Common biological mechanisms between bipolar disorder and type 2 diabetes: Focus on inflammation
Bipolar disorder (BD) patients present a 3–5 fold greater risk of developing type 2 diabetes (T2D) compared to general population. The underlying mechanisms for the increased prevalence of T2D in BD population are poorly understood. The purpose of this review is to critically review evidence suggest...
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Published in | Progress in neuro-psychopharmacology & biological psychiatry Vol. 54; pp. 289 - 298 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier Inc
03.10.2014
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Bipolar disorder (BD) patients present a 3–5 fold greater risk of developing type 2 diabetes (T2D) compared to general population. The underlying mechanisms for the increased prevalence of T2D in BD population are poorly understood.
The purpose of this review is to critically review evidence suggesting that inflammation may have an important role in the development of both BD and T2D.
The literature covered in this review suggests that inflammatory dysregulation take place among many BD patients. Such dysregulated and low grade chronic inflammatory process may also increase the prevalence of T2D in BD population. Current evidence supports the hypothesis of dysregulated inflammatory processes as a critical upstream event in BD as well as in T2D.
Inflammation may be a factor for the development of T2D in BD population. The identification of inflammatory markers common to these two medical conditions will enable researchers and clinicians to better understand the etiology of BD and develop treatments that simultaneously target all aspects of this multi-system condition.
•Inflammatory is a critical upstream event in bipolar disorder and type-2 diabetes.•Inflammation in bipolar disorder may heighten vulnerability for type-2 diabetes.•Add-on anti-inflammatory/anti-diabetic agents may lessen bipolar disorder burden. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0278-5846 1878-4216 |
DOI: | 10.1016/j.pnpbp.2014.06.005 |