BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a multifactorial disease with a complex pathophysiology. The clinical features of NAFLD include obesity, insulin resistance (IR) and dyslipidemia. Consumption of a diet high in saturated fats and sucrose is an important factor in the increasing occurrence of these metabolic disorders, primarily NAFLD and IR. We sought to assess the role of a high-fat, high-sucrose (HFS) diet in the promotion of NAFLD and to evaluate the effects of quercetin (Q), berberine (BB) and o-coumaric acid (CA) on modulation of these disorders. METHODS: Fifty male rats were divided into 2 main groups as follows: group 1 comprised 10 rats fed a standard diet (SD), and group 2 comprised 40 rats fed an HFS diet for 6 weeks and then subdivided equally into 4 groups; one of these groups served as the HFS diet and each of the other three groups received daily supplementation with either Q, CA or BB for 6 weeks. RESULTS: In the present study, several metabolic disorders were induced in our laboratory animal model, as evidenced by histological and biochemical changes. These alterations included serum and hepatic dyslipidemia (i.e., increased triglyceride, total cholesterol and low-density lipoprotein levels and decreased high-density lipoprotein levels), alterations in metabolic enzyme activities (lipase, glycerol-3-phosphate dehydrogenase, and glucose-6-phosphate dehydrogenase), histological changes in the liver (micro- and macrovesicular steatosis) and the downregulation of peroxisome proliferator-activated receptor γ (PPARγ) in adipose tissue and the liver. Daily oral supplementation with Q, CA or BB for 6 weeks after NAFLD induction had a hypolipidemic action and modulated metabolic markers. CONCLUSION: We showed that an HFS diet is able to promote NAFLD, and our results suggest that CA and BB are promising complementary supplements that can ameliorate the metabolic disorders associated with an HFS diet; however, Q requires further investigation.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is a multifactorial disease with a complex pathophysiology. The clinical features of NAFLD include obesity, insulin resistance (IR) and dyslipidemia. Consumption of a diet high in saturated fats and sucrose is an important factor in the increasing occurrence of these metabolic disorders, primarily NAFLD and IR. We sought to assess the role of a high-fat, high-sucrose (HFS) diet in the promotion of NAFLD and to evaluate the effects of quercetin (Q), berberine (BB) and o-coumaric acid (CA) on modulation of these disorders. METHODS: Fifty male rats were divided into 2 main groups as follows: group 1 comprised 10 rats fed a standard diet (SD), and group 2 comprised 40 rats fed an HFS diet for 6 weeks and then subdivided equally into 4 groups; one of these groups served as the HFS diet and each of the other three groups received daily supplementation with either Q, CA or BB for 6 weeks. RESULTS: In the present study, several metabolic disorders were induced in our laboratory animal model, as evidenced by histological and biochemical changes. These alterations included serum and hepatic dyslipidemia (i.e., increased triglyceride, total cholesterol and low-density lipoprotein levels and decreased high-density lipoprotein levels), alterations in metabolic enzyme activities (lipase, glycerol-3-phosphate dehydrogenase, and glucose-6-phosphate dehydrogenase), histological changes in the liver (micro- and macrovesicular steatosis) and the downregulation of peroxisome proliferator-activated receptor γ (PPARγ) in adipose tissue and the liver. Daily oral supplementation with Q, CA or BB for 6 weeks after NAFLD induction had a hypolipidemic action and modulated metabolic markers. CONCLUSION: We showed that an HFS diet is able to promote NAFLD, and our results suggest that CA and BB are promising complementary supplements that can ameliorate the metabolic disorders associated with an HFS diet; however, Q requires further investigation.

