LAUSR

Hyperglycemia is an independent risk factor for the development of respiratory diseases, including influenza infections. Although the lung is a major organ to utilize glucose, the regulation of glucose transport in the healthy and diabetic lung has received little attention. We hypothesized that hyperglycemia would predispose diabetic mice to alterations in pulmonary glucose transport and pulmonary complications during Influenza A infection. To test this hypothesis, we used a streptozotocin-induced type 1 diabetic mouse model (n=8-12/group). A subset of diabetic mice was treated with insulin via a subcutaneous insulin pump to restore euglycemia. After 8 weeks, an additional subset of mice was intranasally infected with influenza A H1N1 (A/PR/8/34; 250 PFU). Viral titer was determined from bronchoalveolar lavage (BAL) fluid by plaque assay. Glucose concentration in BAL fluid was measured spectrophotometrically. Glucose transporter (GLUT) protein content was quantified in whole lung homogenates by Western blotting. Both infected and uninfected diabetic mice had higher glucose concentrations in BAL fluid than their control or insulin-treated counterparts (p Disclosure A. Campolo: None. Z. Maria: None. M. Hinsdale: None. L. Liu: None. V. Lacombe: None.