Relevant bibliographies by topics / Fatty liver syndrome of chickens

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Academic literature on the topic 'Fatty liver syndrome of chickens'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Fatty liver syndrome of chickens"

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Tan, Xiaodong, Ranran Liu, Siyuan Xing, Yonghong Zhang, Qinghe Li, Maiqing Zheng, Guiping Zhao, and Jie Wen. "Genome-Wide Detection of Key Genes and Epigenetic Markers for Chicken Fatty Liver." International Journal of Molecular Sciences 21, no. 5 (March 5, 2020): 1800. http://dx.doi.org/10.3390/ijms21051800.

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Chickens are one of the most important sources of meat worldwide, and the occurrence of fatty liver syndrome (FLS) is closely related to production efficiency. However, the potential mechanism of FLS remains poorly understood. An integrated analysis of data from whole-genome bisulfite sequencing and long noncoding RNA (lncRNA) sequencing was conducted. A total of 1177 differentially expressed genes (DEGs) and 1442 differentially methylated genes (DMGs) were found. There were 72% of 83 lipid- and glucose-related genes upregulated; 81% of 150 immune-related genes were downregulated in fatty livers. Part of those genes was within differentially methylated regions (DMRs). Besides, sixty-seven lncRNAs were identified differentially expressed and divided into 13 clusters based on their expression pattern. Some lipid- and glucose-related lncRNAs (e.g., LNC_006756, LNC_012355, and LNC_005024) and immune-related lncRNAs (e.g., LNC_010111, LNC_010862, and LNC_001272) were found through a co-expression network and functional annotation. From the expression and epigenetic profiles, 23 target genes (e.g., HAO1, ABCD3, and BLMH) were found to be hub genes that were regulated by both methylation and lncRNAs. We have provided comprehensive epigenetic and transcriptomic profiles on FLS in chicken, and the identification of key genes and epigenetic markers will expand our understanding of the molecular mechanism of chicken FLS.
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Trott, K. A., F. Giannitti, G. Rimoldi, A. Hill, L. Woods, B. Barr, M. Anderson, and A. Mete. "Fatty Liver Hemorrhagic Syndrome in the Backyard Chicken." Veterinary Pathology 51, no. 4 (October 3, 2013): 787–95. http://dx.doi.org/10.1177/0300985813503569.

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Zhu, Yaling, Huirong Mao, Gang Peng, Qingjie Zeng, Qing Wei, Jiming Ruan, and Jianzhen Huang. "Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens." Animal Bioscience 34, no. 1 (January 1, 2021): 143–53. http://dx.doi.org/10.5713/ajas.19.0874.

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Objective: To explore the molecular mechanisms of fatty liver hemorrhagic syndrome (FLHS) in laying hens, an experiment was conducted to reveal the differences in histopathological observation and gene expression between FLHS group and normal group.Methods: We compared the histopathological difference using hematoxylin and eosin staining and proceeded with RNA sequencing of adipose tissue to search differentially expressed genes and enriched biological processes and pathways. Then we validated the mRNA expression levels by real-time polymerase chain reaction and quantified protein levels in the circulation by enzyme-linked immunosorbent assay.Results: We identified 100 differentially expressed transcripts corresponding to 66 genes (DEGs) were identified between FLHS-affected group and normal group. Seven DEGs were significantly enriched in the immune response process and lipid metabolic process, including phospholipase A2 group V, WAP kunitz and netrin domain containing 2, delta 4-desaturase sphingolipid 2, perilipin 3, interleukin-6 (<i>IL-6</i>), ciliary neurotrophic factor (<i>CNTF</i>), and suppressor of cytokine signaling 3 (<i>SOCS3</i>). And these genes could be the targets of immune response and be involved in metabolic homeostasis during the process of FLHS in laying hens. Based on functional categories of the DEGs, we further proposed a model to explain the etiology and pathogenesis of FLHS. <i>IL-6</i> and <i>SOCS3</i> mediate inflammatory responses and the satiety hormone of leptin, induce dysfunction of Jak-STAT signaling pathway, leading to insulin resistance and lipid metabolic disorders. Conversely, <i>CNTF</i> may reduce tissue destruction during inflammatory attacks and confer protection from inflammation-induced insulin resistance in FLHS chickens.Conclusion: These findings highlight the therapeutic implications of targeting the JAK-STAT pathway. Inhibition of <i>IL6</i> and <i>SOCS3</i> and facilitation of <i>CNTF</i> could serve as a favorable strategy to enhance insulin action and improve glucose homoeostasis, which are of importance for treating obesity-related disorders for chickens.
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Bryden, W. L. "Tissue depletion of biotin in chickens and the development of deficiency lesions and the fatty liver and kidney syndrome." Avian Pathology 20, no. 2 (June 1991): 259–69. http://dx.doi.org/10.1080/03079459108418762.

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Karikalan, M., M. Asok Kumar, R. Raguvaran, M. Palanivelu, Umesh Dimri, and A. K. Sharma. "Fatty liver kidney syndrome (FLKS) in peafowl chicks (Pavo cristatus) and its management." Indian Journal of Veterinary Pathology 41, no. 4 (2017): 321. http://dx.doi.org/10.5958/0973-970x.2017.00077.3.

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Bannister, D. W., D. I. Sales, and Alison Lee. "Biotin deficiency and susceptibility to fatty liver and kidney syndrome in broiler chicks: reduced 6-phosphofructokinase (EC 2.7.1.11) activity but normal fructose 2,6-bisphosphate content in birds with hepatomegaly." British Journal of Nutrition 54, no. 2 (September 1985): 535–43. http://dx.doi.org/10.1079/bjn19850138.

