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Статті в журналах з теми "Non-Alcoholic fatty liver diseases":

1

Fujioka, Kazumi. "Link between Non-Alcoholic Fatty Liver Disease and Hypertension: Non-Alcoholic Fatty Liver Disease as a Multisystem Disease." International Journal of Clinical Case Reports and Reviews 10, no. 5 (March 11, 2022): 01–04. http://dx.doi.org/10.31579/2690-4861/203.

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The prevalence and incidence of non-alcoholic fatty liver disease (NAFLD) is increasing due to the epidemics of obesity and type 2 diabetes mellitus (T2DM). Many studies provided the evidence of the decreased flow-mediated vasodilation (FMD), increased carotid intima-media thickness (IMT), and increased brachial ankle pulse wave velocity (baPWV) in patients with NAFLD. Recently, a link between NAFLD and hypertension along with new genetic expression, ADIPOQ C11377G and AGTR1 has been shown. It is putative that NAFLD may induce systemic inflammation, insulin resistance, oxidative stress, and increased vasoconstriction and decreased vasodilation, subsequently leading to hypertension. Under the systemic inflammation, it has been suggested that NAFLD may promote sympathetic nervous system (SNS) and renin-angiotensin system (RAS) activation, and local vasculature and renal inflammation, subsequently leading to hypertension. The author has reviewed the current knowledge of the link between NAFLD and hypertension along with new genetic expression in this article. It plausible that NAFLD is a multisystem disease and is associated with hepatic and extrahepatic disease.
2

Alp, Hayriye. "Acupuncture and Phytotherapy Applications in Non-Alcoholic Fatty Liver." Gastroenterology Pancreatology and Hepatobilary Disorders 5, no. 2 (June 2, 2021): 01–03. http://dx.doi.org/10.31579/2641-5194/026.

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Phytotherapy, medicinal and aromatic plants, algae, fungi and lichens, or their extracts, such as gum, balsam and resin, extracts, essential oils, candles and fixed oils with herbal preparations prepared in various forms (tea, capsule, tablet, syrup, drop , lozenges, sachets, etc.) to be protected from diseases, to treat diseases or to support treatment. Phytotherapy; It is based on scientific research and clinical studies. Historically, it has been the primary support of doctors in the treatment of diseases. Objective:We offer here; In addition to the treatment of obesity with acupuncture and phytotherapeutically artichoke (Cynara scolymus L.) and thistle (Silybum marianum (L.) Gaertn.), dandelion (Taraxacum officinale FH Wigg.) using antidepressants for many years, the treatment of obesity with impaired obesity and elevated liver enzymes. It is a case where a positive decrease is achieved in liver enzymes by giving mix extract. Methods: Yin-tan, Memory, Kid-3, Liv-3, St-36,24,25 in body acupuncture, Shen-men, stomach, larynx, jerome, kidney points were pinned in ear acupuncture. When patients who apply to the outpatient clinic need phytotherapeutic support, liver enzymes are routinely checked. Results:The patient lost both weight and liver enzymes. Conclusions and Recommendations: The biggest disadvantage of these preparations is their uncontrolled and high-dose use. It is most appropriate to give this kind of support treatments by people who are trained and licensed in this regard, especially under the control of a doctor. For this purpose, the Department of Traditional Complementary Medicine provides the development of physicians and pharmacists who have received phytotherapy training.
3

Narayan, Smriti, Sonu Kumar Gupta, Priyanka Singh, Villayat Ali, and Malkhey Verma. "Non-alcoholic fatty liver disease progression and current research." Asian Pacific Journal of Health Sciences 6, no. 1 (March 2019): 189–98. http://dx.doi.org/10.21276/apjhs.2019.6.1.26.

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4

Singla, Bharti, Gesu Singla, and Harsharan Kaur. "Lipid profile variations in non alcoholic fatty liver disease." Asian Pacific Journal of Health Sciences 6, no. 3 (September 2019): 1–4. http://dx.doi.org/10.21276/apjhs.2019.6.3.1.

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5

Fitzpatrick, Emer. "PAEDIATRIC NON ALCOHOLIC FATTY LIVER DISEASE: AN EMERGING THREAT." Paediatrics Today 11, no. 1 (March 15, 2015): 1–9. http://dx.doi.org/10.5457/p2005-114.104.

