Association Between the 1291-C/G Polymorphism in the Adrenergic α-2a Receptor and the Metabolic Syndrome

Risselada, Arne; Vehof, Jelle; Bruggeman, Richard; Wilffert, Bob; Cohen, Dan; Hadithy, Asmar F. Al; Arends, Johan; Mulder, Hans

doi:10.1097/jcp.0b013e3181fbfac4

Cited by 13 publications

(11 citation statements)

References 18 publications

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“…Arg347 allele in Alpha-1A adrenergic receptor (ADRA1A)[123] has been demonstrated to be associated with a high prevalence and alpha-2A adrenergic receptor (ADRA2A) 1291-G allele with lower prevalence of MetS. [124] Similarly COMT158Val allele was shown to be associated with MetS prevalence in one of the studies. [30] Kang et al .…”

Section: Predictors Of Mets In Schizophreniamentioning

confidence: 99%

Metabolic Syndrome in Schizophrenia

Malhotra¹,

Grover²,

Chakrabarti³

et al. 2013

Indian Journal of Psychological Medicine

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To review the data with respect to prevalence of metabolic syndrome (MetS) and its correlates in schizophrenia. For this review, electronic search engines PUBMED, Sciencedirect, and Google Scholar were used. Available data suggests that most of the studies have been of cross-sectional design. Prevalence rates of MetS have varied from 11% to 69% in medicated patients, and 4-26% in drug naive patients in cross-sectional evaluations. Longitudinal studies have shown the prevalence rates to range from 0% to 14% at the baseline in drug naive patients, which increase to as high as 52.4% by 3 months of antipsychotic medication treatment. The prevalence rates of MetS in patients with schizophrenia are much higher than that seen in general population or healthy controls. Though there is no causal association with any demographic or clinical variables, the risk increases with increase in age. Among antipsychotics, there seems to be an association between MetS and atypical antipsychotics like clozapine and olanzapine. Therefore, the psychiatrists should be more vigilant regarding the presence of MetS in these high risk groups. Research on biological correlates of MetS in schizophrenia is still in its primitive stage, however, these is some evidence to suggest an association of MetS with adiponectin levels, hematological indices, methylenetetrahydrofolate reductase (MTHFR) and Alpha-1A adrenergic receptor (ADRA1A) gene. These areas hold promise, and targeting these with appropriate interventions may help us to prevent the occurrence of MetS in patients with schizophrenia in future.

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Section: Predictors Of Mets In Schizophreniamentioning

confidence: 99%

Metabolic Syndrome in Schizophrenia

Malhotra¹,

Grover²,

Chakrabarti³

et al. 2013

Indian Journal of Psychological Medicine

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“…One study reported an association with the leptin promoter SNP, but not with the -759C/T HTR2C SNP;46) however an interaction between the two polymorphisms was observed. Another group did find, and replicated, association of metabolic syndrome with another HTR2C SNP47) and with the α2A adrenoceptor gene 48)…”

Section: Pharmacogenetic Findingsmentioning

confidence: 89%

Pharmacogenetic Aspects of Antipsychotic Drug-induced Weight Gain - A Critical Review

Reynolds

2012

Clin Psychopharmacol Neurosci

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Treatment with several antipsychotic drugs can result in weight gain, which may lead to further morbidity such as type 2 diabetes and cardiovascular disease via the development of metabolic syndrome. These important and problematic metabolic consequences of antipsychotic drug treatment probably reflect a pharmacological disruption of the mechanisms involved in control of food intake and body weight. The extent of weight gain following antipsychotic drug treatment shows substantial variability between individuals, due in part to genetic factors. Common functional polymorphisms in many candidate genes implicated in the control of body weight and various aspects of energy and lipid metabolism have been investigated for association with weight gain in subjects receiving antipsychotic drug treatment, and with metabolic pathology in chronic schizophrenia. Perhaps the strongest and most replicated findings are the associations with promoter polymorphisms in the 5-HT2C receptor and leptin genes, although many other possible genetic risk factors, including polymorphisms in the fat mass and obesity associated (FTO) gene and genes for the alpha2A adrenoceptor and melanocortin4 receptor, have been reported. Genome-wide association studies (GWAS) have also addressed antipsychotic-induced weight gain and other indicators of metabolic disturbances. However there is as yet little consistency between these studies or between GWAS and classical candidate gene approaches. Identifying common genetic factors associated with drug-induced weight gain and its metabolic consequences may provide opportunities for personalized medicine in the predictive assessment of metabolic risk as well as indicating underlying physiological mechanisms.

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“…No significant association was found for ADRA2A. 152 Polymorphisms in the apolipoprotein A-V (APOA5) and C-III (APOC3) genes, but not in LEP, showed an influence on triglyceride and cholesterol levels in patients treated with clozapine or olanzapine. 74 Agranulocytosis is a serious adverse effect associated with clozapine.…”

Section: Studies Assessing the Adverse Effects Of Clozapinementioning

confidence: 90%

Pharmacogenetics in schizophrenia: a review of clozapine studies

Kohlrausch

2013

Rev. Bras. Psiquiatr.

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Objectives: Clozapine is quite effective to treat schizophrenia, but its use is complicated by several factors. Although many patients respond to antipsychotic therapy, about 50% of them exhibit inadequate response, and ineffective medication trials may entail weeks of unremitted illness, potential adverse drug reactions, and treatment nonadherence. This review of the literature sought to describe the main pharmacogenetic studies of clozapine and the genes that potentially influence response to treatment with this medication in schizophrenics. Methods: We searched the PubMed database for studies published in English in the last 20 years using keywords related to the topic. Results and Conclusions: Our search yielded 145 studies that met the search and selection criteria. Of these, 21 review articles were excluded. The 124 studies included for analysis showed controversial results. Therefore, efforts to identify key gene mechanisms that will be useful in predicting clozapine response and side effects have not been fully successful. Further studies with new analysis approaches and larger sample sizes are still required.

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Association Between the 1291-C/G Polymorphism in the Adrenergic α-2a Receptor and the Metabolic Syndrome

Cited by 13 publications

References 18 publications

Metabolic Syndrome in Schizophrenia

Metabolic Syndrome in Schizophrenia

Pharmacogenetic Aspects of Antipsychotic Drug-induced Weight Gain - A Critical Review

Pharmacogenetics in schizophrenia: a review of clozapine studies

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