Abstract
To investigate the different effects of acute pulmonary infection induced by Escherichia coli (E. coli) on lipid metabolism between diet-induced obesity (DIO, fed with high-fat diet) mice and lean mice. A total of 180 ICR mice were selected to be challenged intranasally with phosphate-buffered saline or 109 CFUs/mL of E. coli, and the body character indexes, biochemical indexes and expressions of genes and proteins involved in lipid metabolism were examined pre- and post-infection. Results revealed that, before infection, DIO mice had significantly higher body weight, adipose and liver indexes, free fatty acid and triglyceride contents than lean mice. After infection, increased free fatty acid and triglyceride contents, increased expressions of resistin, SREBP-1c, ACC1, FAS and SCD-1, and declined PPARα, CPT-1α expressions and AMPKα phosphorylation were detected in the infected group, while the change rates were more serious in the lean mice than the DIO mice. The above-mentioned findings verified that, after being infected with E. coli, hepatic lipid metabolism disorder was aggravated by activating SREBP-1c related lipid synthesis pathway and inhibiting PPARα related fatty acid oxidation pathway. However, infection-induced lipid metabolic disorders was slighter in the DIO mice than the lean mice through AMPKα pathway.
Highlights
With the improvement of living standards, nonalcoholic fatty liver disease (NAFLD) has become a global public health problem affecting approximately 15-20% of the general population in Asia and over 30% in West [1]
After infection, increased free fatty acid and triglyceride contents, increased expressions of resistin, SREBP‐1c, ACC1, FAS and SCD‐1, and declined Peroxisome proliferator-activated receptor α (PPARα), CPT‐1α expressions and AMPKα phosphorylation were detected in the infected group, while the change rates were more serious in the lean mice than the DIO mice
Our preliminary studies found that obese mice exhibited improved host defenses against infection, and promoting recovery in E. coli-induced acute non-fatal bacterial pneumonia with enhanced immune response [5]
Summary
With the improvement of living standards, nonalcoholic fatty liver disease (NAFLD) has become a global public health problem affecting approximately 15-20% of the general population in Asia and over 30% in West [1]. Obesity is an independent factor for NAFLD, which can increase the prevalence of NAFLD by 40%-50%, and almost 2/3 of obese patients are hepatic steatosis [2]. Insulin resistance and low-grade inflammation in obesity were suggested to be involved with the development of NAFLD [3]. Patients with bacterial or viral infections and animals treated with lipopolysaccharide (LPS) or lipoteichoicacid (LTA) exhibited increased serum triglycerides levels and hepatic lipid accumulation [4]. Our preliminary studies found that obese mice exhibited improved host defenses against infection, and promoting recovery in E. coli-induced acute non-fatal bacterial pneumonia with enhanced immune response [5]. Other studies showed that obesity was a risk factor for pneumonia [6], nosocomial infections [7], and surgical infections [8]
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