Early microcystin-LR exposure-linked inflammasome activation in mice causes development of fatty liver disease and insulin resistance.
Early microcystin-LR exposure-linked inflammasome activation in mice causes development of fatty liver disease and insulin resistance.
复制标题
小鼠的早期微囊LR暴露于小鼠的炎性体激活会导致脂肪肝病和胰岛素抵抗的发展。
DOI：
10.1016/j.etap.2020.103457
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发表时间：
2020-11
影响因子：
4.3
通讯作者：
Chatterjee S
中科院分区：
文献类型：
--
作者：
Al-Badrani M;Saha P;Mondal A;Seth RK;Sarkar S;Kimono D;Bose D;Porter DE;Scott GI;Brooks B;Raychoudhury S;Nagarkatti M;Nagarkatti P;Chatterjee S
来自儿科研究的证据表明，婴儿和儿童存在早期接触微囊藻毒素的风险。本报告验证了这样一种假设，即生命早期暴露于微囊藻毒素（MC）（有害藻华的主要成分），随后幼年暴露于高脂肪饮食喂养，可增强成年期非酒精性脂肪性肝病表型的发展。结果显示早期NAFLD相关炎症的典型症状。细胞因子和趋化因子如CD68、il -1 β、MCP-1、TNF-α以及α-SMA在高脂饮食中暴露于MC-LR组中与对照组相比有所增加。此外，在机制上，NLRP3 KO小鼠表现出炎症和NAFLD表型的显著降低，并抵抗肝脏胰岛素抵抗和葡萄糖代谢等代谢变化。数据表明，儿童时期MC-LR暴露和随后的NLRP3炎性体激活可能影响青少年的肝脏健康。
Evidence from pediatric studies show that infants and children are at risk for early exposure to microcystin. The present report tests the hypothesis that early life exposure to microcystin (MC), a principal component of harmful algal blooms followed by a juvenile exposure to high-fat diet feeding potentiate the development of nonalcoholic fatty liver disease phenotype in adulthood. Results showed classical symptoms of early NAFLD linked inflammation. Cytokines and chemokines such as CD68, IL1β, MCP-1, and TNF-α, as well as α-SMA were increased in the groups that were exposed to MC-LR with the high-fat diet compared to the vehicle group. Also, mechanistically, NLRP3 KO mice showed a significant decrease in the inflammation and NAFLD phenotype and resisted the metabolic changes such as insulin resistance and glucose metabolism in the liver. The data suggested that MC-LR exposure and subsequent NLRP3 inflammasome activation in childhood could impact liver health in juveniles.
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影响因子：
10.4
作者：
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通讯作者：
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作者：
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影响因子：
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作者：
Abdelmegeed MA;Song BJ
通讯作者：
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