ABSTRACT
AIM:To study whether the pulmonary infection of Escherichia coli (E.coli) interferes the glu-colipid metabolism in high-fat diet-induced obese mice.METHODS:High-fat diet-induced obese mice (n=48) and nor-mal chow-fed control mice ( n=48) were intranasally infused with 40 μL fluid containing 4 ×109 CFUs E.coli.The ser-um, periepididymal adipose tissue and liver were obtained at 0 d, 1 d, 2 d, 3 d and 4 d after infection.The body mass, periepididymal adipose tissue and liver were weighed , and the levels of fasting blood glucose (FBG), fasting blood insulin ( FINS) , free fatty acid ( FFA) and very-low-density lipoprotein ( VLDL) were measured by ELISA .The serum total cho-lesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol ( LDL-C) , and hepatic TG contents were detected , and the hepatic steatosis was observed under microscope with oil red O staining.RESULTS:Compared with day 0, the body mass, fat mass and fat index were decreased significantly from day 1 to day 4 after infection (P<0.05).The levels of FBG, FINS and HOMA-IR were apparently raised from day 2 to day 4 af-ter infection (P<0.05).The contents of serum FFA, TG and VLDL were increased markedly from day 1 to day 4 after in-fection (P<0.05).However, the concentrations of serum TC, LDL-C and HDL-C were decreased obviously from day 1 to day 3 ( P<0.05 ) .The liver mass , liver index and TG content were significantly increased from day 1 to day 4 ( P<0.05 ) .Consistently , the lipid droplet accumulation in the liver cells was increased obviously at day 2 and day 4 after infec-tion.Compared with control group , except the levels of serum TC , LDL-C and HDL-C in obese group substantially de-creased, the other indexes were increased by different degrees during the whole experiment period (P<0.05).CONCLU-SION:Pulmonary infection of Escherichia coli exacerbates the disorder of glucose and lipid metabolism in high-fat diet-in-duced obese mice , which contributes the development of insulin resistance and hepatic steatosis .