Hepatitis C virus (HCV) infection is a worldwide healthcare problem; however, traditional treatment methods have failed to cure all patients, and HCV has developed resistance to new drugs. Systems biology-based analyses could play an important role holistic analysis of the impact of HCV on hepatocellular metabolism. Here, we integrated HCV assembly reactions with a genome-scale hepatocyte metabolic model to identify the metabolic targets for HCV assembly and the metabolic alterations that occur between different HCV progression states (cirrhosis, dysplastic nodule, and early and advanced hepatocellular carcinoma (HCC)) and healthy liver tissue. We found that diacylglycerolipids were essential for HCV assembly. In addition, the metabolism of keratan sulfate and chondroitin sulfate was significantly changed in the cirrhosis stage, whereas the metabolism of acyl-carnitine was significantly changed in the dysplastic nodule and early HCC stages. Our results explained the role of the upregulated expression of BCAT1, PLOD3 and six other methyltransferase genes involved in carnitine biosynthesis and S-adenosylmethionine metabolism in the early and advanced HCC stages. Moreover, GNPAT and BCAP31 expression was upregulated in the early and advanced HCC stages and could lead to increased acyl-CoA consumption. By integrating our results with copy number variation analyses, we observed that GNPAT, PPOX and five of the methyltransferase genes (ASH1L, METTL13, SMYD2, TARBP1 and SMYD3), which are all located on chromosome 1q, had increased copy numbers in the cancer samples relative to the normal samples. Finally, we confirmed our predictions with the results of metabolomics studies and proposed that inhibiting the identified targets has the potential to provide an effective treatment strategy for HCV-associated liver disorders. 

Hepatitis C virus (HCV) infection is a worldwide healthcare problem; however, traditional treatment methods have failed to cure all patients, and HCV has developed resistance to new drugs. Systems biology-based analyses could play an important role holistic analysis of the impact of HCV on hepatocellular metabolism. Here, we integrated HCV assembly reactions with a genome-scale hepatocyte metabolic model to identify the metabolic targets for HCV assembly and the metabolic alterations that occur between different HCV progression states (cirrhosis, dysplastic nodule, and early and advanced hepatocellular carcinoma (HCC)) and healthy liver tissue. We found that diacylglycerolipids were essential for HCV assembly. In addition, the metabolism of keratan sulfate and chondroitin sulfate was significantly changed in the cirrhosis stage, whereas the metabolism of acyl-carnitine was significantly changed in the dysplastic nodule and early HCC stages. Our results explained the role of the upregulated expression of BCAT1, PLOD3 and six other methyltransferase genes involved in carnitine biosynthesis and S-adenosylmethionine metabolism in the early and advanced HCC stages. Moreover, GNPAT and BCAP31 expression was upregulated in the early and advanced HCC stages and could lead to increased acyl-CoA consumption. By integrating our results with copy number variation analyses, we observed that GNPAT, PPOX and five of the methyltransferase genes (ASH1L, METTL13, SMYD2, TARBP1 and SMYD3), which are all located on chromosome 1q, had increased copy numbers in the cancer samples relative to the normal samples. Finally, we confirmed our predictions with the results of metabolomics studies and proposed that inhibiting the identified targets has the potential to provide an effective treatment strategy for HCV-associated liver disorders. 

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Out of ninety eight of camels (Camelus dormadarius) examined, only forty eight (48.9 %) were found to be infected with blood protozoan parasites (Trypanosoma evansi, Theileria sp. and Babesia sp.). The higher incidence of infection were found in males (36.7%) whereas, (12.24%) in females. Microscopical examination revealed that longitudinal binary fission, the stumpy, slender forms of Trypanosoma evansi, trophozoites of both Theileria sp. And Babesia sp. Experimental infection revealed that both of Babesia and Theileria have a zoonotic importance for their transmissible to the experimental animals.

Out of 195 Camelus dromedarius examined only 19 were infected (9.7 %) with this parasite. The life cycle of T. sp. involves many morphologically distinct stages-more than described for any other genus in the Trypanosomatidae. This parasite was appeared for the first time in Camelus dromedarius at Assiut, Egypt. Most of stages of T. dromedarius (n.sp.) which were appeared in the blood of Camelus dromedarius are amastigotes stages. At the same time spheromastigots, epimastigote stages and trypomastigote stages with two shapes slender and broad. In experimental infection, the trypanosome was found to be transmissible to laboratory white mice, also metacyclic and amstigote formes were seen.

