VLDL-C and LDL-C levels were calculated according to the Friedewald formula  LDL-C = (Total cholesterol) ? (HDL-C) ? (Triglycerides/5). are particularly susceptible to diarrhea caused by enteropathogens in neonatal period, especially if they have failure of passive transfer of immunoglobulins [5-7]. Bovine placenta does not permit the passive transfer of antibody to the fetus. After bird, the immune system is not fully PTC-028 developed, and the production of endogenous antibody does not rich protective levels until 1 month of age. Therefore, resistance of newborn calf to enteropathogens depends on an adequate passive transfer of colostral immunoglobulins. Failure of passive transfer predisposes neonates to contamination and septicemia and often results in severe and fatal disease [4,8,9]. In diarrhea, metabolic changes such as dehydration, metabolic acidosis, electrolyte imbalance, unfavorable energy balance, and/or hypoglycemia occur at various degrees depending on the severity of the contamination. The severity of the metabolic alterations significantly influences the survivability of diarrheic neonates [10,11]. In case of negative energy balance and/or disease, animal has to provide the majority of energy via lipolysis. On the other hand, lipids play an important role on synthesis of several organic substances together with carbohydrates and proteins. They have also used in biomembrane structures and as hormone precursors . Thus, changes in plasma lipid levels affect other organ or tissue functions [12,13]. The lipids are stored as triglycerides and transported as fatty acid bound to PTC-028 albumin in the blood. The majority of these fatty acids in the blood are metabolized into carbon Rabbit polyclonal to AAMP dioxide and/or ketone bodies by the liver. The remaining, cholesterol, is usually combined with phospholipid and released into the blood as very low-density lipoprotein-cholesterol (VLDL-C) [14,15]. The degradation of VLDL-C results in the production of low-density lipoprotein-cholesterol (LDL-C) that carries cholesterol to peripheral tissues, while high-density lipoprotein-cholesterol (HDL-C) that transfers cholesterol from peripheral tissues to the liver is produced from degradation of LDL-C [13,14]. It has been reported that infections and inflammations impair lipid and lipoprotein metabolism, like lipid oxidation and cholesterol transport to stimulate anti-inflammatory response [16-18]. During the contamination or endotoxemia, a systemic inflammatory response develops and, if it is severe enough, it may damage and impair several organ or systems functions such as liver, kidney, respiratory, and circulatory system [19-21]. Depending on organ or system dysfunction, several metabolic disorders such as metabolic acidosis, hypoglycemia, hyperlactatemia, and hyperfibrinogenemia occur and the severity of these alterations determine the prognosis of the diarrheic calves [21,22]. In view of such concern, the aim of this study was to evaluate the possible changes in lipid variables, alkaline phosphatase (ALP), and bilirubin values to estimate a possible liver failure in neonatal calves affected by diarrhea. Materials and Methods Ethical approval This study was conducted after obtaining approval from the Kafkas University Animal Experiments Local Ethics Committee (KAU HADYEK-Submission 2016/77). Animals In this study, 25 calves with diarrhea that were brought to Department of Internal Medicine, School of Veterinary Medicine, Kafkas University and 10 clinically healthy calves aged 1-30 days aged were used. The etiologic diagnosis was not considered in diarrheic calves, and routine clinical examination was performed in all animals. Blood samples were collected into tubes with ethylenediaminetetraacetic acid and then centrifuged at 3000 rpm for 10 min. Plasma samples were then kept at ?20C until analysis. Biochemical analysis Plasma levels of triglycerides, total cholesterol, HDL-C, ALP, PTC-028 direct and total bilirubin were decided colorimetrically (Epoch, BioTek, USA) using commercial kits (DDS-Turkey). VLDL-C and LDL-C levels were calculated according to the Friedewald formula  LDL-C = (Total cholesterol) ? (HDL-C) ? (Triglycerides/5). VLDL-C was calculated as [VLDL-C (mg/dL) = Triglyceride (mg/dL)/5] in case triglyceride (mg/dL) was 400 mg/dL. Statistical analysis SPSS  for Windows 20.0 was used for the statistical analyses. The distribution of the data obtained from the groups was shown as normal distribution according to the KolmogorovCSmirnov test. Therefore, Students.