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1. In two separate experiments, using different strains, broiler chicks were reared on either a commercial-type chick mash (control) or a fatty liver and kidney syndrome (FLKS)-inducing diet.2. In Expt a, chicks were killed on day 29 and in Expt b, on day 32. Body-weights and liver weights were measured, and values from those given the control ration used to construct a hepatomegaly index by employing a variant of linear discriminant analysis.3. Application of the index to FLKS birds revealed a statistically significant bimodal distribution of liver size.4. The birds with enlarged livers (high index) also possessed metabolic abnormalities in that 6- phosphofructokinase (EC 2. 7. 1. 11; PFK-1) activity (measured at low substrate concentration) was depressed despite the presence of normal, or even slightly elevated fructose 2,6-bisphosphate concentration.5. This indicates the presence of an uncharacterized regulatory mechanism for PFK- 1 in FLKS-susceptible birds.
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PROUDFOOT, F. G., and H. W. HULAN. "THE PERFORMANCE OF ONE NORMAL AND TWO DWARF MEAT MATERNAL GENOTYPES AND THEIR PROGENY AS AFFECTED BY REARING AND ADULT DIETARY TREATMENTS." Canadian Journal of Animal Science 66, no. 1 (March 1, 1986): 245–56. http://dx.doi.org/10.4141/cjas86-025.

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The performances of one normal and two dwarf meat maternal genotypes were compared in a factorial experiment designed to estimate the combined effects of feeding two juvenile diets (low protein (LP) high energy (HE) versus high protein (HP) low energy (LE)) from 106 to 140 days and four adult dietary treatments (LPHE, HPHE, HPLE and an HPLE excluding canola meal) fed from 141 to 420 days. The performance of the three genotypes differed significantly (P < 0.05) for egg production, egg fertility at 322 days, feed efficiency, live body weights and monetary returns less the cost of chicks and feed. One of the dwarf gentoypes exhibited the highest monetary returns. Juvenile dietary treatments had no significant (P > 0.05) effect on the traits measured except age at sexual maturity and female body weights at 154 d. Several traits were affected by the adult dietary treatments including mortality, incidence of fatty liver syndrome, hen-day egg production, feed efficiency up to 322 and 420 days and live body weights. Mortality due to fatty liver syndrome was significantly (P < 0.01) lower among hens fed the high protein, low energy diet without canola meal compared with hens fed the other three adult diets, all of which included canola meal as a feed ingredient. Key words: Dwarf, meat breeders, hens, broilers, diets, fatty liver syndrome, genotypes
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Mirderikvandi, Maryam, Heshmatollah Khosravinia, and Bahman Parizadian Kavan. "Independent and combined effects of Satureja khuzistanica essential oils and acetic acid on prevalence and intensity of fatty liver syndrome in broiler chickens." Journal of Animal Physiology and Animal Nutrition 104, no. 1 (October 17, 2019): 166–77. http://dx.doi.org/10.1111/jpn.13220.

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Liu, Xueqin, Shailendra Kumar Mishra, Tao Wang, Zhongxian Xu, Xiaoling Zhao, Yan Wang, Huadong Yin, et al. "AFB1 Induced Transcriptional Regulation Related to Apoptosis and Lipid Metabolism in Liver of Chicken." Toxins 12, no. 5 (May 4, 2020): 290. http://dx.doi.org/10.3390/toxins12050290.

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Aflatoxin B1 (AFB1) leads to a major risk to poultry and its residues in meat products can also pose serious threat to human health. In this study, after feeding 165-day-old Roman laying hens for 35 days, the toxic effects of aflatoxin B1 at different concentrations were evaluated. The purpose of this study was to explore the mechanism of liver toxicosis responses to AFB1. We found that highly toxic group exposure resulted in liver fat deposition, increased interstitial space, and hepatocyte apoptosis in laying hens. Furthermore, a total of 164 differentially expressed lnRNAs and 186 differentially expressed genes were found to be highly correlated (Pearson Correlation Coefficient > 0.80, p-value < 0.05) by sequencing the transcriptome of control (CB) and highly toxic group (TB3) chickens. We also identify 29 differentially expressed genes and 19 miRNAs that have targeted regulatory relationships. Based on the liver cell apoptosis and fatty liver syndrome that this research focused on, we found that the highly toxic AFB1 led to dysregulation of the expression of PPARG and BCL6. They are cis-regulated by TU10057 and TU45776, respectively. PPARG was the target gene of gga-miR-301a-3p, gga-miR-301b-3p, and BCL6 was the target gene of gga-miR-190a-3p. In summary, highly toxic AFB1 affects the expression levels of protein-coding genes and miRNAs in the liver of Roman layer hens, as well as the expression level of long non-coding RNA in the liver, which upregulates the expression of PPARG and downregulates the expression of Bcl-6. Our study provides information on possible genetic regulatory networks in AFB1-induced hepatic fat deposition and hepatocyte apoptosis.
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Tramunt, Blandine, Alexandra Montagner, Nguan Soon Tan, Pierre Gourdy, Hervé Rémignon, and Walter Wahli. "Roles of Estrogens in the Healthy and Diseased Oviparous Vertebrate Liver." Metabolites 11, no. 8 (July 30, 2021): 502. http://dx.doi.org/10.3390/metabo11080502.

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The liver is a vital organ that sustains multiple functions beneficial for the whole organism. It is sexually dimorphic, presenting sex-biased gene expression with implications for the phenotypic differences between males and females. Estrogens are involved in this sex dimorphism and their actions in the liver of several reptiles, fishes, amphibians, and birds are discussed. The liver participates in reproduction by producing vitellogenins (yolk proteins) and eggshell proteins under the control of estrogens that act via two types of receptors active either mainly in the cell nucleus (ESR) or the cell membrane (GPER1). Estrogens also control hepatic lipid and lipoprotein metabolisms, with a triglyceride carrier role for VLDL from the liver to the ovaries during oogenesis. Moreover, the activation of the vitellogenin genes is used as a robust biomarker for exposure to xenoestrogens. In the context of liver diseases, high plasma estrogen levels are observed in fatty liver hemorrhagic syndrome (FLHS) in chicken implicating estrogens in the disease progression. Fishes are also used to investigate liver diseases, including models generated by mutation and transgenesis. In conclusion, studies on the roles of estrogens in the non-mammalian oviparous vertebrate liver have contributed enormously to unveil hormone-dependent physiological and physiopathological processes.
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Dissertations / Theses on the topic "Fatty liver syndrome of chickens"

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Schumann, Bruce Ezra. "Evaluation of Omega-3 fatty acids and antioxidants in the prevention of fatty liver hemorrhagic syndrome in laying hens." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0032/MQ47359.pdf.

