Synergistic influence of asthma and obesity on hepatic metabolism in a mouse model

Background Obesity is a widespread disease with increasing case numbers and serious health consequences. Asthma is the most common chronic respiratory disease. Asthma and obesity frequently co-occur and usually negatively influence the respective disease course. Recent epidemiological studies suggest a pathomechanistic link between obesity and asthma. Molecular biology studies on the mechanism of this interaction, however, are missing.

Methods Four groups of C57BL/6 mice (n=6 animals each) were fed either a high-fat diet (HFD) or normal diet (ND) until 20 weeks of age. During the last 4 weeks mice were additionally treated by repeated intranasal applications of house dust mite extract (HDM) or PBS as a control. Liver samples were analyzed by qRT-PCR and immunohistochemistry for biochemical markers of glucose metabolism and inflammatory parameters.

Results In all groups with HFD or HDM exposure, genes of glucose metabolism were regulated. In particular, expression of glycolysis associated enzymes such as phosphofructokinase 1 and aldolase were decreased in the HDM/HFD group. In addition, a decrease of succinyl-CoA synthetase was detected in liver tissue by both, qRT-PCR and immunohistochemistry. While IL-10 as a parameter of hepatic anti-inflammatory immune response was increased in the HDM group, markers for Th1 immune response were downregulated in the HDM/HFD group.

Conclusion Our results demonstrate the potentiated morbidity of asthma and obesity on parameters of hepatic glucose metabolism and hepatic inflammation. Therefore, asthma and obesity show a synergistic negative impact on liver function and thus increasing liver injury.

Publication History

Article published online:
23 January 2024