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6

DELLA CORTE, Claudia. "PEDIATRIC NON-ALCOHOLIC FATTY LIVER DISEASE: A GROWING PROBLEM." Paediatrics Today 11, no. 2 (October 8, 2015): 81–83. http://dx.doi.org/10.5457/p2005-114.114.

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7

Mitra, Souveek, Arka De, and Abhijit Chowdhury. "Epidemiology of non-alcoholic and alcoholic fatty liver diseases." Translational Gastroenterology and Hepatology 5 (April 2020): 16. http://dx.doi.org/10.21037/tgh.2019.09.08.

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8

Kanda, Tatsuo, Shunichi Matsuoka, Motomi Yamazaki, Toshikatsu Shibata, Kazushige Nirei, Hiroshi Takahashi, Tomohiro Kaneko, et al. "Apoptosis and non-alcoholic fatty liver diseases." World Journal of Gastroenterology 24, no. 25 (July 7, 2018): 2661–72. http://dx.doi.org/10.3748/wjg.v24.i25.2661.

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9

Federico, A., M. Trappoliere, M. V. D'Auria, C. Del Vecchio Blanco, and C. Loguercio. "Diet and non alcoholic fatty liver diseases." Digestive and Liver Disease 38 (April 2006): S95. http://dx.doi.org/10.1016/s1590-8658(06)80254-9.

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10

Lamichaney, Rachna. "Biochemical and Radiological Changes in Non Alcoholic Fatty Liver Diseases Compare with Obesity." Journal of Medical Science And clinical Research 05, no. 05 (May 28, 2017): 22367–73. http://dx.doi.org/10.18535/jmscr/v5i5.177.

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Дисертації з теми "Non-Alcoholic fatty liver diseases":

1

Bayard, Max, and Jim Holt. "Non-Alcoholic Fatty Liver Disease." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etsu-works/6495.

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2

Levene, Adam Phillip. "Steatosis in non alcoholic fatty liver disease." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9691.

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Non-alcoholic fatty liver disease is the commonest cause of chronic liver disease in developed countries. The accurate assessment of steatosis is central to the diagnosis of non-alcoholic fatty liver disease. I compared the assessment of steatosis by histology, biochemical triglyceride assays, digital image analysis, with and without Oil Red-O staining, in mouse livers and human liver biopsies. In each case Oil Red-O digital image analysis was the most reliable technique for quantitating steatosis. I then investigated a potential, non-invasive technique for distinguishing steatosis from steatohepatitis as only the latter causes progressive liver disease. The liver contains fluorophores which can be detected by autofluorescence spectroscopy. The fluorophore levels vary depending on the levels of oxidative stress and fibrosis within the liver. Mouse and human livers, were assessed to measure the fluorescence intensity at different wavelengths and this was compared with the histology. The probe was able to accurately identify biopsies which had inflammation and fibrosis with a high degree of sensitivity and specificity. Autophagocytosis has recently been suggested to play a role in fat metabolism. Using liver differentiated HUH7 cells grown in normal or oleate containing media with or without Rapamycin (an autophagocytosis activator) the role of autophagocytosis was investigated. This involved examining steatosis by Oil Red-O digital image analysis, biochemical triglyceride assays, electron microscopy and confocal immunofluorescence. I concluded that activating autophagocytosis decreased the levels of steatosis within the cells. This work has shown Oil Red-O digital image analysis is the most accurate way of assessing steatosis within the liver, that autofluorescence spectroscopy has the ability to distinguish, in real-time, isolated steatosis from steatohepatitis and that autophagocytosis has a role in fat metabolism within the liver which may be exploited therapeutically.
3

De, Alwis Nimantha M. W. "Mitochondrial dysfunction in non alcoholic fatty liver disease." Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493235.

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Non Alcoholic fatty Liver disease (NAFLD) is the commonest chronic liver disease worldwide and is a spectrum which includes simple fatty liver (simple steatosis), non-alcoholic steatohepatitis (NASH) and cirrhosis. Simple steatosis is a benign condition but NASH may progress to liver fibrosis and cirrhosis. Why only some develop progressive disease is not known and maybe dependant on the pathophysiology.
4

Liu, Yang-Lin. "Genomic studies in non-alcoholic fatty liver disease." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3822.

