期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 13, 期 -, 页码 5187-5194出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/3074
关键词
diabetes; inflammation; cytokine; macrophage; insulin resistance; review
资金
- NIDDK NIH HHS [DK064862] Funding Source: Medline
The incidence of type 2 diabetes (T2D) is rapidly expanding. Some of the more obvious pathologies associated with it include: defective glucose metabolism, obesity, cardiovascular disease and an inability to mount an effective immune response to infection by certain pathogenic organisms, leading to sepsis and death. A common tie linking these seemingly disparate complications is chronic inflammation. Today we know that inflammation is regulated locally and systemically by numerous biochemical signals. One of the most important of these signals is a class of molecules called cytokines. Cytokines can be generally classified as proinflammatory or anti-inflammatory and allow an organism to respond rapidly to an immune challenge by coordinating an appropriate immune response. In T2D, the balance between proinflammatory and anti-inflammatory cytokines is shifted toward proinflammation, potentially causing or exacerbating the health complications found in T2D. Overnutrition has been shown to trigger the innate immune system but activation of the innate immune system, itself, induces hyperglycemia and insulin resistance. In all likelihood, diabetes and chronic inflammation are inseparable and act as a reciprocal feed-forward loop.
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