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HIGHLIGHTED TOPICS
Role of Exercise in Reducing the Risk of Diabetes and Obesity

Voluntary exercise training enhances glucose transport but not insulin signaling capacity in muscle of hypertensive TG(mREN2)27 rats

Muscle Metabolism Laboratory, Department of Physiology, University of Arizona College of Medicine, Tucson, Arizona

Submitted 27 January 2005 ; accepted in final form 16 February 2005

Male heterozygous TG(mREN2)27 rats (TGR) overexpress a murine renin transgene, display marked hypertension, and have insulin resistance of skeletal muscle glucose transport and insulin signaling. We have shown previously that voluntary exercise training by TGR improves insulin-mediated skeletal muscle glucose transport (Kinnick TR, Youngblood EB, O’Keefe MP, Saengsirisuwan V, Teachey MK, and Henriksen EJ. J Appl Physiol 93: 805–812, 2002). The present study evaluated whether this training-induced enhancement of muscle glucose transport is associated with upregulation of critical insulin signaling elements, including insulin receptor substrate-1 (IRS-1), phosphatidylinositol 3-kinase, Akt, and glycogen synthase kinase-3. TGR remained sedentary or ran spontaneously in activity wheels for 6 wk, averaging 7.1 ± 0.8 km/day by the end of week 3 and 4.3 ± 0.5 km/day over the final week of training. Exercise training reduced total abdominal fat by 20% (P < 0.05) in TGR runners (2.64 ± 0.01% of body weight) compared with sedentary TGR controls (3.28 ± 0.01%). Insulin-stimulated (2 mU/ml) glucose transport activity in soleus muscle was 36% greater in TGR runners compared with sedentary TGR controls. However, the protein expression and functionality of tyrosine phosphorylation of insulin receptor and IRS-1, IRS-1 associated with the p85 regulatory subunit of phosphatidylinositol 3-kinase, and Ser⁴⁷³ phosphorylation of Akt were not altered by exercise training. Only insulin-stimulated glycogen synthase kinase-3 Ser⁹ phosphorylation was increased (22%) by exercise training. These results indicate that voluntary exercise training in TGR can enhance insulin-mediated glucose transport in skeletal muscle, as well as reduce total abdominal fat mass. However, this adaptive response in muscle occurs independently of modifications in the proximal elements of the insulin signaling cascade.

spontaneous running; insulin receptor substrate-1; phosphatidylinositol 3-kinase; Akt; glycogen synthase kinase-3; soleus

This article has been cited by other articles:

				E. J. Henriksen Improvement of insulin sensitivity by antagonism of the renin-angiotensin system Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2007; 293(3): R974 - R980. [Abstract] [Full Text] [PDF]