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Cain, James. "Characterizing the role of dietary fat in the development and progression of liver dysfunction." OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/903.

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Obesity and metabolic dysfunction are worldwide health epidemics and they have grown to unprecedented levels. Human NAFLD is directly linked to obesity and metabolic dysfunction, so attention was given to elucidating a more complete understanding of the liver's role in mediating the metabolically healthy obese phenotype and to better characterizing the potential contribution of dietary fat and fatty acids as a therapeutic supplement to obesogenic diets. Specifically, flaxseed is high in α-linolenic acid (ALA; 18:3 n-3) and low in linoleic acid (LA; 18:2 n-6), and contains multiple other components such as fiber and lignans, and was investigated for its high potential to modify obesity phenotype and fatty liver disease. Additionally, we explored the temporal effect of initiating high-fat diets in various phases of adulthood. However, work in this field is complicated by an ongoing search for appropriate preclinical animal models of NAFLD as they have not been able to replicate the full spectrum of human NAFLD. As such, this dissertation sought to explore fatty liver disease in popular murine models of overnutrition, as well as a novel hen model. Major findings from this work showed that (1) exposure to a high-fat diet during early adulthood preserves metabolic homeostasis, modifies liver morphology, and protects against obesity-related disease, (2) dietary enrichment with flaxseed is capable of increasing tissue n3PUFA content, but this appeared to be only weakly related to metabolic and histological outcomes, and (3) there are limitations to the laying hen as a model of NAFLD as the pathogenic changes may not adequately match the human condition.
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Ghadieh, Hilda E. "Impaired Hepatic Insulin Clearance Links Fatty Liver Disease to Atherosclerosis." University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1533216686796754.

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Baghdadi, Hussam Hussein. "Hepatic injury in metabolic syndrome : the role of selenium in models of hepatic injury and healing." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4235.

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Oxidative stress, lipid peroxidation, and endotoxaemia with cytokine-mediated injury have been implicated as factors in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). The degree of insulin resistance together with co-existing inadequacies of vital antioxidant defence mechanisms may be important determinants of progression to fibrosis in patients with non-alcoholic steatohepatitis (NASH). Current therapies are targeted at improving insulin sensitivity as well as addressing hepatic repair including anti-inflammatory strategies. Anti-oxidants remedies have also been tested but the role of selenoenzymes with antioxidant action, namely thioredoxin reductase 1 (TR1) and glutathione peroxidase 1 (GPX1) have been ignored. The aim of this thesis is to investigate the role of selenium in the pathophysiology of NAFLD both in vitro and in vivo. The in vitro studies used cell lines representing the cell types involved in the disorder; hepatocytes (C3A line) and hepatic stellate cells (LX-2 line). In order to assess the influence of selenium status and selenoenzymes expression on the pathogenesis of NAFLD it was necessary to develop a culture system which allowed good cell viability in selenium free culture medium. This was achieved by the use of an insulin and transferrin (IT)-supplemented medium which importantly was free of any animal serum additions. Using this IT culture medium, selenium addition (as selenite) produced a significant increase in the expression of GPX1 and TR1 in both C3A and LX2 cells. TR1 and GPX1 were expressed at similar levels in both C3A and LX-2 cells. It was also necessary to develop an in-vitro model for fat loading C3A cells to mimic fatty liver pathophysiology. Two models of fat loading were investigated. One model used lactate, pyruvate, octanoate and ammonium (LPON). LPON has been previously used to increase the functionality of C3A cells but it was observed that fat droplets accumulated in these LPON treated cells. Dissection of the agents in the LPON revealed that octanoate was the factor that increased the triglyceride accumulation. Interestingly, octanoate also increased the expression of TR1 and GPX1, suggesting that it could induce oxidative stress leading to the induction of selenoenzymes to afford a protective defence mechanism. In the second model, oleate and/or palmitate were used to fat-load C3A cells. These cells had significantly higher triglyceride content than the LPON-fat-loaded cells. However, oleate and/or palmitate treatments did not increase the expression of either TR1 or GPX1 in C3A cells suggesting perhaps these cells were not under oxidative stress. LPON and oleate/palmitate were also capable of fat loading LX2 cells. Selenium-supplementation of C3A and LX-2 cells efficiently protected (measured by their lactate dehydrogenase retention) them from oxidative damage induced by t-butylhydroperoxide. This suggests that selenium supplementation through its incorporation into selenoenzymes could protect the cells from the oxidative damage. The role of selenium was also investigated in the regulation of α-1 pro-collagen mRNA expression. In LX-2 cells, the expression of α-1 pro-collagen mRNA was unaffected by the selenium status of the cell. Similarly the selenium status of C3A cells had no effect on modifying α-1 pro-collagen mRNA of LX2 cells when co-culture or conditioned medium experiments were performed. These results suggest that LX-2 cells were already largely activated and at a stage unable to be ameliorated by selenium treatment. In contrast, studies on C3A cells revealed that TGF-β1 (common inducer of α-1 pro-collagen mRNA in hepatic stellate cells) dramatically increased the expression of α-1 pro-collagen mRNA in C3A cells to the levels observed in LX-2 cells. More interestingly, selenium supplementation of C3A cells notably decreased α-1 pro-collagen mRNA expression in response to TGF-1. In the in vivo study, plasma selenium in type 2 diabetics (high risk of developing NAFLD) were inversely related to the body mass index and in most patients selenium levels were below that required to maximally express GPX1 in red cells. Furthermore, type 2 diabetics had lower plasma selenium levels compared to the healthy control group. Collectively, this suggests that in the UK population, obesity is a risk factor for both insulin resistance and decreased selenium status leading to sub-optimal antioxidant protection. In conclusion, this study provides evidence that selenium through increasing the expression of selenoenzymes is beneficial in protecting liver cells from oxidative stress. Furthermore, selenium is capable of suppressing α-1 pro-collagen mRNA expression in hepatocytes although not in activated hepatic stellate cells. Taken together these data support the view that suboptimal selenium intake in the UK may be a risk factor in the pathogenesis of NAFLD.
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Liu, Jingjing. "THE ABSENCE OF ABCD2 REVEALS A NOVEL ROLE FOR PEROXISOMES IN THE PROTECTION FROM METABOLIC SYNDROME." UKnowledge, 2011. http://uknowledge.uky.edu/gradschool_diss/819.

