Background: This study investigated the possible association between common and potentially functional polymorphisms of antioxidant enzymes and metabolic abnormalities in patients with schizophrenia.
Methods: The possible associations of the glutathione S-transferase (GST) M1 null and GSTT1 null genotypes, and the superoxide dismutase 2 (SOD2) Val16Ala polymorphism with the risks of being overweight and having metabolic syndrome were examined using a logistic regression analysis in 154 schizophrenic Japanese patients and 203 controls.
Results: Among smokers with schizophrenia, the risks of being overweight and having decreased high-density lipoprotein cholesterol were significantly higher in those with the GSTM1 null genotype than in those with the present genotype (odds ratio 3.20 and 3.15, P=0.03 and P=0.04, respectively), while among nonsmokers with schizophrenia, the risk of an abnormal waist circumference was lower in those with the GSTM1 null genotype (odds ratio 0.34, P=0.04). The risk of a decreased high-density lipoprotein cholesterol level was significantly higher in patients with the combined GSTM1 null and GSTT1 present genotypes than in those with the present genotypes of both genes (odds ratio 3.60, P<0.01). The SOD2 Val16Ala polymorphism was not associated with risk of metabolic abnormalities in either group.
Conclusion: The present study suggests that the GSTM1 null genotype, in combination with smoking status or GSTT1 genotype, might be associated with the metabolic abnormalities in patients with schizophrenia.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3818100 | PMC |
| http://dx.doi.org/10.2147/NDT.S52585 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Bronchopulmonary dysplasia (BPD) is a chronic lung disease, with its own clinical, radiological and histopathological characteristics, which mainly affects premature newborns, resulting from a combination of factors that include immaturity, inflammation and lung injury, in addition to therapy with mechanical ventilation and exposure to high concentrations of oxygen. However, even with advances in care for critically ill newborns, BPD continues to be a challenge for the care team and family members. This has been identified as one of the most important causes of morbidity and mortality due to prematurity, and can have significant impacts on the quality of life of the affected patients.
View Article and Find Full Text PDFnull genotype underpins recurrence of meningiomas.
Front Oncol
December 2024
Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States.
Introduction: Meningiomas are the most common primary central nervous system (CNS) tumor in adults, comprising one-third of all primary adult CNS tumors. Although several recent publications have identified molecular alterations in meningioma including characteristic mutations, copy number alterations, and gene expression signatures, our understanding of the drivers of meningioma recurrence is limited.
Objective: To identify gene expression signatures of 1p22qNF2 meningioma recurrence, with concurrent biallelic inactivation of and loss of chr1p that are heterogenous but enriched for recurrent meningiomas.
Machine learning approaches and genetic determinants that influence the development of type 2 diabetes mellitus: a genetic association study in Brazilian patients.
Braz J Med Biol Res
December 2024
Laboratório de Patologia Molecular, Instituto de Ciências Biológicas, Universidade Federal de Goiás, Goiânia, GO, Brasil.
This genetic association study including 120 patients with type 2 diabetes mellitus (T2DM) and 166 non-diabetic individuals aimed to investigate the association of polymorphisms in the genes GSTM1 and GSTT1 (gene deletion), GSTP1 (rs1695), ACE (rs4646994), ACE2 (rs2285666), VEGF-A (rs28357093), and MTHFR (rs1801133) with the development of T2DM in the population of Goiás, Brazil. Additionally, the combined effects of these polymorphisms and the possible differences between sexes in susceptibility to the disease were evaluated. Finally, machine learning models were integrated to select the main risk characteristics for the T2DM diagnosis.
View Article and Find Full Text PDFRole of GSTM1 and GSTT1 Gene Polymorphisms on Lung Cancer Susceptibility and Effect on Platinum-Based Chemotherapy-Induced Toxicity in Bangladeshi Lung Cancer Patients.
J Cancer Epidemiol
November 2024
Department of Biochemistry and Molecular Biology, University of Dhaka, Dhaka, Bangladesh.
Glutathione S-transferases (GSTs) play a significant role in carcinogen detoxification, and hence, polymorphisms of this gene may lead to lung cancer susceptibility. Accordingly, this study is aimed at investigating GSTM1 and GSTT1 polymorphisms' association with lung cancer risk and their effects on the toxicities of platinum-based chemotherapy used to treat Bangladeshi lung cancer patients. The study subjects comprised 180 lung cancer patients and 200 healthy volunteers.
View Article and Find Full Text PDFGSTM1 and GSTT1 deletions in penile cancer are associated with TNM stage but not with HPV DNA status.
Pathol Res Pract
December 2024
Post-Graduate Program in Adult Health (PPGSAD), Federal University of Maranhão (UFMA), Av. dos Portugueses, 1966, São Luís, Maranhão 65080-805, Brazil. Electronic address:
Deletions of the GSTT1 and GSTM1 are associated with chemical carcinogenesis and genitourinary malignancies like bladder cancer, where they correlate with increased tumor aggressiveness. In uterine cervical lesions, GSTT1 and GSTM1 deletions have also been suggested to facilitate the persistence of human papillomavirus (HPV) infection and HPV-induced carcinogenesis. This work addresses the hypothesis that GSTT1/GSTM1 deletions are associated with presence of HPV DNA and aggressiveness in penile cancer, a rare malignancy with HPV+ and HPV- subtypes.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!