N-Acetyl-chitobiose ameliorates metabolism dysfunction through Erk/p38 MAPK and histone H3 phosphorylation in type 2 diabetes mice

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• 作者：Xia Wu^a ; Jing Wang^b ; Yuqin Shi^b ; Sai Chen^a ; Qiaojuan Yan^a ; Zhengqiang Jiang^b ; ^{zhqjiang@cau.edu.cn} ; Hao Jing^b
• 关键词：ALX ; alloxan ; COS ; chitooligosaccharide ; Erk ; extracellular signal-regulated kinase ; (GlcNAc)2 ; N-acetyl-chitobiose (PubChem CID ; 160244) ; H&E ; haematoxylin and eosin ; HOMA-IR ; homeostasis model assessment of insulin resistance ; IC50 ; the 50% inhibitory concentration ; IL-1β ; interleukin-1 beta ; JNK ; c-Jun terminal kinase ; MAPK ; mitogen-activated protein kinase ; MDA ; malondialdehyde ; MKK ; MAPK kinases ; MSK ; mitogen and stress activated protein kinase ; NF-κB ; nuclear factor-kappaB ; SOD ; superoxide
• 刊名：Journal of Functional Foods
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：28
• 期：Complete
• 页码：96-105
• 全文大小：2562 K
• 卷排序：28

文摘

This is the first study on the improvement of N-acetyl-chitobiose on diabetes-related metabolism disorders. N-Acetyl-chitobiose lowered blood glucose and improved glucose intolerance and insulin sensitivity. N-Acetyl-chitobiose inhibited MAPK signaling pathways in type 2 diabetes model mice.