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ABCD2 (D2) is a peroxisomal ATP binding cassette (ABC) transporter that is expressed in brain, adrenal and liver. D2 is transcriptionally regulated by key transcriptional factors that control lipid and glucose metabolism. Therefore, we examined its role in adipose tissue. These studies revealed that D2 is highly abundant in adipose tissue and upregulated during adipogenesis. However, D2 deficiency does not affect either adipogenesis or lipid accumulation. An examination of the lipid profile of adipose tissue revealed the accumulation of C20 and C22 fatty acids in D2 deficient (D2‐/‐) mice. When challenged with a diet enriched in erucic acid (C22:1, 10% kcal), this lipid accumulated in both liver and adipose tissue. Following 8 weeks of diet, D2‐/‐ mice showed increased adiposity, glucose intolerance, dyslipidemia and steatosis. Analysis of the hepatic lipid profile showed significant changes away from poly unsaturated fatty acids (PUFAs) and toward C18‐22 mono‐unsaturated fatty acids (MUFA). RT‐PCR of the mRNA from the adipose tissue and liver revealed significant changes in lipogenic (ACC, SCD1 & 2) and PUFA synthesis (Δ5 & 6‐desaturase) genes in D2‐/‐ mice. The molecular mechanisms by which D2 regulates lipid metabolism in adipose tissue remains unclear. To explore potential mechanisms, the subcellular localization of D2 in adipose tissue was determined. Our results demonstrated that D2 resides in a distinct subclass of peroxisomes that does not containing classical peroxisomal markers such as pex19 or PMP70, but are positive for pex14. In conclusion, our studies reveal a novel role of D2 and peroxisomes in the protection from disruptions of lipid metabolism induced by dietary erucic acid and that D2 resides in a unique compartment within adipocytes that plays a yet to be elucidated role in the regulation of lipid metabolism.
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Neeb, Zachary P. "Diet-induced dyslipidemia drives store-operated Ca2+ entry, Ca2+ dysregulation, non-alcoholic steatohepatitis, and coronary atherogenesis in metabolic syndrome." Thesis, Connect to resource online, 2010. http://hdl.handle.net/1805/2209.

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Thesis (Ph.D.)--Indiana University, 2010.
Title from screen (viewed on July 21, 2010). Department of Cellular and Integrative Physiology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Michael Sturek, Jeffrey A. Breall, Robert V. Considine, Alexander Obukhov, Johnathan D. Tune. Includes vitae. Includes bibliographical references (leaves 212-240).
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Sliz, E. (Eeva). "Genetics and molecular epidemiology of metabolic syndrome-related traits:focus on metabolic profiling of lipid-lowering therapies and fatty liver, and the role of genetic factors in inflammatory load." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526222554.

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Abstract Metabolic syndrome is a constellation of metabolic abnormalities predisposing to cardiovascular diseases (CVD), type 2 diabetes, and increased mortality. Due to the high prevalence and severe co-morbidities, metabolic syndrome constitutes a major burden for both public health and the global economy. Improved understanding of the detailed molecular mechanisms could provide novel strategies for the treatment and preferably prevention of the metabolic syndrome-related health issues. Recent advancements in ‘omics’ technologies have facilitated the development of novel tools to examine the links between genetic variation and human health. The new techniques allow determination of millions of genotypes or quantification of hundreds of metabolic measures from a single blood sample. In this thesis, genomics and metabolomics approaches are coupled to improve our understanding of the metabolic syndrome-related health issues. More precisely, my projects evaluate the metabolic effects of two lipid-lowering therapies and non-alcoholic fatty liver, as well as assess genetic determinants of chronic inflammation. The present results indicate generally consistent metabolic effects of statins and proprotein convertase subtilisin/kexin type 9 (PCSK9) genetic inhibition. The subtle discrepancies observed could potentially contribute to differences in the efficacy to lower CVD risk between statins and PCSK9 inhibitors. The dissimilar metabolic effects of the four genetic variants that increase the risk of non-alcoholic fatty liver disease (NAFLD) highlight the heterogeneity of the molecular mechanisms involved in NAFLD pathogenesis. The results further suggest that fatty liver by itself might not promote unfavourable metabolic aberrations associated with fatty liver on a population level. The newly identified loci associating with inflammatory phenotypes elucidate the genetic mechanisms contributing to the inflammatory load. In particular, the present results suggest the important role of the locus determining the ABO blood types in the regulation of the soluble adhesion molecule levels. To conclude, this thesis successfully complements the knowledge of the molecular mechanisms involved in metabolic syndrome-related traits and provides examples of how to couple omics technologies in the study of complex traits or in the evaluation of drug effects
Tiivistelmä Metabolinen oireyhtymä on tila, jossa useiden aineenvaihdunnallisten riskitekijöiden kasautuminen suurentaa riskiä sairastua tyypin 2 diabetekseen ja sydän- ja verisuonitauteihin sekä lisää kokonaiskuolleisuutta. Vakavista liitännäissairauksista ja suuresta esiintyvyydestä johtuen metabolinen oireyhtymä kuormittaa merkittävästi sekä terveydenhuoltoa että kansantaloutta. Jotta metabolisen oireyhtymän hoitoon ja ennaltaehkäisyyn voitaisiin kehittää uusia keinoja, on tärkeää ymmärtää paremmin oireyhtymän syntyyn vaikuttavat täsmälliset molekyylimekanismit. Niin sanottujen ’omiikka-tekniikoiden’ viimeaikainen kehitys tarjoaa uusia mahdollisuuksia tutkia geenimuutosten vaikutuksia terveyteen. Uusien tekniikoiden avulla voidaan määrittää miljoonia genotyyppejä tai satoja aineenvaihdunnan merkkiaineita yhdestä verinäytteestä. Tässä väitöskirjatyössä yhdistetään genomiikan ja metabolomiikan menetelmiä metaboliseen oireyhtymään liittyvien terveysongelmien tutkimiseksi. Väitöskirjani osatöissä arvioin kahden lipidilääkkeen sekä ei-alkoholiperäisen rasvamaksan aineenvaihdunnallisia vaikutuksia sekä pyrin tunnistamaan krooniseen tulehdukseen vaikuttavia geneettisiä tekijöitä. Tulosten mukaan statiinien ja PCSK9:n (engl. proprotein convertase subtilisin/kexin type 9) geneettisen eston aineenvaihduntavaikutukset ovat hyvin samankaltaiset. Kuitenkin havaitut pienet poikkeavuudet tietyissä merkkiaineissa voivat vaikuttaa eroavaisuuksiin siinä, kuinka tehokkaasti lääkeaineet alentavat sydäntautiriskiä. Suuret erot rasvamaksan riskiä lisäävien geenimuutosten vaikutuksissa aineenvaihduntaan korostavat rasvamaksaan liittyvien molekyylimekanismien monimuotoisuutta. Tulosten perusteella vaikuttaa siltä, että rasvan kertyminen maksaan ei luultavasti itsessään aiheuta suuria muutoksia verenkierron aineenvaihduntatuotteiden pitoisuuksiin. Tulehdusmerkkiaineisiin assosioituvat uudet geenialueet täydentävät tulehduksen molekyylimekanismeihin liittyvää tietoa. Tulokset korostavat ABO-veriryhmän määräävän geenin vaikutusta liukoisten adheesiomolekyylien pitoisuuksiin. Kaiken kaikkiaan väitöskirjan osatyöt tuovat uutta tietoa metaboliseen oireyhtymään liittyvien terveysongelmien molekyylimekanismeihin. Projektit havainnollistavat, miten omiikka-tekniikoita voidaan hyödyntää monitekijäisten fenotyyppien tutkimuksessa sekä lääkeaineiden aineenvaihduntavaikutusten arvioinnissa
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Almeida, André Guerra de. ""Correlações entre achados laboratoriais e doença hepática gordurosa não alcoólica em pacientes portadores de obesidade mórbida"." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5154/tde-11042006-163614/.

