본문 바로가기
KERD
논문KCI 등재

Lack of Association between Glutathione S-Transferase-M1, -T1, and -P1 Polymorphisms and Olanzapine-Induced Weight Gain in Korean Schizophrenic Patients

2

조회

0

다운로드

0

인용

0

참고문헌

키워드

주제분류정신과학

초록

ObjectiveaaOxidative stress may be an important pathogenic mechanism in the obesity and metabolic syndrome. The aims of this study was to assess the possible association between the oxidative stress related Glutathione S-Transferase genes (GST-M1, GST-T1, and GST-P1)variants and the olanzapine-induced weight gain in Korean schizophrenic patients. MethodsaaWe categorized 78 schizophrenic patients into two groups the more than 7% weight gain from baseline (weight gain ≥7%) and the less weight gain (weight gain <7%) groups according to weight change between before and after long-term olanzapine treatment (440±288 days). All participants were genotyped for the GST-M1, GST-T1 and GST-P1 genes. Differences in allele frequencies between cohorts with different body weight changes were evaluated by a chi-square analysis and Fisher’s exact test. The multifactor dimensionality reduction (MDR) approach was used to analyze gene-gene interactions. ResultsaaMean body weight gain was 5.42 kg. There was no difference in the null genotype distribution of GST-M1 and -T1 between subjects with body weight gain ≥7% compared to subjects with body weight gain <7% (p>0.05). No significant difference in GST-P1 genotype and allele frequencies were observed between the groups (p>0.05). MDR analysis did not show a significant interaction between the three GST gene variants and susceptibility to weight gain (p>0.05). ConclusionaaThese findings do not support a relationship between the genetic variants of three GST genes (GST-M1, -T1 and -P1) and weight gain in Korean schizophrenic patients receiving olanzapine treatment.

Abstract

ObjectiveaaOxidative stress may be an important pathogenic mechanism in the obesity and metabolic syndrome. The aims of this study was to assess the possible association between the oxidative stress related Glutathione S-Transferase genes (GST-M1, GST-T1, and GST-P1)variants and the olanzapine-induced weight gain in Korean schizophrenic patients. MethodsaaWe categorized 78 schizophrenic patients into two groups the more than 7% weight gain from baseline (weight gain ≥7%) and the less weight gain (weight gain <7%) groups according to weight change between before and after long-term olanzapine treatment (440±288 days). All participants were genotyped for the GST-M1, GST-T1 and GST-P1 genes. Differences in allele frequencies between cohorts with different body weight changes were evaluated by a chi-square analysis and Fisher’s exact test. The multifactor dimensionality reduction (MDR) approach was used to analyze gene-gene interactions. ResultsaaMean body weight gain was 5.42 kg. There was no difference in the null genotype distribution of GST-M1 and -T1 between subjects with body weight gain ≥7% compared to subjects with body weight gain <7% (p>0.05). No significant difference in GST-P1 genotype and allele frequencies were observed between the groups (p>0.05). MDR analysis did not show a significant interaction between the three GST gene variants and susceptibility to weight gain (p>0.05). ConclusionaaThese findings do not support a relationship between the genetic variants of three GST genes (GST-M1, -T1 and -P1) and weight gain in Korean schizophrenic patients receiving olanzapine treatment.

참고문헌 (44)