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Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum that spans simple steatosis, through steatohepatitis (NASH) to fibrosis and ultimately cirrhosis. NAFLD is characterised by substantial inter-patient variation in rate of progression and disease outcome: whilst up to 25% of the general population are at risk of progressive disease, only a minority experience associated liver-related morbidity. Inter-patient genetic variation and environment determine severity and progression of NAFLD. This thesis reports a series of studies examining the association of genetic variations in two genes patatin-like phospholipase domain-containing 3 (PNPLA3, rs738409 c.444 C > G, p.I148M) and transmembrane 6 superfamily member 2, (TM6SF2, rs58542926 c.449 C > T, p.E167K) with severity of NAFLD and risk of NAFLD-associated hepatocellular carcinoma (HCC). Addressing first the role of PNPLA3, I demonstrate that the rs738409 variant is associated with steatosis, steatohepatitis and fibrosis in the largest histologically characterised NAFLD cohort of European-Caucasian descent (n=1,005) studied to date. Subsequently, adopting a case-control analyses in a cohort of 100 consecutive Northern European Caucasian patients with NAFLD-associated HCC arising and a cohort of patients with histologically characterised NAFLD, I demonstrate that carriage of the rs738409 minor (G) allele is significantly associated with increased risk of developing NAFLD-associated HCC, independent of potential confounding factors including gender, age at diagnosis, presence of advanced fibrosis/cirrhosis, T2DM and BMI. During my studies, a genome-wide association study identified a SNP in TM6SF2 as a modifier of hepatic triglyceride accumulation measured by MR Spectroscopy. It was therefore pertinent to determine whether this variant also affected risk of steatohepatitis or fibrosis in NAFLD. Using the aforementioned cohorts, I demonstrate for the first time that, in addition to its association with steatosis, the rs58542926 SNP is significantly associated with stage of fibrosis in NAFLD. In contrast to PNPLA3 however, no association with NAFLD-HCC was found. In conclusion, the current thesis confirms the association of PNPLA3 with NAFLD severity and provides new evidence of its association with HCC risk. In addition, itdemonstrates for the first time that TM6SF2 is associated with NAFLD-fibrosis severity. These studies provide important new insights into NAFLD pathogenesis and mandate further functional study.
5

Alshaalan, Rasha. "Non-invasive diagnostic methods for non-alcoholic fatty liver disease." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=119567.

