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Objective: 12,13-Dihydroxy-9Z-octadecenoic acid (12,13-diHOME) is a lipokine secreted from brown adipose tissue, and it has positive effects on dyslipidemia. Acute exercise has been shown to lead to an increase in its secretion. In this study, it was aimed to investigate the relationship of 12,13-diHOME with obesity, exercise and dyslipidaemia for the first time in the adolescent age group., Design: Prospective study., Patients: Twenty-eight male adolescents with obesity and the same number of age-matched healthy normal-weight male controls., Measurements: Fasting serum glucose, insulin, lipid and 12,13-diHOME levels were measured. Cardiopulmonary exercise testing was performed in all subjects using a stress test treadmill. Peak oxygen consumption (peak VO2) and anaerobic threshold heart rate (ATHR) were measured., Results: Adolescents with obesity had lower 12,13-diHOME levels than normal-weight adolescents both before and after acute exercise (p = .025 and p = .019, respectively), and after acute exercise, 12,13-diHOME levels significantly increased in both groups (p = .001 for both). 12,13-diHOME levels negatively correlated with triglyceride, total cholesterol, LDL-C, and positively correlated with HDL-C. Also, peak VO 2 and ATHR levels showed positive correlation with 12,13-diHOME levels., Conclusion: 12,13-diHOME levels were found to be lower in adolescents with obesity than normal-weight adolescents and increased with acute exercise. Also, the close relationship of this molecule with dyslipidaemia in addition to that with obesity suggests that it has an important role in the pathophysiology of these disorders. Further molecular studies will further elucidate the role of 12,13-diHOME in obesity and dyslipidaemia., (© 2023 John Wiley & Sons Ltd.)

This study aimed to investigate the role of endoplasmic reticulum (ER) stress in polycystic ovary syndrome (PCOS) and the effect of salubrinal (SAL) on this role. Animals were divided into four groups as control, PCOS, PCOS+SAL and SAL. Weights and serum testosterone levels were increased in the PCOS group while serum LH and ATF4 expressions were decreased. Morphometrically, number of follicles with a diameter between 150 and 300 µm were declined and number of follicles larger than 300 µm as well as the percentage of cystic follicles (CFs) were increased. Immunoreactivities of GRP78 and p-eIF2α were decreased, whereas oxidative stress (OS) dependent PAR expression was increased. Ultrastructurally, the PCOS group had no ER enlargement which was observed in the control group, while there were mitochondrial damage in granulosa cells (GCs). Elevated OS levels did not induce but rather decreased ER stress in GCs, and SAL injection in the PCOS model was ineffective on searched parameters. Since ER stress plays roles in certain physiological processes, we suggest that inhibitors of ER stress may not be always useful for reproductive tissues.

In this study, we investigated the mechanism of oxidative damage induced by nicotine and the efficacy of vitamin E, an integral component of cellular membranes, against the damage in follicular/granulosa cells of rat ovaries. The animals were randomly divided into 4 groups; control, nicotine, nicotine + vitaminE, vitamin E (n = 8, per each group). Nicotine and vitamin E were administrated intraperitoneally 1 mg/kg/day and 200 mg/kg/day, respectively, once daily for 2 weeks. Nicotine increased lipid peroxide levels such as lipid peroxide (LPO) and malondialdehyde (MDA) in serum, 4-hydroxynonenal (4-HNE) in granulosa cells and apoptotic granulosa cells in the ovary. Positive correlation occurred between the findings of LPO markers and TUNEL labeling. Level of 17-β estradiol (E 2 ), number of follicles and granulosa cell proliferation decreased with nicotine treatment and negatively correlated with LPO levels and apoptosis in granulosa cells. Ultrastructural study of nicotine treated rat ovaries showed mitochondrial damage and autophagosomes in the granulosa cells. The administration of nicotine and vitamin E together, revealed an increase in E 2 level, granulosa cell proliferation and the number of healthy follicles associated with decrease in LPO, MDA, 4-HNE levels and TUNEL reactivity in a manner correlated with each other, compared to the nicotine group. Vitamin E showed to alleviate mitochondrial damage and decrease the number of autophagosomes in granulosa cells. These results suggest that lipid peroxidation may be one of the nicotine' damage mechanisms on folliculogenesis and vitamin E may prevent nicotine-induced follicular damage through reducing lipid peroxidation level in granulosa cells., Competing Interests: Declaration of Competing Interest The authors declare that they have no conflict of interest., (Copyright © 2019 Society for Biology of Reproduction & the Institute of Animal Reproduction and Food Research of Polish Academy of Sciences in Olsztyn. Published by Elsevier B.V. All rights reserved.)

