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Praziquantel treatment after Schistosoma japonicum infection maintains hepatic insulin sensitivity and improves glucose metabolism in mice

BACKGROUND: Epidemiological studies in China have revealed that Schistosoma japonicum infection is inversely correlated with metabolic syndrome, even after repeated chemotherapy with praziquantel (PZQ). We investigated the effect of chronic S. japonicum infection, PZQ chemotherapy, and soluble egg a...

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Detalles Bibliográficos
Autores principales: Luo, Xiaofeng, Zhu, Yuxiao, Liu, Ran, Song, Jingwei, Zhang, Fan, Zhang, Wenyue, Xu, Zhipeng, Hou, Min, Yang, Bingya, Chen, Lin, Ji, Minjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5625765/
https://www.ncbi.nlm.nih.gov/pubmed/28969688
http://dx.doi.org/10.1186/s13071-017-2400-5
Descripción
Sumario:BACKGROUND: Epidemiological studies in China have revealed that Schistosoma japonicum infection is inversely correlated with metabolic syndrome, even after repeated chemotherapy with praziquantel (PZQ). We investigated the effect of chronic S. japonicum infection, PZQ chemotherapy, and soluble egg antigen (SEA) treatment on whole-body metabolic homeostasis and hepatic insulin sensitivity in mouse models. RESULTS: Infection with S. japonicum was found to increase whole-body and hepatic insulin sensitivity in mice. PZQ chemotherapy significantly improved the physiological status of infected mice, maintaining Th2 immune-deviation and enhancing hepatic insulin sensitivity. Multiple linear regression analysis revealed positive correlations between anti-inflammatory cytokine expression and insulin signalling-related genes in the liver, as demonstrated by an in vitro stimulated hepatic cell line with IL-13 and IL-22. SEA treatment also improved the glucose tolerance and insulin sensitivity in Lepr (db/db) mice. CONCLUSIONS: This study indicated that chronic S. japonicum infection with PZQ chemotherapy and SEA treatment can regulate metabolic homeostasis and protect against metabolic syndrome by promoting Th2 and regulatory responses in the liver. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13071-017-2400-5) contains supplementary material, which is available to authorized users.