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Sport and Exercise Science, School of Physical Activity and Human Services, and Department of Food Science and Nutrition, The Ohio State University, Columbus, Ohio 43210
Received 10 October 1995; accepted in final form 5 June 1996.
Ferrara, Cynthia M., W. Michael Sherman, Nicole Leenders,
Sylvia A. McCune, and Karla Roehrig. Exercise training and the
glucose transport system in obese
SHHF/Mcc-facp
rats. J. Appl. Physiol. 81(4):
1670-1676, 1996.
The effects of a similar exercise training
stimulus on maximal insulin-stimulated (MIS) plasma membrane glucose
transporter number and glucose transport were determined in lean and
obese
SHHF/Mcc-facp
rats. Six-week-old lean and obese male rats were randomly divided into
four groups: lean sedentary (LSed), obese sedentary (OSed), lean
exercise (LEx), and obese exercise (OEx). An 8- to 12-wk treadmill
running program equalized daily muscular work for LEx and OEx. Plasma
membranes were isolated from control and MIS muscles of mixed fiber
types. MIS significantly increased glucose transport (3.4- and
2.8-fold) in LSed and OSed, respectively. MIS significantly increased glucose transporter number (2.5-fold) in LSed, but there was
no increase in glucose transporter number in OSed. Peak oxygen uptake
and citrate synthase activity were increased a similar amount for LEx
and OEx groups, demonstrating a similar training stimulus. MIS
significantly and similarly increased glucose transport in LEx and OEx
(4.4- and 5.1-fold, respectively). The effects of MIS on plasma
membrane glucose transporter number in the exercise-trained rats were
similar to the responses observed in the sedentary lean and obese
groups. MIS significantly increased glucose transporter number
(2.6-fold) in LEx, whereas there was no increase in glucose transporter
number in OEx. The reduction in MIS glucose transport in OSed appears
to be related to a defect in the processes associated with the
translocation of glucose transporters to the plasma membrane. Exercise
training of the obese rats apparently did not alter this defect.
Similar increases in peak oxygen uptake, citrate synthase, and MIS
glucose transport in LEx and OEx groups suggest that insulin resistance
does not limit the ability of the glucose transport system to adapt to
exercise training in the obese male
SHHF/Mcc-facp
rats.
exertion; obesity; non-insulin-dependent diabetes; insulin resistance
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