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Background: NAFLD is one of the most common causes of liver disease worldwide. It is a spectrum of disease characterized by macrovesicular steatosis of the liver that ranges from simple fatty liver (steatosis), to non-alcoholic steatohepatitis (NASH). NASH may eventually evolve to cirrhosis and end stage complication. Liver biopsy has long been considered the gold standard of reference to diagnose NAFLD but it is costly and invasive. Recently, non-invasive methods have been proposed. Aims and methods: The aim of this study was to investigate the accuracy of non-invasive methods including (Ultrasound, computed tomography scan, Xenon-133 scan, Hepatic steatosis index, Fibroscan, NAFLD fibrosis score, APRI index, and FIB-4 index) and their combination to diagnose steatosis and to diagnose significant liver fibrosis (>F2) and cirrhosis (F4) as compared to liver biopsy. We conducted a retrospective study of 114 NASH patients (79 males, mean age 49.6±10.6). All had adequate liver histology. Results: The distribution of fibrosis stage was as follows: F0-F1= 50%, F2=16.8%, F3=19.2%, F4=14%. The distribution of steatosis grade was as follows: grade 0-1=16%, grade2=53.3%, grade3=30.7%. The following tests correlated with fibrosis: APRI index (r=0.554), FIB-4(r=0.555), NAFLD fibrosis score (r=0.473), Fibroscan(r=0.586) and Hepatic Steatosis Index (HSI) (r=0.245). The FIB-4 and APRI index showed the best diagnostic accuracy for significant fibrosis as indicated by an Area Under the Curve (AUC) of 0.801 and 0.782, respectively. The FIB-4 showed the best AUC= 0.886 for cirrhosis. None of the following tests US, CT, HSI, and xenon-133 scan were considered correlated significantly. The best combination algorithm for the detection of cirrhosis was gender and FIB-4 with an AUC of 0.8937. Conclusion: this study demonstrates that non-invasive methods for liver fibrosis are accurate to diagnose >F2 and F4. Severe steatosis cannot be reliably diagnosed by non-invasive methods. Notably, a combination of FIB-4 and gender significantly improves the performance of the single method for cirrhosis. These methods may help reducing the number of liver biopsies stratifying NASH patients that should start a screening program for HCC and esophageal varices.
Contexte : La stéatose hépatique non alcoolique (SHNA) est l'une des causes les plus répandues des maladies du foie à l'échelle mondiale. Il s'agit d'un spectre de maladies qui se caractérise par une stéatose hépatique macrovésiculaire allant de la stéatose hépatique simple (stéatose) à la stéatohépatite non alcoolique (NASH). La NASH peut éventuellement évoluer vers une cirrhose et des complications en phase terminale. La biopsie du foie a longtemps été considérée comme la norme de référence par excellence pour le diagnostic de la SHNA, mais elle est coûteuse et invasive. Des méthodes non invasives ont récemment été proposées. Objectifs et méthodes : La présente étude avait pour objectif d'évaluer la précision de certaines méthodes non invasives (notamment les ultrasons [US], la tomographie par ordinateur [TO], la scintigraphie au xénon 133, l'indice de stéatose hépatique (ISH), la technique Fibroscan, le score de fibrose de SHNA, l'indice de ratio entre l'aspartate aminotransférase et les plaquettes [APRI] et l'indice FIB-4) et de l'utilisation combinée de ces méthodes pour le diagnostic de la stéatose et pour le diagnostic d'une fibrose hépatique significative (> F2) et de la cirrhose (F4), par comparaison à la biopsie du foie. Nous avons réalisé une étude rétrospective sur 114 patients atteints de NASH (79 patients de sexe masculin, âge moyen de 49,6 ans ± 10,6). Tous ces patients présentaient une histologie hépatique adéquate.Résultats : La répartition des stades de fibrose était la suivante : F0 F1 = 50 %, F2 = 16,8%, F3 = 19,2 %, F4 = 14 %. La répartition des stades de stéatose était la suivante : stade 0-1 = 16 %, stade 2 = 53,3 %, stade 3 = 30,7 %. Les tests suivants ont été mis en corrélation avec la fibrose : l'indice APRI (r = 0,554), l'indice FIB-4 (r = 0,555), le score de fibrose de SHNA (r = 0,473), la technique Fibroscan (r = 0,586) et l'indice de stéatose hépatique (r = 0,245). L'indice FIB-4 et l'indice APRI ont offert la meilleure précision diagnostique en ce qui concerne la fibrose significative, comme l'indiquent la surface sous la courbe (SSC) de 0,801 et la SSC de 0,782 respectivement. L'indice FIB-4 a présenté la meilleure SSC, soit 0,886, pour ce qui est de la cirrhose. Aucun des tests suivants, c'est à dire les tests aux US, la TO, l'ISH, et la scintigraphie au xénon 133, n'était considéré comme étant corrélé significativement. Le meilleur algorithme de combinaison pour le dépistage de la cirrhose était le sexe et l'indice FIB-4 avec une surface sous la courbe de 0,8937. Conclusion: cette étude démontre que les méthodes non invasives de diagnostic de la fibrose hépatique sont précises en ce qui concerne les stades > F2 et F4. La Stéatose sévère ne peut être diagnostiqué de façon fiable par des méthodes non invasives Notamment, une combinaison de l'indice FIB-4 et du sexe améliore considérablement le rendement de la méthode unique en ce qui a trait à la cirrhose. Ces méthodes pourraient aider à réduire le nombre de biopsies du foie visant à stratifier les patients atteints de NASH qui devraient entreprendre un programme de dépistage du carcinome hépatocellulaire (CHC) et des varices œsophagiennes.
6

Hallsworth, Kate. "Physical activity, exercise and non-alcoholic fatty liver disease." Thesis, University of Newcastle upon Tyne, 2012. http://hdl.handle.net/10443/1510.

