Hu Yan1, Jin-Dong Chen, Xiao-Yan Zheng. 1. Institute of Mental Health, the Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Abstract
RATIONALE AND BACKGROUND: The development of atypical antipsychotic (AAP) drugs has brought about dramatic improvement in the function of many patients with schizophrenia and related mental disorders. However, prescription of AAPs is frequently associated with the emergence of weight gain, hypertriglyceridemia, and other metabolic disturbances. Although the mechanisms involved in AAP-induced hypertriglyceridemia remain to be fully elucidated, several studies have proposed that this side effect may be associated with weight gain and obesity. Recently, special emphasis has been placed on the evidence indicating a direct effect of AAPs on triglyceride metabolism. OBJECTIVES: In this review, we highlight recent findings discussing the potential mechanisms by which AAPs may contribute to hypertriglyceridemia. In addition, we summarize the adjunctive pharmacologic treatments for AAP-associated dyslipidemia. CONCLUSIONS: There is evidence that AAPs may cause hypertriglyceridemia through several possible mechanisms: (1) a direct effect on triglyceride metabolism either by stimulation of hepatic triglyceride production and secretion or by inhibition of lipoprotein lipase-mediated triglyceride hydrolysis and (2) an indirect mechanism associated with obesity and insulin resistance. The practical applications of this manuscript provide new insights for the future investigation of AAPs.
RATIONALE AND BACKGROUND: The development of atypical antipsychotic (AAP) drugs has brought about dramatic improvement in the function of many patients with schizophrenia and related mental disorders. However, prescription of AAPs is frequently associated with the emergence of weight gain, hypertriglyceridemia, and other metabolic disturbances. Although the mechanisms involved in AAP-induced hypertriglyceridemia remain to be fully elucidated, several studies have proposed that this side effect may be associated with weight gain and obesity. Recently, special emphasis has been placed on the evidence indicating a direct effect of AAPs on triglyceride metabolism. OBJECTIVES: In this review, we highlight recent findings discussing the potential mechanisms by which AAPs may contribute to hypertriglyceridemia. In addition, we summarize the adjunctive pharmacologic treatments for AAP-associated dyslipidemia. CONCLUSIONS: There is evidence that AAPs may cause hypertriglyceridemia through several possible mechanisms: (1) a direct effect on triglyceride metabolism either by stimulation of hepatic triglyceride production and secretion or by inhibition of lipoprotein lipase-mediated triglyceride hydrolysis and (2) an indirect mechanism associated with obesity and insulin resistance. The practical applications of this manuscript provide new insights for the future investigation of AAPs.
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