Abstract:

Objective To investigate the responsive ability to acute inflammatory stimulus of type 2 diabetic rats and obese non-diabetic rats induced by high-fat diet. Methods Type 2 diabetic GK rats (GK group) and Wistar rats (Wistar group) were fed with high-fat diet for 14 weeks, and the body weight of rats in two groups were observed. Then rats were allocated to GK high-fat feeding baseline group (GK+HFF group), Wistar+HFF group, GK highfat feeding+lipopolysaccharide (LPS) injection group (GK+HFF+LPS group) and Wistar+HFF+LPS group by random number table, with 6 rats in each group. Severe sepsis model was established by intraperitoneal injection of 5 mg/kg LPS in GK+HFF+LPS group and Wistar+HFF+LPS group. The blood glucose fluctuation was observed, and the expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-10 mRNA in liver, lung, kidney and myocardial tissues was determined by Real-Time PCR. Results After feeding with highfat diet for 14 weeks, the body weight of rats in Wistar group was significantly higher than that in GK group (P<0.05), and the blood glucose concentration of rats in GK group was significantly higher than that in Wistar group (P<0.05). After LPS injection, the blood glucose concentration of rats in GK+HFF+LPS group significantly increased, while the blood glucose concentration of rats in Wistar+HFF+LPS group did not change significantly. Real-Time PCR revealed that the expression of TNF-α, IL-1β, IL-6 and IL-10 mRNA in Wistar+HFF+LPS group was significantly higher than that in Wistar+HFF group (P<0.05), and the expression of TNF-α, IL-1β, IL-6 and IL-10 mRNA in GK+HFF+LPS group was significantly higher than that in GK+HFF group (P<0.05). The increase of expression of TNF-α, IL-1β, IL-6 and IL-10 mRNA in Wistar+HFF+LPS group was not significantly different from that in GK+HFF+LPS group (P>0.05). Conclusion After feeding with high-fat diet, the tolerance to acute inflammation may increase in obese non-diabetic rats, which is more significant than that in type 2 diabetic rats.

Key words: diabetes mellitus, obesity, stress hyperglycemia, inflammation, type 2 diabetic rat