Browsing by Author "Ulus, İsmail Hakki"
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Item Choline, CDP-choline or phosphocholine increases plasma glucagon in rats: Involvement of the peripheral autonomic nervous system(Elsevier, 2008-07-28) Cansev, Mehmet; İlçöl, Yeşim Özarda; Yılmaz, Mustafa Sertaç; Hamurtekin, Emre; Ulus, İsmail Hakki; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Biyokimya Anabilim Dalı.; 0000-0001-9496-1475; 0000-0003-2918-5064; M-9071-2019; AAH-1571-2021; D-5340-2015; AAL-8873-2021; 8872816100; 35741320500; 8895544100; 8717648500; 7004271086The present study was designed to test the effects of choline, cytidine-5'-diphosphocholine (CDP-choline) and phosphocholine on plasma glucagon concentrations in rats. Intraperitoneal (i.p.) injection of 200-600 mu mol/kg of choline, CDP-choline or phosphocholine produced a dose-dependent increase in plasma glucagon and choline concentrations. Pretreatment with hexamethonium (15 mg/kg: i.p.), a peripherally-acting ganglionic nicotinic acetylcholine receptor antagonist, entirely blocked the increases in plasma glucagon by 600 mu mol/kg of choline, CDP-choline or phosphocholine. The increases in plasma glucagon by these choline compounds was reduced significantly (P<0.01) by about 25% by pretreatment with atropine methylnitrate (2 mg/kg), a peripherally-acting muscarinic acetylcholine receptor antagonist. Blockade of central acetylcholine receptors did not alter the increase in plasma glucagon induced by i.p. choline (600 mu mol/kg). While alpha(2)-adrenoceptor blockade or bilateral adrenalectomy attenuated the increase in plasma glucagon evoked by choline compounds, blockade of alpha(1)- or beta-adrenoceptors or chemical sympathectomy failed to alter this increase. Intracerebroventricular (i.c.v.) choline (1.5 mu mol) administration also increased plasma glucagon; the effect was blocked by central pretreatment with a neuronal type nicotinic acetylcholine receptor antagonist, mecamylamine (50 mu g; i.c.v.) or the neuronal choline uptake inhibitor, hemicholinium-3 (20 mu g; i.c.v.). These data show that choline, CDP-choline or phosphocholine increases plasma glucagon concentrations by increasing peripheral nicotinic and muscarinic cholinergic neurotransmissions. Central choline also increases plasma glucagon by augmenting central nicotinic cholinergic neurotransmission by acting presynaptically. Stimulation of adrenal medullary catecholamine release and subsequent activation of alpha(2)-adrenoceptors are mainly involved in the increase in plasma glucagon induced by choline, CDP-choline or phosphocholine.Item Endotoxin alters serum-free choline and phospholipid-bound choline concentrations, and choline administration attenuates endotoxin-induced organ injury in dogs(Lippincott Williams & Wilkins, 2005-09) Ilçol, Yeşim Özarda; Yılmaz, Zeki; Ulus, İsmail Hakki; Uludağ Üniversitesi/Tıp Fakültesi/Biyokimya Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Dahiliye Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Biyokimya ve Klinik Biyokimya Anabilim Dalı.; 0000-0001-9836-0749; A-9637-2008; D-5340-2015; AAL-8873-2021This study in dogs was performed to assess circulating choline status during endotoxemia and to determine whether choline administration can protect dogs from endotoxin-induced tissue injuries. Baseline serum-free and phospholipid-bound choline concentrations were 19.2 +/- 0.6 mu mol/L and 3700 +/- 70 mu mol/L, respectively. After intravenous endotoxin infusion, serum-free choline concentrations decreased by 14% to 49% (P < 0.05-0.001) at 2 to 6 h after 0.02 mg/kg endotoxin, and increased by 23% to 98% (P < 0.05-0.001) at 1 to 48 h after 1 mg/kg endotoxin. Serum phospholipid-bound choline concentrations increased by 19% to 27% (P < 0.05) at 12 to 24 h or by 18% to 53% (P < 0.05-0.001) at 1 to 48 h after 0.02 or 1 mg/kg endotoxin, respectively. The changes in serum-free and -bound choline levels in response to endotoxin were accompanied by dose- and time-related elevations in serum cortisol and biochemical markers for tissue injury and/or organ dysfunction. Intravenous administration of choline (20 mg/kg) 5 min before, and 4 and 8 h after endotoxin (11 mg/kg) attenuated endotoxin-induced elevations in serum alanine aminotransferase (P < 0.05-0.001), aspartate aminotransferase (P < 0.05-0.001), -y-glutamyl transferase (P < 0.05-0.001), alkaline phosphatase (P < 0.05-0.001), lactate dehydrogenase (P < 0.05-0.001), myocardial creatine kinase (P < 0.001), urea (P < 0.05-0.01), creatinine (P < 0.05), uric acid (P < 0.010.001), and tissue necrosis factor-alpha (P < 0.001). Choline also attenuated alanine ami notransf erase (P < 0.05-0.01), alkaline phosphatase (P < 0.05-0.01), lactate dehydrogenase (P < 0.05-0.01), creatine kinase (P < 0.05-0.001), myocardial creatine kinase (P < 0.05-0.001), and uric acid (P < 0.05-0.01), but failed to alter the serum urea, creatinine, aspartate aminotransf erase, and gamma-glutamyl transferase responses to 0.02 mg/kg endotoxin. These data show that choline status is altered during endotoxemia and that choline administration diminishes endotoxin-induced tissue injury.