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EXERCISE INCREASES GLUCOSE TRANSPORTER-4 LEVELS IN MONONUCLEAR CELLS IN SLED DOGS AND STUDENT ATHLETES

Abstract

The principle role of insulin is to stimulate the redistribution of the glucose transporter, GLUT4, from intracellular vesicles to the plasma membrane. Exercise has been a cornerstone treatment for individuals with insulin resistance (IR) because, in part, exercise causes an increase in GLUT4 in skeletal muscle in humans and animals, independent of insulin. There is currently no direct method for diagnosing IR that has widespread clinical application. Insulin resistance is typically diagnosed with indirect methods that rely on fasting insulin and glucose levels such as the Homeostatic Model of Assessment (HOMA-IR) or indicators of prolonged elevated glucose such as glycosylated hemoglobin (HbA1c) and/or oral glucose tolerance test along with an array of comorbidities. Interestingly, in the past decade, GLUT4 has been shown to increase in peripheral blood mononuclear cells (PBMC) in response to insulin. A similar increase in GLUT4 in PBMC in response to exercise had not been reported. PURPOSE: To measure the effects of exercise on GLUT4 in PBMC in both canine and human athletes. METHODS: Initially, we compared GLUT4 in PBMC between 12 conditioned sled dogs and 12 sedentary sled dogs. A follow-up study compared GLUT4 in PMBC between 16 NCAA cross-country ski student-athletes and 16 sedentary students at the University of Alaska. For both studies, other indices of insulin resistance were measured including, but not limited to HbA1C, HOMA-IR, and BMI. RESULTS: All biochemical and demographic parameters were comparable between groups. However, GLUT4 in conditioned sled dogs (6690 ± 184 ng/g protein vs. 4290 ± 773 ng/g protein) and conditioned humans (116±49.8 mg/g protein vs. 65.6±58.5 mg/g protein) were significantly higher than in their sedentary counterparts (p

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