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Non-alcoholic fatty liver disease (NAFLD) represents a spectrum of liver conditions ranging from hepatic steatosis through steatohepatitis to cirrhosis. Its prevalence has been estimated at between one-in-five and one-in-three of the adult population depending on country and diagnostic criteria used. Prevalence increases with degree of obesity, and is very common in those with Type 2 diabetes (T2DM). Rising prevalence of obesity and T2DM, particularly in younger people, will ensure that NAFLD remains a growing clinical concern for the future. Lifestyle modification, which encompasses diet, weight loss, physical activity, and/or exercise related behaviours, is the primary recommended therapy for NAFLD, especially in the absence of approved pharmaceutical agents. Despite lifestyle modifications being central to the management of NAFLD, the evidence base upon which these guidelines are based is lacking, and this is particularly true for physical activity and exercise. The focus of this thesis is on defining, exploring and developing the evidence for physical activity and exercise in NAFLD with a view to improving clinical care. The work contained within this thesis demonstrates that low levels of physical activity are prominent in people with NAFLD and that targeting this with resistance exercise therapy confers benefits to both liver lipid and the factors promoting its accumulation. It also highlights alterations in cardiac structure and function in people with NAFLD in the absence of overt cardiac disease, which may provide a therapeutic avenue in which to decrease cardiac disease risk in people with fatty liver. Over the duration of the work described in this thesis, the number of studies reporting on exercise and liver fat in people with NAFLD has increased markedly. The new information contained within this thesis contributes to this body of knowledge and, over time, will improve the management of a condition that is an increasing burden to the people of the Western world.
7

Scorletti, Eleonora. "Effect of omega-3 fatty acids in non-alcoholic fatty liver disease." Thesis, University of Southampton, 2017. https://eprints.soton.ac.uk/422265/.

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The first chapter (Introduction) of the thesis summarises the pathogenesis of NAFLD and its associated risk factors such as type 2 diabetes and cardiovascular disease. Moreover, it describes: a) the potential beneficial effects of long chain omega-3 fatty acid treatment [docosahexaenoic acid (DHA) plus eicosapentaenoic acid (EPA)] in NAFLD; b) the effect of genotypes patatin-like phospholipase domain-containing protein-3 (PNPLA3 I148M) and the transmembrane 6 superfamily member 2 protein (TM6SF2 E167K), on the level of DHA and EPA enrichment and end of study liver fat percentage after DHA+EPA treatment; and c) the effect of fatty acid desaturase (FADS) and Elongase (ELOVL) polymorphisms influencing omega-3 fatty acid metabolism. The second chapter describes the overall aim of this thesis. The aim of my research was to investigate in patients with NAFLD: a) the effect of long-chain omega-3 fatty acid treatment on liver fat percentage and liver fibrosis biomarkers; b) the effect of genotypes influencing NAFLD severity on treatment with DHA+EPA; and c) the effect of genotypes influencing omega-3 fatty acid metabolism in NAFLD. The third chapter describes in details the design and methods used in my research. Chapter four highlights my novel results from the WELCOME study. This chapter describes the baseline and end of study characteristics of the WELCOME study participants and shows the results of the DHA+EPA treatment on liver fat percentage and liver fibrosis biomarkers. This chapter also describes the association between DHA erythrocyte enrichment and decrease in liver fat percentage after DHA+EPA treatment. Chapter five illustrates the association between PNPLA3 I148M and DHA erythrocyte enrichment percentage and end of study liver fat percentage after DHA+EPA treatment. The chapter shows that PNPLA3 I148M was associated with higher end of study liver fat percentage and lower DHA tissue enrichment. Chapter six shows the negative association between FADS polymorphisms and omega-3 fatty acid metabolism in NAFLD. The chapter also shows that there was a gene-DHA+EPA interaction between the minor allele of the FADS1 rs174556 and Δ-5 desaturase activity after treatment with DHA+EPA. Finally, chapter seven, summarises my results in the context of current evidence and knowledge about the subject matter.
8

Spanos, Christos. "Quantitative liver proteomics for biomarker discovery in non-alcoholic fatty liver disease." Thesis, University of Surrey, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.616323.