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Devido a controvérsias sobre a freqüência, diagnóstico e possibilidade de progressão para doença crônica da degeneração gordurosa do fígado em portadores de obesidade mórbida, planejou-se uma investigação retrospectiva em pacientes candidatos à cirurgia bariátrica. Foram analisados 60 indivíduos com indicação de gastroplastia com derivação intestinal em Y de Roux. Os pacientes foram submetidos a questionário clínico, provas bioquímicas e posteriormente, à biópsia hepática intraoperatória. A freqüência de EHNA e esteatose hepática foi elevada, e detectou-se 5% de cirrose. Na análise univariada houve correlação de diversos testes bioquímicos com as enzimas hepáticas. Na análise multivariada a albumina foi a variável determinante; apesar de seu debilitado valor preditivo. Nestas condições, apenas a avaliação histológica configura-se como critério definitivo para diagnóstico e acompanhamento desta população
Because of controversies about frequency, diagnosis and possibility of progression toward chronic disease of fatty degeneration of the liver in morbidly obese patients, a retrospective study was done in patients who underwent bariatric surgery. Sixty individuals with indication for gastroplasty with Roux-en-Y jejunal bypass were enrolled. They were submitted to clinical questionnaire, biochemistry tests and subsequently, intraoperative liver biopsy. Frequency of NASH and steatosis was high, and 5.0% suffered from cirrhosis. In univariate analysis there was correlation between various biochemical measurements and liver enzymes. In multivariate analysis only serum albumin was a determinant variable, with low predictive value. The histological grading system remains the definitive criterion for diagnosis and follow-up of this population
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Bellio, Marie. "La plaquette sanguine : un nouvel acteur du syndrome hémorragique de Noonan et du développement des maladies métaboliques." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30010.