  1. Allison DB, "Antipsychotic-induced weight gain: a comprehensive research synthesis", Am J Psychiatry, 156, pp.1686~1696 (1999)
  2. Taylor DM, "Atypical antipsychotics and weight gain--a systematic review", Acta Psychiatr Scand, 101, pp.416~432 (2000)
  3. Allison DB, "The impact of weight gain on quality of life among persons with schizophrenia", Psychiatr Serv, 54, pp.565~567 (2003)
  4. Strassnig M, "Body mass index and quality of life in community-dwelling patients with schizophrenia", Schizophr Res, 62, pp.73~76 (2003)
  5. Perkins DO, "Adherence to antipsychotic medications", J Clin Psychiatry, 60(21), pp.25~30 (1999)
  6. Vauth R, "Understanding adherence to neuroleptic treatment in schizophreniaí", Psychiatry Res, 126, pp.43~49 (2004)
  7. Jibson MD, "New atypical antipsychotic medications", J Psychiatr Res, 32, pp.215~228 (1998)
  8. Casey DE, "The pharmacology of weight gain with antipsychotics", J Clin Psychiatry, 62(7), pp.4~10 (2001)
  9. Pillai A, "Long-term antipsychotic treatments and crossover studies in rats: differential effects of typical and atypical agents on the expression of antioxidant enzymes and membrane lipid peroxidation in rat brain", J Psychiatr Res, 41, pp.372~386 (2007)
  10. Walss-Bass C, "Clozapine causes oxidation of proteins involved in energy metabolism: a possible mechanism for antipsychotic-induced metabolic alterations", Int J Neuropsychopharmacol, 11, pp.1097~1104 (2008)
  11. Palmieri VO, "Systemic oxidative alterations are associated with visceral adiposity and liver steatosis in patients with metabolic syndrome", J Nutr, 136, pp.3022~3026 (2006)
  12. Eriksson JW, "Metabolic stress in insulin’s target cells leads to ROS accumulation- a hypothetical common pathway causing insulin resistance", FEBS Lett, 581, pp.3734~3742 (2007)
  13. Andreassen OA, "Neurotoxicity associated with neuroleptic- induced oral dyskinesias in rats. Implications for tardive dyskinesia?", Prog Neurobiol, 61, pp.525~541 (2000)
  14. Fridlyand LE, "Reactive species and early manifestation of insulin resistance in type 2 diabetes", Diabetes Obes Metab, 8, pp.136~145 (2006)
  15. Silva Mdo C, "GSTM1, GSTT1, and GSTP1 genotypes and the genotoxicity of hydroquinone in human lyphocytes", Environ Mol Mutagen, 43, pp.258~264 (2004)
  16. Mannervik B, "The isoenzymes of glutathione transferase", Adv Enzymol Relat Areas Mol Biol, 57, pp.357~417 (1985)
  17. Hayes JD, "Glutathione S-transferase polymorphisms and their biological consequences", Pharmacology, 61, pp.154~166 (2000)
  18. Houstis N, "Reactive oxygen species have a causal role in multiple forms of insulin resistance", Nature, 440, pp.944~948 (2006)
  19. Kuzuya M, "Glutathione peroxidase 1 Pro198Leu variant contributes to the metabolic syndrome in men in a large Japanese cohort", Am J Clin Nutr, 87, pp.1939~1944 (2008)
  20. Lee YS, "Dysregulation of adipose glutathione peroxidase 3 in obesity contributes to local and systemic oxidative stress", Mol Endocrinol, 22, pp.2176~2189 (2008)
  21. Pemble S, "Human glutathione S-transferase θ (GSTT1): cDNA coloning and the characterization of a genetic polymorphism", Biochem J, 300, pp.271~276 (1994)
  22. Seidegård J, "Isoenzyme(s) of glutathione transferase (class Mu) as a marker for the susceptibility to lung cancer: a follow up study", Carcinogenesis, 11, pp.33~36 (1990)
  23. Sundberg K, "Differences in the catalytic efficiencies of allelic variants of glutathione transferase P1-1 towards carcinogenic diol epoxides of polycyclic aromatic hydrocarbons", Carcinogenesis, 19, pp.433~436 (1998)
