Inflammatory Process in Type 2 Diabetes: The Role of Cytokines

Authors: ALEXANDRAKI, KRYSTALLENIA1; PIPERI, CHRISTINA1; KALOFOUTIS, CHRISTOS1; SINGH, JAIPAUL2; ALAVERAS, ANTONIS1; KALOFOUTIS, ANASTASIOS1

Source: Annals of the New York Academy of Sciences, Volume 1084, Number 1, November 2006 , pp. 89-117(29)

Publisher: Wiley-Blackwell

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Abstract:

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Population-based studies have shown strong relationship between inflammatory markers and metabolic disturbances, obesity, and atherosclerosis, whereas inflammation has been considered as a “common soil” between these clinical entities and type 2 diabetes (T2D). The accumulation of macrophages in adipose tissue (AT), the common origin of macrophages and adipocytes, the prevalent presence of peripheral mononuclear cells, and apoptotic β cells by themselves seem to be the sources of inflammation present in T2D, since they generate the mediators of the inflammatory processes, namely cytokines. The main cytokines involved in the pathogenesis of T2D are interleukin-1β (IL-1β), with an action similar to the one present in type 1 diabetes, tumor necrosis factor-α (TNF-α), and IL-6, considered as the main regulators of inflammation, leptin, more recently introduced, and several others, such as monocyte chemoattractant protein-1, resistin, adiponectin, with either deleterious or beneficial effects in diabetic pathogenesis. The characterization of these molecules targeted diabetes treatment beyond the classical interventions with lifestyle changes and pharmaceutical agents, and toward the determination of specific molecular pathways that lead to low grade chronic inflammatory state mainly due to an immune system's unbalance.

Keywords: type 2 diabetes mellitus; inflammation; cytokines

Document Type: Research article

DOI: http://dx.doi.org/10.1196/annals.1372.039

Affiliations: 1: Laboratory of Biological Chemistry, University of Athens Medical School, Goudi 11527, Athens, Greece 2: Department of Biological Sciences, University of Central Lancashire, Preston PR1 2HE, UK

Publication date: 2006-11-01

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