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Les plaquettes sanguines jouent un rôle majeur dans le maintien de l’intégrité vasculaire. Elles sont les premiers éléments à intervenir lors d’une brèche vasculaire afin d’arrêter le saignement par la formation d’un thrombus. La plaquette est également un acteur critique dans la survenue d’évènements thrombotiques associées à certaines pathologies comme par exemple le syndrome métabolique, ce qui en fait une cible pharmacologique majeure. Au cours de ma thèse, je me suis focalisée sur deux axes de recherche : (i) l’étude de l’activation plaquettaire dans le syndrome de Noonan (SN) et le syndrome de Noonan avec Lentigines Multiples (SNLM) et (ii) la caractérisation du rôle des plaquettes dans le développement des maladies hépatiques non alcooliques (NAFLD). Dans un premier temps, motivée par le fait que les patients atteints du SN présentent des troubles de l’hémostase encore inexpliqués, mes travaux de recherche ont eu pour but de caractériser l’activation plaquettaire dans le SN et le SNLM causés respectivement par une hyper- ou une hypo-activation de la protéine tyrosine phosphatase SHP2. Nous avons tout d’abord observé que les plaquettes de patients Noonan présentent in vitro une agrégation fortement diminuée en réponse à de faibles doses d’un ligand du récepteur GPVI, le collagène, associée ex vivo à une réduction significative de la formation de thrombi en condition de flux artériel sur matrice de collagène. Le modèle murin mimant phénotypiquement le SN présente également un défaut d’agrégation plaquettaire in vitro induite par de faibles doses d’agonistes de GPVI associé à une diminution de la signalisation en aval de GPVI. La formation de thrombi plaquettaire ex vivo en condition de flux artériel mais aussi in vivo à la suite d’une lésion de la carotide est aussi significativement altérée. L’hémostase primaire des souris Noonan est aussi très fortement affectée, comme montré par une augmentation significative du temps de saignement à la queue. A l’opposé, le modèle murin de SNLM est responsable d’une hyper-activation plaquettaire induite par la stimulation de GPVI et présente un phénotype prothrombotique ex vivo en condition de flux artériel. De façon intéressante, cette hyperactivation plaquettaire est également observée chez les patients atteints du SNLM et est exacerbée dans des conditions de flux à haute vitesse. Ainsi, cette étude permet de mettre en lumière deux nouvelles thrombopathies associées à un dysfonctionnement de la signalisation plaquettaire, ce qui permet une meilleure compréhension et prise en charge des potentiels risques hémorragiques/thrombotiques des patients SN et SNLM. D’un point de vue moléculaire, cette étude a permis de préciser le rôle de SHP2 dans l’activation plaquettaire. Dans un second temps, je me suis intéressée au rôle des plaquettes dans le développement de la NAFLD. Pour ce faire, plusieurs modèles murins ont été mis sous régimes hyperlipidiques mimant différents stades de la pathologie. De façon intéressante, nous avons montré un rôle protecteur des plaquettes sur le statut glucido-lipidique du foie en inhibant le stockage de lipides, mais également sur l’état inflammatoire et fibrotique hépatique en protégeant de l’infiltration des cellules inflammatoires et de l’installation de la fibrose. Ce rôle est associé à un recrutement de plaquettes dans les sinusoïdes hépatiques durant l’installation de la pathologie. De plus, nous démontrons que la délétion de Vps34 plaquettaire permet de ralentir le développement de la NAFLD. Ainsi, ces résultats ont permis de mettre un jour pour la première fois un nouveau rôle protecteur des plaquettes sur le développement de la NAFLD et pourrait permettre d’identifier de potentielles pistes thérapeutiques permettant de réduire ou prévenir la NAFLD. En conclusion, mes travaux de thèse apportent de nouvelles données quant au rôle des plaquettes dans différents contextes pathologiques : le SN, le SNLM et la NAFLD
Blood platelets play a major role in the maintenance of vascular integrity. They are the first blood cells recruited after vessel injury to stop bleeding by thrombus formation. Platelet hyper-activation is also a critical element in thrombotic events associated to several pathologies such as metabolic syndrome, which makes them major pharmacologic targets. My thesis work was focused on two main axis: (i) analysis of platelet activation in Noonan syndrome (NS) and Noonan syndrome with multiple lentigines (NSML) and (ii) characterization of the role of platelets in non-alcoholic fatty liver disease (NAFLD). Firstly, motivated by the occurrence of bleeding anomalies frequently reported in NS, we focused on characterizing platelet activation in NS and NSML caused respectively by a gain or a loss of function of the protein tyrosine phosphatase SHP2. We observed that platelets from NS patients display a defective in vitro aggregation to low concentrations of collagen, a GPVI agonist, associated to a decrease in thrombus growth ex vivo on a collagen surface under arterial shear stress. The mouse model phenocopying NS also exhibit a significant reduction in in vitro platelet aggregation induced by low concentrations of GPVI agonists, which is associated to a deficiency in GPVI signalling. The thrombus formation ex vivo under arterial shear stress as well as in vivo following a local carotid injury was also significantly affected. Primary haemostasis is also defective in NS mice as shown by a significant increase in mouse tail bleeding time. In contrast, NSML mouse platelets exhibited an increased activation after GPVI stimulation and an enhanced platelet thrombotic phenotype on collagen matrix under arterial shear stress. Interestingly, this platelet hyper-activation is also observed in blood samples from NSML patients ex vivo in arterial shear rate and exacerbated in high shear rate condition. This study allows the discovery of two new thrombopathies linked to platelet signalling defects and provides important information for the medical care of patient with NS or NSML in risk of bleeding or thrombosis situations. Besides, this study brings new insights into the understanding of SHP2 function in platelet activation. Secondly, I studied the role of platelets in NAFLD development. Using mouse models fed with different hyperlipidic diets mimicking different step of the NAFLD, we showed a protective role for platelets in hepatic glucidic and lipidic metabolism by inhibition of lipid storage. Furthermore, platelets protect against hepatic inflammation and fibrosis by decreasing inflammatory cells recruitment and fibrosis development. This protective role is associated to the presence of platelet aggregates in liver sinusoids. Interestingly, we demonstrate that platelet Vps34 deletion allows to slow down NAFLD development. Thereby, these innovative results highlight a new protective role of platelet in NAFLD development and could allow the identification of potential pharmacologic targets for preventing or limiting the disease. In conclusion, my thesis work brings new data on the role of platelets in different physiopathologic conditions: NS, NSML and NAFLD
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Oliveira, Cacilda Pedrosa de. ""Alterações hepáticas em grandes obesos: avaliações clínico-laboratoriais e histopatológicas antes do tratamento cirúrgico da obesidade"." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-31052006-150549/.

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A doença hepática gordurosa não-alcoólica (DHGNA) e a esteatohepatite (EHNA) são freqüentes nos obesos. O objetivo foi determinar a prevalência de DHGNA/EHNA e Síndrome Metabólica (SM) nos grandes obesos; definir preditores de EHNA; estabelecer critérios histológicos para o diagnóstico da EHNA. Avaliados 325 pacientes encaminhados à cirurgia bariátrica (IMC = 35 kg/m2), dos quais 146 foram submetidos à análise histológica; as variáveis clínicas e bioquímicas analisadas e correlacionadas com a histologia. A DHGNA ocorreu em 111 (76%) pacientes e a prevalência de EHNA, conforme critério histológico usado, em 25,3% a 55,5%; SM ocorreu em 57,2%. Os preditores da EHNA foram: SM; alterações glicêmicas; hipertrigliceridemia e HAS. Foram preditores de fibrose: idade acima de 30 anos e AST elevada
Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) has been associated with obesity. Determine prevalence of NAFLD/NASH and metabolic syndrome (MS) in severe obesity; define clinical predictor of steatohepatitis; establish histological criteria necessary to diagnose NASH. Evaluation of 325 patients submitted to bariatric surgery (BMI = 35 kg/m2), among which 146 were submitted to histological analysis; variables clinical and biochemical were analyzed and correlated to histological characteristics. NAFLD occurred in 111 (76%) patients and NASH, according to histological criteria used, in 25.3% to 55.5%; MS was present in 57.2%. Predictors of NASH: MS; glycaemic alterations; hypertriglyceridaemia and high blood pressure (HBP). Predictors of fibrosis: age above 30 years and high AST
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Books on the topic "Fatty liver syndrome of chickens"

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1946-, Gershwin M. Eric, and Day Christopher Paul, eds. Falk Liver Conference. Basel: Karger, 2010.