  24. Han OS, "Structured Clinical Interview for DSM-IV Axis I Disorder-Korean Version" (2000), Hana Medical Publishing
  25. Park YM, "Weight gain associated with the alpha2a-adrenergic receptor -1,291 C", G polymorphism and olanzapine treatment, 2006, pp.141B, 394~397
  26. Park YM, "Lack of association between the -759C", T polymorphism of the 5-HT2C receptor gene and olanzapine-induced weight gain among Korean schizophrenic patients, 2008, pp.33, 55~60
  27. Kang SG, "Possible association between the -2548A", G polymorphism of the leptin gene and olanzapine-induced weight gain, 2008, pp.32, 160~163
  28. Young-Min Park, "G-protein β3 Subunit Gene 825C", T Polymorphism Is Not Associated with Olanzapine-Induced Weight Gain in Korean Schizophrenic Patients, 2009, pp.6(1), 39~43[DOI]
  29. Kang SG, "Association study between glutathione S-transferase GST-M1, GST-T1, and GST-P1 polymorphisms and tardive dyskinesia", Hum Psychopharmacol, 24, pp.55~60 (2009)
  30. Zhong SL, "Relationship between genotype and enzyme activity of glutathione S-transferases M1 and P1 in Chinese", Eur J Pharm Sci, 28, pp.77~85 (2006)
  31. Hahn LW, "Multifactor dimensionality reduction software for detecting gene-gene and gene-environment interactions", Bioinformatics, 19, pp.376~382 (2003)
  32. Ritchie MD, "Multifactor-dimensionality reduction reveals high-order interactions among estrogen-metabolism genes in sporadic breast cancer", Am J Hum Genet, 69, pp.138~147 (2001)
  33. Motsinger AA, "The effect of reduction in crossvalidation intervals on the performance of multifactor dimensionality reduction", Genet Epidemiol, 30, pp.546~555 (2006)
  34. Ritchie MD, "Power of multifactor dimensionality reduction for detecting gene-gene interactions in the presence of genotyping error, missing data, phenocopy, and genetic heterogeneity", Genet Epidemiol, 24, pp.150~157 (2003)
  35. Velez D, "A balanced accuracy function for epistasis modeling in imbalanced datasets using multifactor dimensionality reduction", Genet Epidemiol, 31, pp.306~315 (2007)
  36. Brassat D, "Multifactor dimensionality reduction reveals gene-gene interactions associated with multiple sclerosis susceptibility in African Americans", Genes Immun, 7, pp.310~315 (2006)
  37. Motsinger AA, "Complex gene-gene interactions in multiple sclerosis: a multifactorial approach reveals associations with inflammatory genes", Neurogenetics, 8, pp.11~20 (2007)
  38. Agirbasli D, "Interaction among 5,10 methylenetetrahydrofolate reductase, plasminogen activator inhibitor and endothelial nitric oxide synthase gene polymorphisms predicts the severity of coronary artery disease in Turkish patients", Coron Artery Dis, 17, pp.413~417 (2006)
  39. Hsieh CH, "Analysis of epistasis for diabetic nephropathy among type 2 diabetic patients", Hum Mol Genet, 15, pp.2701~2708 (2006)
  40. Rösen P, "The role of oxidative stress in the onset and progression of diabetes and its complications: a summary of a Congress Series sponsored by UNESCO- MCBN, the American Diabetes Association and the German Diabetes Society", Diabetes Metab Res Rev, 17, pp.189~212 (2001)
  41. Packer L, "Molecular aspects of lipoic acid in the prevention of diabetes complications", Nutrition, 17, pp.888~895 (2001)
  42. Sagara Y, "nduction of reactive oxygen species in neurons by haloperidol", J Neurochem, 71, pp.1002~1012 (1998)
  43. Nasrallah H, "A review of the effect of atypical antipsychotics on weight", Psychoneuroendocrinology, 28(1), pp.83~96 (2003)
  44. Ryu S, "-759 C", T polymorphism of 5-HT2C receptor gene and early phase weight gain associated with antipsychotic drug treatment, 2007, pp.31, 673~677

관련 논문AI추천

이 간행물의 다른 논문 (4건)