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Non-alcoholic fatty liver disease (NAFLD) is now the most common liver disease worldwide. Given that NAFLD can progress from steatosis to non-alcoholic steatohepatitis (NASH), fibrosis and potentially hepatocellular carcinoma, early diagnosis and accurate disease staging are primary clinical concerns. Hypothesizing that a subset of liver proteins will exhibit differential expression in NAFLD and that these proteins may represent candidate disease biomarkers; the aims of this project were to use proteomics to identify differentially expressed proteins both in an in vitro and an in vivo model of NASH. Preliminary studies developed and characterised both models used here; experiments utilized a relative quantitative proteomic approach with isobaric tags for relative and absolute quantitation labelling combined with nano-liquid chromatography and tandem mass spectrometry.
9

Cheng, Lik-fai, and 鄭力暉. "Non-alcoholic fatty liver disease in Asia: a systematic review." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45171117.

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10

MARIN, VERONICA. "Non-Alcoholic and Alcoholic Fatty Liver disease: two sides of the same coin." Doctoral thesis, Università degli Studi di Trieste, 2017. http://hdl.handle.net/11368/2908152.

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Background and aims: The booming prevalence of obesity and diabetes in young age and the increased consumption of alcohol in adolescents lead to the development of Non-Alcoholic Fatty Liver Disease (NAFLD) and Alcoholic Liver Disease (ALD). Task 1 of this work is focused on the development of an in vivo model of pediatric NAFLD and in the study of the therapeutic properties of Silymarin. The task 2 investigated the source of MIF, a cytokine involved in the pathogenesis of ALD. Materials and Methods: NAFLD in vivo study: C57BL/6 male and female mice were exposed to HFHCD or chow diet (CTRL diet) for 16 weeks. Biochemical and biomolecular analysis were performed to follow the progression of the damage. In the second phase Silymarin properties were evaluated (33mg/animal/day). ALD in vitro study: MIF expression was measured in HuH7 and macrophages cells in response to 50mM ethanol. The ethanol-induced liver injury was assessed in C57BL/6 (WT) and Mif-/- bone marrow chimeras. MIF was measured in serum, as well as visualized by immunohistochemistry in liver biopsies, from patients with alcoholic hepatitis (AH). Results: NAFLD in vivo study: HFHCD induced immediately a significant body weight gain in both genders. Males presented an early epididymal fat-pads hyperplasia and after week 12, a significant hepatomegaly, with alteration of glycemia, insulinemia, lipid profile, and ALT. Comparable body/blood changes were observed in females after week 16. Liver histology showed in both genders a mixed macro-microvesicular steatosis. Inflammatory foci were observed only in males, confirmed also by an increase in MCP-1 and TNF-α mRNA. Conversely, females had no signs of inflammation but rather presented enhanced lipid peroxidation (MDA) and a reduced GSH/GSSG ratio, signs of oxidative stress. By week 8 both genders developed progressive fibrosis. HFHCD+Silymarin decreased liver and visceral fat weight and improved ALT and lipid profile. HFHCD→CTRL diet reverted all altered parameters under study. Histologically, Silymarin slightly reduced inflammatory foci and fibrosis. ALD in vitro study: HuH7, but not THP-1 macrophages, released MIF in response to ethanol challenge in cell culture. In chimeric mice expressing MIF in non-myeloid cells (Mif-/- →WT), chronic ethanol feeding increased ALT/AST, hepatic steatosis, and cytokine/chemokine mRNA expression. In contrast, chimeric mice not expressing MIF in non-myeloid cells (WT→ Mif-/-) were protected from ethanol-induced liver injury. Immunohistochemical staining of liver biopsies from patients with AH revealed a predominant localization of MIF to hepatocytes. Interestingly, the concentration of MIF in suprahepatic serum, but not peripheral serum, was positively correlated with clinical indicators of disease severity and with an increased risk of mortality in patients with AH. Conclusions: Data collected suggested that our juvenile NAFLD model had a faster and more aggressive liver injury progression compared with published adult models, with different molecular mechanisms between males and females. Silymarin exerted some beneficial effects without requiring lifestyle improvements, relevant aspect considering the general low compliance of obese subjects in modifying their nutritional behavior. ALD project provided evidence that hepatocyte-derived MIF was critical to the pathogenesis of ALD in mice and likely contributes to liver injury in patients with AH. Altogether these new findings can lead to new therapeutic perspective.