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Xu Zhao, Shan Zhang, Yiru Shen, Y.M. Guo, and S.R. Shi. Changes in liver triglyceride metabolism in broiler chickens with cold-induced ascites syndrome. Verlag Eugen Ulmer, 2016. http://dx.doi.org/10.1399/eps.2016.151.

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Eating yourself sick: How to stop obesity, fatty liver, and diabetes from killing you and your family. 2018.

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Avand, Ghazal. Metabolic syndrome in non-alcoholic fatty liver disease: A comparison between simple steatosis and non-alcoholic steatohepatitis. 2006.

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Mancell, Sara, and Deepa Kamat. Nutritional management of liver disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0068.

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The chapter on nutrition and liver disease describes the pathophysiology of the malnutrition that frequently accompanies chronic liver disease in children and then discusses the suggested management as well as ways of nutritional assessment and monitoring of the children. There is also a section of specific suggestions for various conditions such as biliary atresia, Alagille syndrome, Wilson disease, non-alcoholic fatty liver disease, as well as an overview of the various special feeds and supplements used in these conditions.
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Wiles, Kate, and Catherine Nelson-Piercy. Pre-eclampsia and related disorders. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0296_update_001.

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Pre-eclampsia is a pregnancy-specific condition diagnosed by new-onset hypertension and proteinuria after 20 weeks’ gestation. The incidence of pre-eclampsia means that it is both the most prevalent cause of acute kidney injury (AKI) in pregnancy and the commonest glomerular disease in the world. This chapter outlines the diagnosis and management of pre-eclampsia. Particular emphasis is given to the post-partum disease course as this is when a specialist nephrology opinion may be sought. HELLP (haemolysis, elevated liver enzymes, low platelets) syndrome is a variant of severe pre-eclampsia. The most important differential diagnoses of HELLP syndrome are the thrombotic microangiopathies. Pregnancy can act as a trigger for both for new disease and flare of thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome. AKI is a common complication of acute fatty liver of pregnancy. The diagnosis and supportive management of this condition are considered.
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Wiles, Kate, and Catherine Nelson-Piercy. Acute kidney injury in pregnancy. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0297.

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The diagnosis of acute kidney injury in pregnancy is complicated by physiological changes to both kidney and circulation; although a serum creatinine of higher than 90 μ‎‎‎mol/L is considered diagnostic of kidney injury in pregnancy. The aetiology of acute kidney injury in pregnancy mirrors that of the non-pregnant patient with the addition of pregnancy-specific conditions such as pre-eclampsia, HELLP syndrome (haemolysis, elevated liver enzymes, low platelets), post-partum haemorrhage, and acute fatty liver of pregnancy. In early pregnancy, the major additional concerns are septic abortion and hyperemesis. Urinary tract infection is common in pregnancy. Surveillance and treatment thresholds reflect the recognized association between urinary tract infection and adverse pregnancy outcome. Obstructive nephropathy is difficult to diagnose in pregnancy due to a physiological dilatation of the renal tract. Radiological assessment and intervention to the renal tract in pregnancy are also discussed in this chapter.
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Anderson, John A., Pierre-Antoine Laloë, and Derek J. Tuffnell. Hypertension in pregnancy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0036.

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The hypertensive disorders of pregnancy encompass a spectrum of disease, including gestational hypertension, haemolysis, elevated liver enzymes, and low platelets (HELLP syndrome), and acute fatty liver of pregnancy through to pre-eclampsia and eclampsia. These conditions can pose significant problems for clinicians and are associated with significant morbidity and mortality for both mother and baby. Pre-eclampsia and eclampsia remain one of the leading causes of maternal death worldwide. The majority of fatalities occur in settings with low healthcare resources. In the developed world, improvements over the last 60 years in antenatal and intrapartum care, along with national surveillance and audit, have led to tenfold and fivefold reductions in absolute mortality and severe morbidity from eclampsia and pre-eclampsia respectively. Conversely, the incidence of pre-eclampsia has been rising in the developed world as the average age of first maternity increases and rates of obesity and other medical conditions rise. It is therefore increasingly likely that hypertension may complicate the obstetric and anaesthetic management of pregnant women.
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Plebani, Mario, Monica Maria Mion, and Martina Zaninotto. Biomarkers of renal and hepatic failure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0039.

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In the last few years, major advances have been achieved in the understanding of the molecular and pathophysiological mechanisms which underlie the complex interactions between the heart and the kidney, as well as between the heart and the liver. According to these new insights, new biomarkers have been proposed for better evaluating and monitoring patients affected by cardiovascular diseases. In addition, some biomarkers should be used as risk factors and for an early identification and treatment of these severe diseases. This chapter reviews the most important biomarkers for evaluating the ‘cardiorenal syndrome’, in particular, the measurement of serum creatinine and its use for calculating the glomerular filtration rate which, with the new and more efficient equation, namely Chronic Kidney Disease Epidemiology Collaboration, still remains the most widely used biomarker. The role of newer biomarkers will be explored. The measurement of cystatin C, representing additional information, particularly in paediatric age groups and in the early phase of kidney disease, plays an increasing role. Neutrophil gelatinase-associated lipocalin is a recently developed and very promising new biomarker for the diagnosis of acute kidney injury, while the well-known albumin/creatinine ratio has been re-evaluated as a simple and useful tool for an early identification of kidney disease. Regarding liver diseases, a growing body of evidence demonstrates the usefulness of non-invasive makers of hepatic fibrosis that may avoid the need for a liver biopsy in most patients. A promising field of research is represented by the role of non-alcoholic fatty liver disease in the pathogenesis of cardiovascular disease.
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Wiles, Kate, Kate Bramham, and Catherine Nelson-Piercy. Kidney disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0044.

