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    Ameliorative Effects of Larazotide Acetate on Intestinal Permeability and Bacterial Translocation in Acute Pancreatitis Model in Rats
    (Springer, 2024) Karahan, Dogu; Harputluoglu, Muhsin Murat Muhip; Gul, Mehmet; Gunduz, Ayten; Ozyalin, Fatma; Inceoglu, Feyza; Satilmis, Basri
    Background Intestinal barrier dysfunction in acute pancreatitis (AP) may progress to systemic inflammatory response syndrome (SIRS) and multi-organ failures by causing bacterial translocation. Larazotide acetate (LA) is a molecule that acts as a tight junction (TJ) regulator by blocking zonulin (Zo) receptors in the intestine. Aims In our study, we aimed to investigate the effects of LA on intestinal barrier dysfunction and bacterial translocation in the AP model in rats. Methods Thirty-two male Sprague-Dawley rats were divided into 4 groups; control, larazotide (LAR), AP, and AP + LAR. The AP model was created by administering 250 mg/100 g bm L-Arginine intraperitoneally 2 times with an hour interval. AP + LAR group received prophylactic 0.01 mg/mL LA orally for 7 days before the first dose of L-Arginine. For intestinal permeability analysis, fluorescein isothiocyanate-dextran (FITC-Dextran) was applied to rats by gavage. The positivity of any of the liver, small intestine mesentery, and spleen cultures were defined as bacterial translocation. Histopathologically damage and zonulin immunoreactivity in the intestine were investigated. Results Compared to the control group, the intestinal damage scores, anti-Zo-1 immunoreactivity H-Score, serum FITC-Dextran levels and bacterial translocation frequency (100% versus 0%) in the AP group were significantly higher (all p < 0.01). Intestinal damage scores, anti-Zo-1 immunoreactivity H-score, serum FITC-Dextran levels, and bacterial translocation frequency (50% versus 100%) were significantly lower in the AP + LAR group compared to the AP group (all p < 0.01). Conclusions Our findings show that LA reduces the increased intestinal permeability and intestinal damage by its effect on Zo in the AP model in rats, and decreases the frequency of bacterial translocation as a result of these positive effects.
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    Effects of intracerebroventricular MOTS-c infusion on thyroid hormones and uncoupling proteins
    (Springer Heidelberg, 2023) Bahar, Mehmet Refik; Tekin, Suat; Beytur, Asiye; Onalan, Ebru Etem; Ozyalin, Fatma; Colak, Cemil; Sandal, Suleyman
    This study was conducted to determine the possible effects of intracerebroventricular MOTS-c infusion on thyroid hormones and uncoupling proteins (UCPs) in rats. Forty male Wistar Albino rats were divided into 4 groups with 10 animals in each group: control, sham, 10 and 100 mu M MOTS-c. Hypothalamus, blood, muscle, adipose tissues samples were collected for thyrotropin-releasing hormone (TRH), UCP1 and UCP3 levels were determined by the RT-PCR and western blot analysis. Serum thyroid hormone levels were determined by the ELISA assays. MOTS-c infusion was found to increase food consumption but it did not cause any changes in the body weight. MOTS-c decreased serum TSH, T3, and T4 hormone levels. On the other hand, it was also found that MOTS-c administration increased UCP1 and UCP3 levels in peripheral tissues. The findings obtained in the study show that central MOTS-c infusion is a directly effective agent in energy metabolism.
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    The importance of lipids in neurodegenerative diseases Neurodegenerative diseases and lipids
    (Bayrakol Medical Publisher, 2026) Kurt, Zeynep Eker; Ozyalin, Fatma
    Lipids are vital for membrane structure, energy storage, and cell signaling. Balanced lipid intake is essential for brain health and function. PUFAs like DHA and AA make the brain prone to oxidative stress and inflammation. Lipid peroxidation contributes to neuronal damage and neurodegenerative diseases. Disrupted lipid metabolism is linked to Alzheimer's, Parkinson's, and schizophrenia. Studying brain lipid changes may uncover disease mechanisms and guide new therapies.