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

Praziquantel treatment after Schistosoma japonicum infection maintains hepatic insulin sensitivity and improves glucose metabolism in mice.
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日本血吸虫感染后吡喹酮治疗可维持小鼠肝脏胰岛素敏感性并改善葡萄糖代谢。

DOI:
10.1186/s13071-017-2400-5
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发表时间:
2017-10-02
影响因子:
3.2
通讯作者:
Ji M
Ji M
中科院分区:
医学2区
文献类型:
--
作者:
Luo X;Zhu Y;Liu R;Song J;Zhang F;Zhang W;Xu Z;Hou M;Yang B;Chen L;Ji M

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中国流行病学研究表明,日本血吸虫感染与代谢综合征呈负相关,即使反复使用吡喹酮(PZQ)化疗后也是如此。我们研究了慢性日本血吸虫感染、PZQ化疗和可溶性卵抗原(SEA)治疗对小鼠全身代谢稳态和肝脏胰岛素敏感性的影响。日本血吸虫感染可增加小鼠全身和肝脏胰岛素敏感性。PZQ化疗可显著改善感染小鼠的生理状态,维持Th2免疫偏差,增强肝脏胰岛素敏感性。多元线性回归分析显示,抗炎细胞因子的表达与肝脏中胰岛素信号相关基因的表达呈正相关,这是由IL-13和IL-22体外刺激的肝细胞系证实的。SEA治疗还改善了Lepr db/db小鼠的葡萄糖耐量和胰岛素敏感性。本研究提示慢性日本血吸虫感染联合PZQ化疗和SEA治疗可通过促进肝脏Th2和调节反应调节代谢稳态,预防代谢综合征。本文的在线版本(10.1186/s13071-017-2400-5)包含补充材料,授权用户可使用。
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. 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. 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. The online version of this article (10.1186/s13071-017-2400-5) contains supplementary material, which is available to authorized users.
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