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This chapter describes the physiological adaptations to pregnancy in women with and without renal disease, reports pregnancy outcomes in women with both acute kidney injury and chronic kidney disease, and discusses a management strategy for antenatal and peripartum care. Acute kidney injury (AKI) is difficult to define in pregnancy because of the physiological increase in glomerular filtration. A normal creatinine can mask renal injury in pregnancy. This chapter considers important causes of AKI in pregnancy including pre-eclampsia, HELLP syndrome, thrombotic microangiopathy, acute fatty liver of pregnancy, systemic lupus erythematosus, urinary tract infection, and obstruction. The trend in the developed world for delaying pregnancy and the increasing prevalence of obesity mean that greater numbers of pregnancies will be complicated by chronic kidney disease. Maternal and fetal complications increase with worsening prepregnancy renal function including the development of pre-eclampsia, fetal growth restriction, premature delivery, and fetal loss. Prepregnancy counselling and the intrapartum management for women with lupus nephritis, immunoglobulin A nephropathy, polycystic kidney disease, and diabetic nephropathy are discussed. Renal replacement therapies in pregnancy including both dialysis and renal transplantation are considered, and practical guidance on renal biopsy, anaesthesia, and the pharmacology of renal disease in pregnancy is offered.
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Book chapters on the topic "Fatty liver syndrome of chickens"

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Smolle, Elisabeth, Sonja M. Kessler, Nicole Golob, and Johannes Haybaeck. "Nonalcoholic Fatty Liver Disease." In Metabolic Syndrome, 641–57. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-11251-0_36.

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Smolle, Elisabeth, Sonja M. Kessler, Nicole Golob, and Johannes Haybaeck. "Non-alcoholic Fatty Liver Disease." In Metabolic Syndrome, 1–21. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12125-3_36-1.

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Ahmed, Mohamed H., and Christopher D. Byrne. "Non-Alcoholic Fatty Liver Disease." In The Metabolic Syndrome, 245–77. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444347319.ch15.

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Futterweit, Walter. "Nonalcoholic Fatty Liver Disease in Polycystic Ovary Syndrome." In Insulin Resistance and Polycystic Ovarian Syndrome, 303–15. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-310-3_23.

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Angulo, Paul. "Metabolic Syndrome and Non-alcoholic Fatty Liver Disease." In Practical Gastroenterology and Hepatology Board Review Toolkit, 522–29. Oxford, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119127437.ch83.

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Najjar, Sonia M. "Non-Alcoholic Fatty Liver Disease and the Metabolic Syndrome." In Metabolic Basis of Obesity, 219–27. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1607-5_12.

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Laron, Zvi. "Nonalcoholic Fatty Liver Disease (Nafld) in Patients with Laron Syndrome." In Laron Syndrome - From Man to Mouse, 143–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11183-9_14.

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Yilmaz, Yusuf. "Is NAFLD different in absence of metabolic syndrome?" In Clinical Dilemmas in Non-Alcoholic Fatty Liver Disease, 44–49. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118924938.ch6.

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Yki-Järvinen, Hannele. "Effects of treatment of NAFLD on the metabolic syndrome." In Clinical Dilemmas in Non-Alcoholic Fatty Liver Disease, 189–95. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118924938.ch21.

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Blackstone, Robin P. "Obesity-Related Diseases and Syndromes: Insulin Resistance, Type 2 Diabetes Mellitus, Non-alcoholic Fatty Liver Disease, Cardiovascular Disease, and Metabolic Syndrome." In Obesity, 83–108. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39409-1_5.

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Conference papers on the topic "Fatty liver syndrome of chickens"

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Yin, Shouyi, Tao Liu, Huafeng Wei, and Guang Ji. "Syndrome differentiation of fatty liver based on the whole network analysis theory." In 2010 IEEE International Conference on Bioinformatics and Biomedicine Workshops (BIBMW). IEEE, 2010. http://dx.doi.org/10.1109/bibmw.2010.5703868.

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Vijayaraman, A., J. Hanje, and S. E. Kirkby. "An Unusual Case of Severe Hepatopulmonary Syndrome as a Result of Endocrine Dysfunction Related Fatty Liver Disease." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3754.

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Wang, Xiaoyong, and Jia Wu. "IDDF2018-ABS-0068 A potential link between polycystic ovary syndrome and non-alcoholic fatty liver disease: an update meta-analysis." In International Digestive Disease Forum (IDDF) 2018, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfabstracts.200.

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Minville, Caroline, Marie-Noelle Hilleret, Renaud Tamisier, Patrick A. Levy, Jean-Pierre Zarski, and Jean-Louis Pepin. "In Sleep Apnea Syndrome, Nonalcoholic Fatty Liver Disease (NAFLD) Is Associated With The Severity Of Intermittent Hypoxia And More Severe Endothelial Dysfunction." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5374.

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Ali, Alyaa Hassan, Shawal Mohamed Faizal, Khairul Najmi Muhammad Nawawi, Wong Zhiqin, Ngiu Chai Soon, Nur Yazmin Yaacob, Shamsul Azhar Shah, Hamad Hamdi Che Hassan, Oteh Maskon, and Raja Affendi Raja Ali. "IDDF2018-ABS-0219 Assessment of correlation between non-alcoholic fatty liver disease and severity of coronary artery disease in young acute coronary syndrome patients." In International Digestive Disease Forum (IDDF) 2018, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfabstracts.235.

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Zhilyakova, Elena, Tatyana Golivets, Zoya Tsvetkova, and Diana Dubonosova. "Search of New Opportunities of Pharmacological Protection at the Early Stages of a Non-Alcoholic Fatty Liver Disease Associated With Obesity and Metabolic Syndrome." In Proceedings of the 1st International Symposium Innovations in Life Sciences (ISILS 2019). Paris, France: Atlantis Press, 2019. http://dx.doi.org/10.2991/isils-19.2019.87.

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Uong, Flaryll Faye, Nirvana Maryam Sana, Maria Angelica Bianca Tech, and Janus Ong. "IDDF2020-ABS-0022 The metabolic syndrome as a risk factor for non-alcoholic fatty liver disease in filipino adults consulting in a philippine tertiary hospital: a retrospective cohort study." In Abstracts of the International Digestive Disease Forum (IDDF), 22–23 November 2020, Hong Kong. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2020. http://dx.doi.org/10.1136/gutjnl-2020-iddf.33.

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