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Insulin Resistance Alters Basal But Not Insulin-Sensitive Glucose Transporter Expression In The Colon"

Insulin Resistance Alters Basal But Not Insulin-Sensitive Glucose Transporter Expression In The Colon

Name:
Alia Houser

Department:
Physiological Sciences

Abstract:
Obesity and type 2 diabetes have been identified as key risk factors in the development of colon cancer. Insulin resistance (IR), the hallmark of obesity and diabetes, has been suggested as a potential underlying mechanism leading to colon cancer. However, the role of insulin and glucose metabolism in the colon of healthy and diabetic patients has received little attention. Glucose uptake from the bloodstream into cells is the rate-limiting step of glucose utilization and is regulated via specific glucose transporter proteins (GLUTs). Although GLUTs -4 and -8 have been identified as insulin- sensitive isoforms, their role and regulation in the colon remains elusive. Therefore, we hypothesized that insulin resistance will impair GLUT expression and trafficking in the colon. To test our hypothesis, we used an insulin resistant (IR) C57Bl/6 mouse model paired with age-matched animals fed a normal control type diet (CD). Mice fed a high-fat-diet, became obese, hyperinsulinemic, and displayed insulin resistance. At 9 months, the distal colons were collected. The protein expression of basal and insulin-sensitive GLUT isoforms (-1, -4, -8, -10) was quantified from total lysate and membrane-enriched fractions by Western blotting (n=11/group). We found that basal GLUT1, the novel GLUT10 isoform, and the insulin-sensitive GLUT -4 and -8 proteins were expressed in the distal colon of healthy mice. There was a significant reduction in the total protein expression of GLUT-1 and -10 in the colon of IR animals compared to healthy controls (by 33% and 38% respectively, p