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Intracerebroventricular (ICV) injection of ouabain, a specific Na-K ATPase inhibitor, induces behavioral changes in rats resembling the manic phenotypes of bipolar disorder. The binding of ouabain to the Na-K ATPase affects signal events in vitro including Akt, a possible molecular target of mood disorders. However, the effects of ouabain on Akt in the brain need further clarification. In this study, we investigated changes in the phosphorylation state of Akt in the rat brain after ICV injection of ouabain. Consistent with our previous report, the locomotor activity of rats within 30 min after ouabain ICV injection changed according to the dose with higher doses of ouabain, 0.5 and 1 mM, inducing significant hyperactivity. In addition, ouabain administration induced a dose-dependent increase in the immunoreactivity of p-Akt (Ser473) in the frontal cortex. striatum, and hippocampus after 30 min, and reached statistical significance with 1 mM of ouabain. Phosphorylation of GSK-3 beta (Ser9), FOX01 (Ser256), and eNOS (Ser1177), which are downstream molecules of Akt, was also increased in a dose-dependent manner within the same brain regions. Moreover, hyperactivity was seen for 8 h after a single 1 mM injection of ouabain and increased phosphorylation of Akt (Ser473), GSK-3 beta, (Ser9), FOX01 (Ser256), and eNOS (Ser1177) was also observed in the cortex, striatum, and hippocampus. Thus, intrabrain injection of ouabain induces activation of Akt signaling accompanied by hyperactivity, suggesting the possible role of Akt in ouabain rat model of mania. (C) 2010 Elsevier Inc. 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Despite growing concerns about the co-morbidity of metabolic syndrome (MetS) and bipolar disorder, few studies have been conducted on this topic in Asian populations This study examined Korean patients with bipolar disorder to assess its co-morbidity with MetS and to compare the prevalence of MetS in patients with medication for bipolar disorder with that of healthy patients We used cross-sectional data from the medical records of patients with bipolar disorder who presented to the psychiatric clinic in Seoul National University Hospital between June 2007 and June 2008. The control group, matched for age and gender, was randomly drawn from visitors to the Health Promotion Center at the same hospital during the same period We compared the prevalence of MetS between these two groups with independent sample t-tests and chi-squared tests We also calculated the indirectly standardized prevalence ratio (ISPR) with a standardization that used the Fourth Korean National Health and Nutrition Examination Survey (KNHNES. 2007) The prevalence of MetS in patients who took medication for bipolar disorder (N = 152) was 270%. 25.0% and 25 7%, based on the definitions of the American Heart Association and the National Heart, Lung and Blood Institute`s adaptation of the Adult Treatment Panel III (AHA), the National Cholesterol Education Program for Adult Treatment Panel III (ATPIII) and the International Diabetes Federation (IDF), respectively The present study determined that the prevalence of MetS was significantly higher in patients with bipolar disorder than in the control group, the odds ratios (OR) (95%CI) were 2.44 (1 35-4 40), 248 (1.34-459) and 257 (1.40-4.74), based on the definition of the ANA. ATPIII and IDF, respectively.The ISPR (95%CI) was 1.48(1 02-1 93), 1.54(1 05-2 03) and 