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Greg Cartee

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Primary Appointment: School of Kinesiology
Primary PIBS Dept.: Molecular and Integrative Physiology
PubMed Name: cartee gd
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  The research in the Muscle Biology Laboratory is focused on skeletal muscle metabolism. We are especially interested in the modulation of glucose transport by exercise and calorie restriction (CR; consuming 60% of ad libitum uptake), and how these interventions are influenced by advancing age. Each of these interventions can lead to a substantial improvement in skeletal muscle insulin sensitivity, which is a significant benefit for health.

Exercise: Even with many years of regular exercise training, a substantial portion of the exercise effect on improved insulin sensitivity is attributable to the effects of the most recent exercise session. This acute exercise effect can last for several hours to several days. Insulin resistance (a lower than normal ability to clear blood glucose in the presence of normal blood insulin) is an essential defect in Type 2 Diabetes, and even in the absence of diabetes, insulin resistance is linked to many other pathologies, including atherogenesis, hypertension, cardiovascular disease, renal disease, some cancers, and cognitive dysfunction. For this reason, improved insulin sensitivity is an especially important health benefit of exercise. In addition, the improved insulin sensitivity has implications for exercise performance because it facilitates the restoration and supercompensation of muscle glycogen stores, thereby improving the capacity for subsequent exercise. Although it has been known for over twenty years that a single exercise bout can lead to a subsequent increase in insulin-stimulated glucose transport, the precise mechanisms that underlie this important benefit remain uncertain. Attempting to explain this elusive process is a primary goal of our research.

Akt Substrate of 160 kDa (AS160): Phosphorylation of the signaling protein called AS160 is the most distal insulin signaling event that has been linked to GLUT4 glucose transporter translocation in adipocytes. We recently demonstrated that AS160 found in skeletal muscle also becomes phosphorylated in response to either insulin or contractile activity, raising the possibility that this protein may represent a convergence between the insulin signaling and exercise/contraction pathways for increasing cell surface GLUT4 and glucose transport. We also found that in vivo exercise can elevate AS160 phosphorylation in skeletal muscle immediately post-exercise in the absence of insulin and 4 hours post-exercise in the presence of insulin. We are currently performing experiments to understand the regulation and function of AS160 in skeletal muscle.

Calorie Restriction (CR): A short period of reduced calorie intake (consuming ~60% of usual ad libitum intake for 20 days) can enhance insulin sensitivity for skeletal muscle glucose uptake. The figure above illustrates some of the key steps in the insulin signaling pathway that leads to increased glucose transport in skeletal muscle. We have found that Akt2 (in skeletal muscle, two isoforms of this protein are abundantly expressed: Akt1 and Akt2) is essential for the full-effect of short-term (20 days) calorie restriction on insulin-stimulated glucose transport. We are currently attempting to understand the signaling steps proximal and distal to Akt2 that are also important for this effect.