Crosstalk between insulin and dopamine signaling: A basis for the metabolic effects of antipsychotic drugs

被引:37
作者
Nash, Abigail I. [1 ]
机构
[1] NIMH, NIH, Bethesda, MD 20892 USA
关键词
Dopamine; DAT; Insulin; Hyperinsulinemia; Antipsychotic; Schizophrenia; WEIGHT-GAIN; TRANSPORTER FUNCTION; ATYPICAL ANTIPSYCHOTICS; CARBOHYDRATE-METABOLISM; HYPOINSULINEMIC RATS; 1ST-EPISODE PATIENTS; DIABETES-MELLITUS; GLUCOSE-TOLERANCE; DORSAL STRIATUM; NAIVE PATIENTS;
D O I
10.1016/j.jchemneu.2016.07.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the setting of rising rates of obesity and metabolic syndrome, characterized in part by hyperinsulinemia, it is increasingly important to understand the mechanisms that contribute to insulin dysregulation. The higher risk for metabolic syndrome imparted by antipsychotic medication use highlights one such mechanism. Though there is great variation in the number and types of signaling pathways targeted by these medications, the one common mechanism of action is through dopamine. Dopamine's effects on insulin signaling begin at the level of insulin secretion from the pancreas and continue through the central nervous system. In a reciprocal fashion, insulin also affects dopamine signaling, with specific effects on dopamine reuptake from the synapse. This review probes the dopamine-insulin connection to provide a comprehensive examination of how antipsychotics may contribute towards insulin resistance. Published by Elsevier B.V.
引用
收藏
页码:59 / 68
页数:10
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