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Diabetes Alters the Translocation of Insulin-Sensitive Glucose Transporters in the Lung

Diabetes Alters the Translocation of Insulin-Sensitive Glucose Transporters in the Lung

Allison Campolo

Physiological Sciences

While the morbidity and mortality of diabetes have recently reached epidemic levels worldwide, respiratory infections have long been a significant cause of death in humans as well. It is now clear that hyperglycemia is an independent risk factor for the development of respiratory infections. Our long term goal is to investigate whether the hyperglycemic state will predispose patients to increased glucose concentrations in the airway surface liquid, promoting bacterial proliferation in the airway. Although the lung is a major organ to utilize glucose, the regulation of glucose transport in the healthy and diabetic lung have received little attention. Glucose transport is regulated by a family of specialized proteins, called the glucose transporters (GLUTs). We hypothesized that the type 2 diabetic condition would alter GLUT activity in the lung. To test this hypothesis, we used a type 2 diabetic mouse model (n=10/group). After feeding a high-fat diet (60% kcal from fat) for 9 months, mice became hyperglycemic, hyperinsulinemic, insulin resistant, and glucose intolerant. GLUT protein content was quantified by Western blotting in the total lysate and membrane-enriched fraction of whole lung homogenates. Cell surface GLUT content was quantified using the biotinylated photolabeled technique. To our knowledge, we are the first to apply this state-of-the-art technique to the study of GLUT trafficking in the lung. In addition, we are the first to report the protein expression of several basal and insulin-sensitive GLUT isoforms, including GLUT-1, -2, -3, -4, -8, - 10 and -12 in the healthy adult rodent lung. Total protein content of these GLUT isoforms was unchanged in the whole lung of diabetic rodents as compared to their healthy counterparts. In contrast, cell surface protein content of GLUT8, a novel insulin-sensitive isoform, was significantly decreased in the diabetic lung (p