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

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.