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Potential role of prolactin in antipsychotic‐mediated association of schizophrenia and type 2 diabetes
Author(s) -
Oberweis Brandon,
Gragnoli Claudia
Publication year - 2012
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.24023
Subject(s) - prolactin , schizophrenia (object oriented programming) , antipsychotic , dopamine , atypical antipsychotic , type 2 diabetes , medicine , endocrinology , typical antipsychotic , serotonin , receptor , diabetes mellitus , psychology , pharmacology , psychiatry , hormone
It remains unclear why atypical antipsychotics confer a risk for hyperglycemia compared to typical antipsychotics. Atypical antipsychotics antagonize dopamine receptors‐2 (D 2 ) and serotonin (5‐HT) receptors‐2, while typical antipsychotics antagonize only D 2 receptors. We aimed at elucidating the mechanistic differences between the role of typical and atypical antipsychotics on prolactin levels and glucose regulation. A Medline search was conducted during 2010 using the search terms type 2 diabetes (T2D), typical/atypical antipsychotics, schizophrenia, prolactin, and serotonin. We discuss the effect of typical and atypical antipsychotics on prolactin levels and glucose regulation. Given that prolactin is under negative control by dopamine and positive control by serotonin, typical antipsychotics induce elevations in prolactin, while atypical antipsychotics do not. Research studies show protective effects of prolactin on T2D. We hypothesize that the difference in induction of T2D between typical and atypical antipsychotics is due to the antipsychotic receptor binding mediated effect in changes in prolactin levels. J. Cell. Physiol. 227: 3001–3006, 2012. © 2011 Wiley Periodicals, Inc.