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Published on: June 24, 2020
Prenatal Exposure to Lipopolysaccharide Induces PTX3 Expression and Results in Obesity in Mouse Offspring
Shugang Qin1, Xin Chen1, Meng Gao1
1Institute of Materia Medical, College of Pharmacy, Third Military Medical University, Chongqing, 400038, China.
Insights
Inflammation during pregnancy, triggered by lipopolysaccharide (LPS), directly causes obesity in offspring. This occurs via increased inflammatory factor PTX3, which disrupts fat development and metabolism, offering new therapeutic targets for obesity.
Area of Science:
- Reproductive biology
- Metabolic disorders
- Immunology
Background:
- Obesity is a complex metabolic disorder with significant public health implications.
- The direct causal link between inflammation and obesity, particularly during prenatal development, remains incompletely understood.
- Inflammatory factors may play a role in metabolic dysregulation, but specific mechanisms are unclear.
Purpose of the Study:
- To investigate whether inflammation during pregnancy can directly cause obesity in offspring.
- To identify key inflammatory mediators involved in inflammation-induced obesity.
- To elucidate the underlying molecular mechanisms by which inflammation affects offspring metabolism and adipogenesis.
Main Methods:
- Pregnant mice were intraperitoneally injected with lipopolysaccharide (LPS) to induce inflammation.
- Offspring were assessed for body fat levels, blood lipid profiles, glucose metabolism, and expression of fat differentiation markers.
- The role of the inflammatory factor PTX3 and the MAPK pathway in mediating obesity was investigated.
Main Results:
- LPS-induced inflammation during pregnancy significantly increased PTX3 levels.
- Offspring exhibited abnormal fat development, dysregulated blood lipids, and impaired glucose metabolism.
- Increased expression of adipogenic markers and PTX3-mediated regulation via MAPK pathway hyperactivation were confirmed.
Conclusions:
- Prenatal inflammation is a direct cause of obesity in offspring.
- PTX3 is identified as a key mediator linking inflammation to obesity by regulating adipogenic markers through the MAPK pathway.
- Findings provide novel therapeutic targets and strategies for obesity prevention and treatment, emphasizing early anti-inflammatory interventions during pregnancy.
Abstract:
This study tested the hypothesis whether inflammation will directly lead to obesity. This study was designed to investigate the relationship between inflammation and obesity by intraperitoneally injecting pregnant mice with lipopolysaccharide (LPS) (75 μg kg-1). The results showed that inflammation during pregnancy could lead to a significant increase in the levels of the inflammatory factor PTX3. The offspring of the LPS-treated mice displayed abnormal levels of fat development, blood lipids, and glucose metabolism, and fat differentiation markers were significantly increased. Our study also confirmed that PTX3 can increase the susceptibility to obesity by regulating the expression of adipogenic markers; this regulatory role of PTX3 is most likely caused by MAPK pathway hyperactivation. Our study is the first to find strong evidence of inflammation as a cause of obesity. We determined that PTX3 was an important moderator of obesity, and we elucidated its mechanism, thus providing new targets and theories for obesity therapy. Moreover, our study provides new ideas and directions for the early intervention of anti-inflammation in pregnancy.
