期刊
BIOMEDICAL RESEARCH-TOKYO
卷 36, 期 1, 页码 63-70出版社
BIOMEDICAL RESEARCH PRESS LTD
DOI: 10.2220/biomedres.36.63
关键词
-
资金
- Vietnam National Foundation for Science and Technology Development (NAFOSTED) [106.05-2011.58]
This study, using C57BL/6J mice with streptozotocin (STZ)-induced diabetes, aimed to determine whether Bifidobacterium species (spp.) both induces the expressions of proteins in the insulin signaling pathway and enhances the expressions of certain adipocytokines. The protein expressions of I kappa B kinase alpha (IKK alpha), I kappa B kinase beta (IKK beta), nuclear factor-kappaB inhibitor alpha (I kappa B alpha), and the mitogen-activated protein kinase (MAPK) pathway were also investigated. Oral administration of Bifidobacterium spp. reduced blood glucose levels significantly and increased the protein expressions of insulin receptor beta, insulin receptor substrate 1, protein kinase B (Akt/PKB), IKK alpha, and I kappa B alpha. Extracellular-signal-regulated kinase 2 (ERK2) showed increased expression. Bifidobacterium spp. also induced the adiponectin expression and decreased both macrophage chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6) expression. In addition, IKK beta, c-Jun NH2-terminal kinase (JNK) and p38 MAP kinase expressions showed no significant changes in both groups. In conclusion, Bifidobacterium spp. may be the promising bacteria for treating diabetes.
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