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• We investigated the possible associations between PLA2G4A and PLA2G6 gene polymorphisms and nicotine dependence in schizophrenia. • This is the first report on PLA2 genes and nicotine dependence. • We observed two significant, though weak, effects of the PLA2G6 polymorphism. • The PLA2G6 polymorphism influences smoking risk in male patients. • The PLA2G6 genotype-smoking interaction influences disease onset in male patients. We investigated the relationship between the rs10798059 (BanI) and rs4375 polymorphisms in the phospholipase A2 (PLA2)G4A and PLA2G6 genes and the risk of nicotine dependence in 263 Croatian patients with schizophrenia. We also examined whether interactions between these polymorphisms and smoking contributed to schizophrenia onset and Positive and Negative Syndrome Scale (PANSS) psychopathology. We found no significant differences in the distribution of PLA2G4A genotypes and alleles according to smoking status, and no effect of the PLA2G4A genotype-smoking interaction on disease onset or PANSS. The PLA2G6-TT homozygous genotype was significantly overrepresented in male smokers compared to nonsmokers (34.7% vs. 17.1%, p < 0.05). These patients had ∼2.6-fold higher risk of becoming smokers than males with heterozygous PLA2G6-CT and homozygous PLA2G6-CC genotypes. In addition, male smokers without the PLA2G6-C allele (PLA2G6-TT homozygous) experienced earlier onset than nonsmoking homozygous PLA2G6-TT males. Thus, the PLA2G6 polymorphism affected the risk of nicotine dependence in male patients and the PLA2G6 genotype-smoking interaction was linked to the age of disease onset. [ABSTRACT FROM AUTHOR]

Objective Patients with schizophrenia are more likely to be smokers than the general population, which makes them an interesting group with which to study the etiology of nicotine dependency. We studied the prevalence of a gene variant of peroxisome proliferator-activated receptor alpha ( PPARα ) in schizophrenia, together with nicotine dependency, to investigate whether the PPARα -L162V polymorphism (rs1800206) influences nicotine dependency in schizophrenia. Given evidence suggesting that smoking influences the severity of schizophrenia, together with our recent data linking the PPARα -L162V polymorphism to clinical manifestations of schizophrenia (in the Croatian population), we hypothesized that interactions between the two (smoking and the PPARα -L162V polymorphism) might contribute to disease onset and scores for the Positive and Negative Syndrome Scale. To the best of our knowledge, this is the first study to investigate the possible associations between the PPARα gene and nicotine dependency. Patients and methods Genotyping was performed for 267 chronically ill schizophrenia patients (males/females: 140/127) by polymerase chain reaction. Results A significant excess of PPARα -L162V genotypes and PPARα -162V alleles were detected among female smokers in comparison to female nonsmokers (18.2% vs. 2.0%, and 9.1% vs. 1.0%, p < 0.01, respectively). We also revealed a significant PPARα genotype–smoking interaction that predicted positive symptom severity among male patients ( F = 4.43, p < 0.05). These data indicated that the PPARα -L162V heterozygous genotype, depending on smoking status, might be of relevance as either protective, or a risk factor, for the severity of positive symptoms. No interaction between the PPARα -L162V polymorphism and smoking for the time of onset of schizophrenia was detected ( p > 0.05, respectively). Conclusion We demonstrated two significant yet weak effects. The first showed an effect of the PPARα -L162V polymorphism on the risk of nicotine dependency. The second linked the PPARα genotype–smoking interaction to positive symptoms severity among schizophrenia patients; both effects manifested in a gender-specific fashion. [ABSTRACT FROM AUTHOR]

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Copyright of Collegium Antropologicum is the property of Croatian Anthropological Society and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

• This is the first investigation of the association between the skin flush response to niacin and lipid and glucose metabolism in schizophrenia. • Skin flush response to niacin was not significantly associated with plasma cholesterol or glucose levels. • Niacin-induced skin flushing was positively and strongly associated with plasma triglyceride levels. The available data suggest that abnormalities of arachidonic acid-related signaling may be of relevance in attenuated niacin-induced flush responses and lipid and glucose metabolism disturbances, which are all common among individuals with schizophrenia. We previously demonstrated attenuated skin flush responses to niacin in patients with schizophrenia. Here we investigated whether these niacin responses might be associated with elevated plasma lipid and glucose concentrations in this patient group. We found that higher plasma triglyceride levels were associated with higher total volumetric niacin response (VNR) values and that the VNR accounted for ~14.2% of the variability in triglyceride levels. Triglyceride levels were significantly higher in patients with a positive niacin skin flush response compared to those with absent niacin skin flushing at the 5-minute interval with niacin concentrations of 0.1 and 0.01 M, and at the 10- and 15-minute intervals with a niacin concentration of 0.001 M. [ABSTRACT FROM AUTHOR]