1 98 (1 36-2 60). respectively Patients with medications for bipolar disorder showed a significantly higher prevalence of increased waist circumference, elevated triglycerides. and reduced HDL-cholesterol than the control group. The prevalence of MetS in patients taking medication for bipolar disorder was higher than that in the general population Obesity and dyslipidemia were particularly prevalent in patients with bipolar disorder (C) 2010 Elsevier Inc All rights reserved ; This study was supported by National Research Foundation of Korea Grant funded by the Korean Government (2009-0077030). ; Meyer JM, 2009, J CLIN PSYCHIAT, V70, P318 ; De Hert M, 2009, WORLD PSYCHIATRY, V8, P15 ; CHANG HH, 2009, J AFFECT DISORD ; Correll CU, 2008, J CLIN PSYCHIAT, V69, P1948 ; Correll CU, 2008, BIPOLAR DISORD, V10, P788, DOI 10.1111/j.1399-5618.2008.00625.x ; Daumit GL, 2008, SCHIZOPHR RES, V105, P175, DOI 10.1016/j.schres.2008.07.006 ; Ader M, 2008, J PSYCHIATR RES, V42, P1076, DOI 10.1016/j.jpsychires.2008.01.004 ; van Winkel R, 2008, J CLIN PSYCHIAT, V69, P1319 ; Fiedorowicz JG, 2008, ANN CLIN PSYCHIATRY, V20, P131, DOI 10.1080/10401230802177722 ; Sicras A, 2008, BIPOLAR DISORD, V10, P607 ; Salvi V, 2008, GEN HOSP PSYCHIAT, V30, P318, DOI 10.1016/j.genhosppsych.2008.04.009 ; Fagiolini A, 2008, J CLIN PSYCHIAT, V69, P678 ; van Winkel R, 2008, BIPOLAR DISORD, V10, P342 ; Sicras-Mainar A, 2008, EUR PSYCHIAT, V23, P100, DOI 10.1016/j.eurpsy.2007.07.005 ; Park HS, 2008, OBES REV, V9, P104, DOI 10.1111/j.1467-789X.2007.00421.x ; Garcia-Portilla MP, 2008, J AFFECT DISORDERS, V106, P197, DOI 10.1016/j.jad.2007.06.002 ; Cardenas J, 2008, J AFFECT DISORDERS, V106, P91, DOI 10.1016/j.jad.2007.05.030 ; Fagiolini A, 2008, CNS DRUGS, V22, P655 ; FAUCI AS, 2008, HARRISONS PRINCIPLES ; Kim B, 2008, J AFFECT DISORDERS, V105, P45, DOI 10.1016/j.jad.2007.04.006 ; Narisawa S, 2008, J EPIDEMIOL, V18, P37, DOI 10.2188/jea.18.37 ; McIntyre RS, 2007, CURR OPIN PSYCHIATR, V20, P406 ; Birkenaes AB, 2007, J CLIN PSYCHIAT, V68, P917 ; Yumru M, 2007, J AFFECT DISORDERS, V98, P247, DOI 10.1016/j.jad.2006.08.009 ; Guo JJ, 2006, J CLIN PSYCHIAT, V67, P1055 ; Alberti KGMM, 2006, DIABETIC MED, V23, P469 ; Correll CU, 2006, J CLIN PSYCHIAT, V67, P575 ; De Hert MA, 2006, SCHIZOPHR RES, V83, P87, DOI 10.1016/j.schres.2005.12.855 ; McEvoy JP, 2005, SCHIZOPHR RES, V80, P19, DOI 10.1016/j.schres.2005.07.014 ; Grundy SM, 2005, CIRCULATION, V112, P2735, DOI 10.1161/CIRCULATIONAHA.105.169404 ; Fagiolini A, 2005, BIPOLAR DISORD, V7, P424 ; Lieberman JA, 2005, NEW ENGL J MED, V353, P1209 ; Lim S, 2005, DIABETES CARE, V28, P1810 ; COHN T, 2004, CAN J PSYCHIAT, V49, P753 ; 2002, CIRCULATION, V106, P3143 ; JIN H, 2002, ANN CLIN PSYCHIAT, V14, P59 ; Koller E, 2001, AM J MED, V111, P716 ; Wetterling T, 2001, DRUG SAFETY, V24, P59 ; Henderson DC, 2000, AM J PSYCHIAT, V157, P975, DOI 10.1176/appi.ajp.157.6.975 ; 4

V-akt murine thymoma viral oncogene homolog 1 (AKT1) has been suggested to be involved in the pathophysiology of schizophrenia Recent, independent studies in Caucasian, Japanese, Iranian, and Chinese populations have reported that the AKT1 gene may be associated with schizophrenia, but these results have yet to be replicated in other populations. In the present study, we performed a case-control association study between AKT1 and schizophrenia in a Korean population. We genotyped six single nucleotide polymorphisms (SNP1 (rs3803300), SNP2 (rs1130214), SNP3 (rs3730358), SNP4 (rs1130233), SNP5 (rs2494732), SNP A (rs2498804)) of AKT1, selected froth previous reports, in a sample of 283 subjects with schizophrenia and 350 controls. No significant difference in single marker polymorphisms or haplotype frequencies of the six SNPs in the AKT1 gene was observed between controls and subjects with schizophrenia In addition, we carried out an updated meta-analysis of the six SNPs, and found no evidence for an association between the six SNPs and schizophrenia Taken together, our results do not support the hypothesis that AKT1 is a susceptibility gene for schizophrenia (C) 2009 Elsevier Ireland Ltd and the Japan Neuroscience Society All rights reserved ; This study was supported by a grant from the Korea Healthcare Technology R&D Project, Ministry for Health, Welfare and Family Affairs (A030001), and by National Research Foundation of Korea Grant funded by the Korean Government (2009-0076274). ; Stefansson H, 2009, NATURE, V460, P744, DOI 10.1038/nature08186 ; Need AC, 2009, PLOS GENET, V5, DOI 10.1371/journal.pgen.1000373 ; O`Donovan MC, 2008, NAT GENET, V40, P1053, DOI 10.1038/ng.201 ; Arguello PA, 2008, J CLIN INVEST, V118, P2018, DOI 10.1172/JCI35931 ; Tan HY, 2008, J CLIN INVEST, V118, P2200, DOI 10.1172/JCI3472S ; Sanders AR, 2008, AM J PSYCHIAT, V165, P497, DOI 10.1176/appi.ajp.2007.07101573 ; Thiselton DL, 2008, BIOL PSYCHIAT, V63, P449, DOI 10.1016/j.biopsych.2007.06.005 ; LIU YC, 2008, J PSYCHOPHARMACOL ; Xu MQ, 2007, J CLIN PSYCHIAT, V68, P1358 ; Norton N, 2007, SCHIZOPHR RES, V93, P58, DOI 10.1016/j.schres.2007.02.006 ; Sutton LP, 2007, J NEUROCHEM, V102, P153, DOI 10.1111/j.1471-4159.2007.04527.x ; Roh MS, 2007, EXP MOL MED, V39, P353 ; Seo MS, 2007, INT J NEUROPSYCHOPH, V10, P359, DOI 10.1017/S1461145706006869 ; Sullivan PF, 2007, BIOL PSYCHIAT, V61, P1121, DOI 10.1016/j.biopsych.2006.11.010 ; Volz TJ, 2007, ADDICTION, V102, P44 ; Turunen JA, 2007, SCHIZOPHR RES, V91, P27, DOI 10.1016/j.schres.2006.11.028 ; Beaulieu JM, 2007, J NEUROSCI, V27, P881, DOI 10.1523/JNEUROSCI.5074-06.2007 ; Ide M, 2006, J NEUROCHEM, V99, P277, DOI 10.1111/j.1471-4159.2006.04033.x ; Bajestan SN, 2006, AM J MED GENET B, V141B, P383, DOI 10.1002/ajmg.b.30291 ; Norton N, 2006, CURR OPIN PSYCHIATR, V19, P158 ; Liu YL, 2006, PSYCHIAT GENET, V16, P39 ; Ikeda M, 2006, INT J NEUROPSYCHOPH, V9, P77, DOI 10.1017/S1461145705005481 ; Ahn YM, 2005, INT J NEUROPSYCHOPH, V8, P607, DOI 10.1017/S1461145705005353 ; Alimohamad H, 2005, J NEUROCHEM, V95, P513, DOI 10.1111/j.1471-4159.2005.03388.x ; Schwab SG, 2005, BIOL PSYCHIAT, V58, P446, DOI 10.1016/j.biopsych.2005.05.005 ; Beaulieu JM, 2005, CELL, V122, P261 ; Alimohamad H, 2005, BIOL PSYCHIAT, V57, P533, DOI 10.1016/j.biopsych.2004.11.036 ; Barrett JC, 2005, BIOINFORMATICS, V21, P263, DOI 10.1093/bioinformatics/bth457 ; Ohtsuki T, 2004, MOL PSYCHIATR, V9, P981, DOI 10.1038/sj.mp.4001559 ; Ikeda M, 2004, BIOL PSYCHIAT, V56, P698, DOI 10.1016/j.biopsych.2004.07.023 ; Joo EJ, 2004, COMPR PSYCHIAT, V45, P225, DOI 10.1016/j.comppsych.2004.02.007 ; Kang UG, 2004, FEBS LETT, V560, P115, DOI 10.1016/S0014-5793(04)00082-1 ; Emamian ES, 2004, NAT GENET, V36, P131, DOI 10.1038/ng1296 ; Srisurapanont M, 2003, INT J NEUROPSYCHOPH, V6, P347, DOI 10.1017/S1461145703003675 ; Dudbridge F, 2003, GENET EPIDEMIOL, V25, P115, DOI 10.1002/gepi.10252 ; Wall JD, 2003, AM J HUM GENET, V73, P502 ; Purcell S, 2003, BIOINFORMATICS, V19, P149 ; Zaykin DV, 2002, HUM HERED, V53, P79 ; NURNBERGER JI, 1994, ARCH GEN PSYCHIAT, V51, P849 ; 4