Pathophysiological changes after lipopolysaccharide-induced acute inflammation in a type 2 diabetic rat model versus normal controls.

Abstract Aims The present study aimed to explore the mechanism of a potential beneficial effect of pre-existing diabetes in acute hyperglycemia during critical illness. Methods Pathophysiological changes including blood glucose variability, changes of inflammatory and oxidative stress responses after lipopolysaccharide (LPS)-induced acute infection were compared between type 2 diabetic rat model (GK rats) and normal controls (Wistar rats). Results After LPS injection, Wistar rats showed serious infective symptoms while GK rats did not. Blood glucose (BG) levels were significantly elevated in both GK and Wistar rats; however, compared to Wistar rats, GK rats had lower BG variability, smaller increases in the serum tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels, a larger increase in the serum IL-10 level, and a smaller decrease in the IκB-α protein level of lung tissue. Serum malondialdehyde (MDA) levels increased and serum total antioxidant capacity (T-AOC) levels decreased for both GK and Wistar rats. Conclusions We found diabetes was associated with adaptive changes at the cellular level that might actually be protective in acute hyperglycemia–mediated damage during sepsis. Chronic exposure to hyperglycemia potentially reduced the acute deleterious effects of acute hyperglycemia on septic mortality by decreasing BG variability, blunting the pro-inflammatory response and elevating the anti-inflammatory response.