Babesia and Theileria are intraerythrocytic parasites which are capable of infecting a wide range of vertebrates causing huge economic losses. Histopathological and hematological changes during Babesia and Theileria inoculation in rat they were reported. Objective of the study is to determine the presence of Babesia & Theileria infected Camelus dromedarius at Assiut locality, Upper Egypt and their effects on hematological and tissues (liver, lung and kidney) of rat by injection in the blood. Blood samples were collected from Camelus dromedarius from different localities of Slaughter houses at Assiut city, Egypt (Dairout, Beni ady and Elethamna). Thick and thin blood smears were made for morphological examination of some protozoan blood parasites with electron microscopic studies. Out of (195) one hundred and ninety five Camelus dromedarius were examined and only twelve (6.1 %) were infected with Th. assiutis (n. sp.) and fifty one were found to be infected (26.1 %) with B. Cameli (n. sp.). For the first time the parasites were infected camels at Assiut. These parasites were injected in the blood of rat and the changes occurred on the organs were seen. Also Hemoglobin concentration, WBCs, RBCs, hematocrite, MCV, MCH and MCHC were measured for detection the hematological effects of these parasites. This study has reported for the first time the presence of Th. assiutis (n. sp.) & B. Cameli (n. sp.). in Camelus dromedarius and the results can lead to the prevention of babesiosis and theileriosis in the region to increase the livestock output.

The valuable effects of antioxidants supplemen- tation on lithium-induced nephrotoxicity has not been understood yet. The purpose of this study was to evaluate the renoprotective effect of zinc sulfate (Zn) and/or vitamin E (Vit. E) against lithium chloride (Li)-induced nephrotoxicity in rats. Forty male rats were divided into five groups. The first worked as controls and the other were treated with Li (20 mg/kg daily for 4 weeks). Group I of Li- treated was left without treatment, however, group II, III and IV were treated with Zn (10 mg/kg daily for 4 weeks), Vit. E (10 mg/kg, twice a week for 4 weeks), and the combination of Zn and Vit. E, respectively. Rats were killed for collection of blood and kidneys for biochemical and histological studies. The results showed a significant increase in Li in kidney tissue in all treated groups with Li, however, Zn was only increased in the groups treated with Zn, whereas Cu was similar in all treated and control groups. Plasma levels of creatinine, urea and glucose showed differences among the treated groups. The levels of lipid peroxidation, nitric oxide, glutathione, superoxide dismutase and catalase in renal tissue were significantly increased in Li-treated groups in comparison with the control and ameliorated by treatment with Zn and the combination of Zn and Vit. E. Histological observation showed perivascular edema and interstitial lymphocytic cell reaction in kidney of rats treated with Li, however co-treatment with Zn and/or Vit. E resulted in improvement of the histological changes. In conclu- sion Li-exposure causes a histological and biochemical changes mediated by oxidative stress and Li accumulation and co-treatment with Zn and/or Vit. E may protect against Li toxicity.

The valuable effects of antioxidants supplemen- tation on lithium-induced nephrotoxicity has not been understood yet. The purpose of this study was to evaluate the renoprotective effect of zinc sulfate (Zn) and/or vitamin E (Vit. E) against lithium chloride (Li)-induced nephrotoxicity in rats. Forty male rats were divided into five groups. The first worked as controls and the other were treated with Li (20 mg/kg daily for 4 weeks). Group I of Li- treated was left without treatment, however, group II, III and IV were treated with Zn (10 mg/kg daily for 4 weeks), Vit. E (10 mg/kg, twice a week for 4 weeks), and the combination of Zn and Vit. E, respectively. Rats were killed for collection of blood and kidneys for biochemical and histological studies. The results showed a significant increase in Li in kidney tissue in all treated groups with Li, however, Zn was only increased in the groups treated with Zn, whereas Cu was similar in all treated and control groups. Plasma levels of creatinine, urea and glucose showed differences among the treated groups. The levels of lipid peroxidation, nitric oxide, glutathione, superoxide dismutase and catalase in renal tissue were significantly increased in Li-treated groups in comparison with the control and ameliorated by treatment with Zn and the combination of Zn and Vit. E. Histological observation showed perivascular edema and interstitial lymphocytic cell reaction in kidney of rats treated with Li, however co-treatment with Zn and/or Vit. E resulted in improvement of the histological changes. In conclu- sion Li-exposure causes a histological and biochemical changes mediated by oxidative stress and Li accumulation and co-treatment with Zn and/or Vit. E may protect against Li toxicity.