Background: Metabolic syndrome (MetS) is one of the high cardiovascular (CV) situations. Endothelial dysfunction, which is a common finding in patients with MetS, is related with increased CV risk. In patients with MetS, the effect of the major CV risk factors, not included in the MetS definition, on endothelial dysfunction is not well known. The aim of this study was to determine the effect of major CV risk factors such as gender, smoking, family history, and biochemical parameters on endothelial dysfunction in patients with MetS., Methods: The study was performed between December 2010 and August 2014. A total of 55 patients (15 females and 40 males) with MetS and 81 healthy controls (37 females and 44 males) with a body mass index <25 kg/m2 were enrolled in the study. Endothelial dysfunction was measured by flow-mediated dilatation (FMD), oxidative stress parameters; high-sensitivity C-reactive protein (hs-CRP), oxidized low-density lipoprotein (ox-LDL), endothelial nitric oxide synthase (e-NOS), nitric oxide, and cell adhesion markers; von Willebrand factor, and e-selectin. Platelet aggregation (endothelial adenosine diphosphate), total platelet count, and mean platelet volume were additionally analyzed and demographic parameters were explored. Student's t- test, Mann-Whitney U-test, and Chi-square test were used to analyze the results., Results: The fasting blood glucose (z= 3.52, P= 0.001), hs-CRP (z = 3.23, P= 0.004), ox-LDL (z = 2.62, P= 0.013), and e-NOS (z = 2.22, P= 0.026) levels and cardiac risk score (z = 5.23, P< 0.001) were significantly higher in patients with MetS compared with the control group. Smoking was correlated with decreased FMD (χ2 = 9.26, P= 0.002) in MetS patients but not in the control group., Conclusions: Increased ox-LDL, hs-CRP, and e-NOS are likely to be a result of oxidative stress, a condition in which an imbalance occurs between the production and inactivation of reactive nitrogen and oxygen species. In addition, in patients with MetS, smoking is independently related to endothelial dysfunction.

Background: Cardiovascular diseases (CVD) account for approximately 50% of the total deaths in Turkey. Most of them are related with atherosclerotic coronary heart disease. Predictive value of endothelial dysfunction markers related with the earliest stage of atherosclerosis has been getting more attention. We hypothesized that differences in endothelial dysfunction biochemical markers among genders would aid to capture proatherogenic activity that was not diagnosed by conventional risk assessment scoring systems., Methods: We assessed the endothelial dysfuntion markers in 92 Turkish adults who were in the »low CV risk group« according to ESC (European Society of Cardiology)-Score Risk Charts. We compared the males and females., Results: We observed higher endothelial dysfunction rates in males, with higher median and mean levels of e-NOS, ox-LDL before and after adjustment for HDL lowness and obesity (P=0.018, P=0.036 for NOS; P=0.000, P=0.004 for ox-LDL, respectively). Men had higher hs-CRP levels than females before adjustment (P=0.021). Decreased e-NOS levels were related with FMD for females before adjustment for confounders (P=0.028). We also found significant correlation between e-NOS and ox-LDL levels both before (r=0.360, P<0.001) and after adjustment (r=0.366, P<0.01) for confounders which pointed out the nitrosative stress. In multivariate regression analyses, after adjusting for other endothelial dysfunction markers which were not included in the ESC-risk scoring system, decreased e-NOS levels were independently asssociated with impaired flow mediated dilatation for females (odds ratio 0.3; P=0.038)., Conclusions: Our results underline the importance of gender in evaluating endothelial dysfunction biochemical markers to assess cardiovascular risk for low CV risk indivuals., Competing Interests: Conflict of interest statement The authors stated that they have no conflicts of interest regarding the publication of this article.