BACKGROUND:Obstructive sleep apnea (OSA) is a common sleep problem, in which patients are at increased risk for metabolic and cardiovascular problems, including metabolic syndrome, diabetes mellitus (DM), and dyslipidemia. Betatrophin is a novel protein that regulates fatty acid and triglyceride (TG) metabolism and is related to obesity and metabolic abnormalities, including metabolic syndrome, DM, and dyslipidemia. Although OSA and betatrophin share common abnormalities, their relationship has not been investigated.AIM:The aim of this study is to investigate the relationships among betatrophin, OSA, and the serum lipid profile.METHODS:Ninety consecutive patients with suspected OSA underwent polysomnography (PSG) to confirm OSA. Plasma betatrophin, leptin, adiponectin, and the full lipid profile were analyzed. The patients were categorized as OSA or control based on the apnea-hypopnea index (AHI).RESULTS:About 61% of patients had OSA, and 39% had normal PSG. The levels of betatrophin, leptin, and adiponectin were higher in patients with OSA (256.59 ± 29.35, 374.20 ± 37.93, and 17.86 ± 2.63 μg/mL, respectively) compared to the controls (141.86 ± 26.20, 205.53 ± 14.75, and 7.52 ± 1.02 μg/mL, respectively). Betatrophin levels were correlated with the AHI, leptin (r = 0.413, P = 0.002, r = 0.782, P = 0.000). TG levels were significantly higher, and high-density lipoprotein cholesterol (HDL-C) levels were lower, in OSA patients compared to controls (244 ± 20.33 vs. 138 ± 14.89, and 37.21 ± 1.26 vs. 43.78 ± 1.62, respectively). The TG level was correlated with betatrophin (r = 0.353, P = 0.013). Multiple regression analysis showed that the AHI, leptin, and arousals were independent predictors of betatrophin level (B = 1.70 P = 0.046 95%, B = 0.56 P < 0.005, and B = 1, 2, P = 0.003, respectively).CONCLUSIONS:Our results suggest a complex relationship between OSA, betatrophin, TG, and HDL, as well as other adipokines. Our results require further investigation to assess this complex association and re-evaluate previous related studies.

Objective. This study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. Materials and Methods. In the study, 56 Wistar Albino rats were equally divided into eight groups. Group 1 was the control group; group 2 was the group receiving cisplatin; group 3 was the group receiving cisplatin + gallic acid; group 4 was the group receiving cisplatin + silymarin; group 5 was the group receiving cisplatin + silymarin + gallic acid; group 6 was the group receiving silymarin; group 7 was the group receiving gallic acid; group 8 was the group receiving gallic acid + silymarin. AST, ALT, urea, creatinine, albumin, globulin, and total protein levels were measured at the end of the study. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione (GSH), and 8-hydroxy-2′-deoxyguanosine (8OH-dG) levels were measured in kidney and liver tissues. Additionally, histopathological evaluations of the tissues were also performed. Results. In kidney and liver tissues, cisplatin significantly increased MDA and 8-OHdG levels compared with treatment groups ( p < 0.05 ). Silymarin-treated group significantly increased the SOD activity and GSH amount in the liver tissue compared with the cisplatin-treated group ( p < 0.05 ). Gallic acid significantly increased CAT activity compared with the cisplatin-treated group ( p < 0.05 ). It was determined that the cisplatin-treated group significantly decreased CAT and SOD activity compared with the control group ( p > 0.05 ). Gallic acid showed a significant increase in CAT and SOD activity in kidney tissue compared with the cisplatin-treated group ( p < 0.05 ). Conclusion. As a result, it was observed that gallic acid silymarin had a protective effect on cisplatin-induced nephrotoxic and hepatotoxic effects.

Doxorubicin (DXR) is a chemotherapeutic antibiotic obtained from Streptomyces peucetius var. (Abd El-Gany, Rasha, Bakry, & Shimaa, 2016). It is an effective and wide-spectrum therapeutic, but has toxic effect, especially on tissues with rapid cellular cycles such as those of the ovaries, testes and intestinal mucosa (Kiyomiya, Matsuo, & Kurebe, 2001). Certain hypotheses have been developed related to DXR-induced toxicity, including suggestions that it may cause DNA damage (Denard et al., 2011), oxidative stress and cellular apoptosis

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