E212, 2006; doi:10.1152/ajpendo.00608.2004
0193-1849/06 $8.00
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Physical training reverses the increased activity of the hepatic ketone body synthesis pathway in chronically diabetic rats

Adil El Midaoui,1 Jean Louis Chiasson,2 Gilles Tancrède,1 and André Nadeau1

1Diabetes Research Unit, Research Center of Laval University Medical Center, Ste Foy; and 2Research Group on Diabetes and Metabolic Regulation, Research Centre, Centre Hospitalier de l’Université de Montréal, Hôtel-Dieu, Montreal, Quebec, Canada

Submitted 23 December 2004 ; accepted in final form 27 July 2005

This study was designed to examine whether the training-induced improvement in the plasma concentration of ketone bodies in experimental diabetes mellitus could be explained by changes in the activity of the hepatic ketone body synthesis pathway and/or the plasma free fatty acid levels. Diabetes mellitus was induced by an intravenous injection of streptozotocin (50 mg/kg), and training was carried out on a treadmill. The plasma concentration of {beta}-hydroxybutyric acid was increased (P < 0.001) in sedentary diabetic rats, and this was partly reversed by training (P < 0.001). The plasma concentration of free fatty acids was increased (P < 0.001) in sedentary diabetic rats, and this was reversed to normal by training (P < 0.001). Diabetes was also associated with an increased activity of the hepatic ketone body synthesis pathway. When the data are expressed as per total liver, physical training decreased the activity of the hepatic ketone body synthesis pathway by 18% in nondiabetic rats (P < 0.05) and by 22% in diabetic rats (P < 0.01), the activity present in trained diabetic rats being not statistically different from that of sedentary control rats. These data suggest that the beneficial effects of physical training on the plasma {beta}-hydroxybutyric acid levels in the diabetic state are probably explained in part by a decrease in the activity of the hepatic ketone body synthesis pathway and in part by a decrease in plasma free fatty acid levels.

{beta}-hydroxybutyric acid; streptozotocin; diabetes



Address for reprint requests and other correspondence: A. El Midaoui, Toronto General Hospital, MBRC, 4R-414 Research 20, 200 Elizabeth St., Toronto, ON M5G 2C4 Canada (e-mail: aelmidaoui{at}sympatico.ca)







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