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ISSN 0188-9796 (Print)

2006, Number 2

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Rev Endocrinol Nutr 2006; 14 (2)

Linking of the inflammatory response, obesity and diabetes with the stress of the endoplasmic reticulum by means of the selenoprotein S actions

Bastarrachea RA, Curran JE, Eugenia BV, Kent JJ, López-Alvarenga JC, Téllez-Mendoza J, Blangero J, Comuzzie AG

Language: Spanish
References: 53
Page: 89-101
PDF size: 188.39 Kb.


ABSTRACT

The inflammatory component in obesity and diabetes is now firmly established with the discovery of causal links between inflammatory mediators, such as tumor necrosis factor-alpha (TNF-α) and insulin receptor signaling and the elucidation of the underlying molecular mechanisms, such as c-Jun NH2-terminal kinase (JNK) and inhibitor of nuclear factor-kappa β kinase-mediated transcriptional and post-translational modifications (IKK) that inhibit insulin action. It has been recently demonstrated that the endoplasmic reticulum (ER) might be a key site where the metabolic signals are sensed, integrated, and transmitted in the form of stress signals, including activation of JNK, IKK, and possibly other pathways. Elimination of misfolded proteins from the endoplasmic reticulum (ER) by retro-translocation is an important physiological adaptation to ER stress. A new protein named mammalian selenoprotein S has been recently identified. It putatively functions in the stress responses of the endoplasmic reticulum (ER) that are linked to the immune and inflammatory signaling pathways. It is encoded by SEPS1 (also called VIMP), a gene involved in stress response in the endoplasmic reticulum and inflammation control. This celuarticle will review the link between stress, inflammation, selenoproteins and metabolic disease, particularly type 2 diabetes, and discuss the impact of genetic variation in selenoprotein S and its influence in regulating the inflammatory response.


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