Endotoxemia induces a series of inflammatory responses that may result in lung injury. However, heat shock protein72 (HSP72) has the potential to protect the lungs from damage. The objective of this study was to determine whether prior exercise conditioning could increase the expression of HSP72 in the lungs and attenuate lung damage in diabetic rats receiving lipopolysaccharide (LPS). Streptozotocin was used to induce diabetes in adult male Wistar rats. Rats were randomly assigned to sedentary or exercise groups. Rats in the exercise condition ran on a treadmill 5 days/week, 30–60 min/day, with an intensity of 1.0 mile/hour over a 3-week period. Rats received an intravenous infusion of LPS after 24？hrs from the last training session. Elevated lavage tumor necrosis factor-alpha (TNF-α) level in response to LPS was more marked in diabetic rats. HSP72 expression in lungs was significantly increased after exercise conditioning, but less pronounced in diabetic rats. After administration of LPS, exercised rats displayed higher survival rate as well as decreased lavage TNF-α level and lung edema in comparison to sedentary rats. Our findings suggest that exercise conditioning could attenuate the occurrence of inflammatory responses and lung damage, thereby reducing mortality rate in diabetic rats during endotoxemia. 1. Introduction Pulmonary edema is a common complication of diabetes mellitus because of the increased capillary permeability [1]. Severely uncontrolled diabetic state may initiate pathologic events leading to the capillary leak of acute respiratory distress syndrome [2]. Due to the lower level and impaired binding activity of cell-surface receptors on monocytes [3], a poorly controlled diabetic state increases susceptibility to infections such as endotoxemia [4]. Additionally, infection can be more serious and difficult to eradicate in diabetic patients [5]. The highest incidence of acute respiratory distress syndrome occurred in endotoxemic patients and resulted in lung injury [6]. However, the severity of lung injury during systemic endotoxemiain type 1 diabetes remains unclear. Endotoxemia is mainly caused by anendotoxin (lipopolysaccharide; LPS) from gram-negative bacteria [7]. Endotoxins induce a great amount of alveolar monocytes and macrophages to release tumor necrosis factor-alpha (TNF-α), which subsequently damages pulmonary vessels and increases lung vascular/epithelial permeability. This change allows more albumins to pass from the vessels to the alveolar space. Consequently, albumin content in the brochoalveolar lavage fluid increases
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