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Stress - pathophysiology of T2DM development

Reviews of the associations of stress and mental illness have been undertaken and also looked at the potential...

Reviews of the associations of stress and mental illness have been undertaken and also looked at the potential underlying mechanisms.

Kelly summarises this in figure 1 (Kelly & Ismail, 2015). The role of inflammatory markers increases the risk of developing T2DM however this paper does not make clear during discussion the pathophysiological link between inflammation, insulin resistance and rising glucose.

A key association is increasing stress itself leading to individuals engaging in adverse-health promoting activities which lead to increasing physiological responses of insulin resistance e.g., quality and quantity of food, smoking, reduced exercise and increased alcohol abuse (Bonnet, et al., 2005; Rod, Grønbaek, Schnohr, Prescott, & Kristensen, 2009).

Suggested chronic stress explanations by Pouwer et al (2010) include the inflammation pathway (through pro-immune activity). The inflammatory cytokines and raised glucocorticoids contribute to neuroendocrine and neurotransmitter changes that are similar to those in physical or psychological stressors (Anisman, 2009). The full cascade of understanding this pathway remains incomplete.

Research looks into this but notes the gap of clarity with these pathways (Lontchi-Yimagou, Sobngwi, Matsha, & Kengne, 2013). White adipose tissue increases activates inflammatory pathways and is implicated with the increased release of a number of markers including TNF-alpha, IL1, IL6, IL10, leptin, adiponectin amongst many others (Shoelson, Lee, & Goldfine, 2006). Low grade inflammation is associated between adipose tissue and increased risk of developing T2DM (Nikolajczyk, Jagannathan-Bogdan, Shin, & Gyurko, 2011).

CRP has been investigated in T2DM and it is possible that it could alter signalling pathways of insulin (Xu, Morita, & Ikeda, 2007). There is some suggestion this might increase inflammation within the pancreas, where insulin is produced, and also the liver, hypothalamus and muscle, but evidence remains unclear (Lontchi-Yimagou, Sobngwi, Matsha, & Kengne, 2013).



Anisman, H. (2009). Cascading effects of stressors and inflammatory immune system activation: implications for major depressive disorder. Journal of Psychiatry Neuroscience, 34(1), 4-20.

Bonnet, F., Irving, K., Terra, J. L., Nony, P., Berthezène, F., & Moulin, P. (2005). Anxiety and depression are associated with unhealthy lifestyle in patients at risk of cardiovascular disease. Atherosclerosis, 178(2), 339-344.

Kelly, S. J., & Ismail, M. (2015). Stress and type 2 diabetes: a review of how stress contributes to the development of type 2 diabetes. Annual review of public health, 36, 441-462.

Shoelson, S. E., Lee, J., & Goldfine, A. B. (2006). Inflammation and insulin resistance . Journal of Clinical Investigation, 116, 1793-1801.

Lontchi-Yimagou, E., Sobngwi, E., Matsha, T. E., & Kengne, A. P. (2013). Diabetes mellitus and inflammation. Current diabetes reports, 13(3), 435-444

Nikolajczyk, B. S., Jagannathan-Bogdan, M., Shin, H., & Gyurko, R. (2011). State of the union between metabolism and the immune system in type 2 diabetes. ;12:239–50~. Genes & Immunity, 12, 239-250.

Xu, J. W., Morita, I., & Ikeda, K. (2007). C-reactive protein suppresses insulin signaling in endothelial cells: role of spleen tyrosine kinase. . Molecular Endocrinology, 21, 564–573.

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