Книги з теми "Non-Alcoholic fatty liver diseases":

1

Bugianesi, Elisabetta, ed. Non-Alcoholic Fatty Liver Disease. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6.

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2

Farrell, Geoffrey C., Arthur J. McCullough, and Christopher P. Day, eds. Non-Alcoholic Fatty Liver Disease. Oxford, UK: Wiley-Blackwell, 2013. http://dx.doi.org/10.1002/9781118556153.

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3

Chalasani, Naga, and Gyongyi Szabo, eds. Alcoholic and Non-Alcoholic Fatty Liver Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20538-0.

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4

Taylor-Robinson, Simon D., and Roger Williams. Clinical dilemmas in non-alcoholic fatty liver disease. Chichester, West Sussex: John Wiley & Sons Inc., 2016.

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5

Farrell, Geoffrey C., Arthur J. McCullough, and Christopher Paul Day. Non-alcoholic fatty liver disease: A practical guide. Chichester, West Sussex: John Wiley & Sons, 2013.

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6

Williams, Roger, and Simon D. Taylor-Robinson, eds. Clinical Dilemmas in Non-Alcoholic Fatty Liver Disease. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118924938.

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Buko, V. U. Prostaglandiny pri alkogolʹnom porazhenii pecheni. Minsk: "Navuka i tėkhnika", 1991.

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8

Fitzpatrick, Emer. Non-alcoholic fatty liver disease. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0061.

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Анотація:
The chapter on non-alcoholic fatty liver disease includes the risk factors for this ever-increasing condition, the pathophysiology, as well as the differential of hepatic steatosis. Finally it includes the most current principles of its management.
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Khanna, Sudeep. Non-Alcoholic Fatty Liver Disease. Elsevier - Health Sciences Division, 2010.

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10

Chalasani, Naga, and Gyongyi Szabo. Alcoholic and Non-Alcoholic Fatty Liver Disease: Bench to Bedside. Springer, 2015.

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Частини книг з теми "Non-Alcoholic fatty liver diseases":

1

Hardy, Timothy, and Christopher P. Day. "Non-Alcoholic Fatty Liver Disease." In Sherlock's Diseases of the Liver and Biliary System, 540–60. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119237662.ch28.

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2

Targher, Giovanni, and Alessandro Mantovani. "NAFLD, Diabetes, and Other Endocrine Diseases: Clinical Implications." In Non-Alcoholic Fatty Liver Disease, 147–68. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6_8.

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3

Arteel, Gavin E., and David W. Crabb. "Pathogenesis of Alcoholic Liver Disease." In Alcoholic and Non-Alcoholic Fatty Liver Disease, 41–69. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20538-0_3.

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4

Awai, Hannah I., Kimberly P. Newton, and Jeffrey B. Schwimmer. "Nonalcoholic Fatty Liver Disease in Children." In Alcoholic and Non-Alcoholic Fatty Liver Disease, 339–62. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20538-0_17.

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Engin, Atilla. "Non-Alcoholic Fatty Liver Disease." In Obesity and Lipotoxicity, 443–67. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48382-5_19.

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Marjot, Thomas, and Jeremy Cobbold. "Non-alcoholic Fatty Liver Disease." In In Clinical Practice, 111–29. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43126-0_7.

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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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Chang, Charissa Y. "Non-Alcoholic Fatty Liver Disease." In Mount Sinai Expert Guides: Hepatology, 132–41. Oxford, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118748626.ch11.

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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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Koeckerling, David, Thomas Marjot, and Jeremy Cobbold. "Non-alcoholic Fatty Liver Disease." In In Clinical Practice, 127–49. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-10012-3_7.

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Тези доповідей конференцій з теми "Non-Alcoholic fatty liver diseases":

1

Male, E., H. Liaquat, N. Agrawal, A. J. Mamary, K. Carney, T. Bronzell-Wynder, G. J. Criner, and P. Mulhall. "Non-Alcoholic Fatty Liver Disease in Lung Transplant." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4744.

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2

Pivtorak, Kateryna, Olga Yakovleva, and Irina Fedzhaga. "ENDOTHELIAL DYSFUNCTION IN NON-ALCOHOLIC FATTY LIVER DISEASE." In EDUCATION AND SCIENCE OF TODAY: INTERSECTORAL ISSUES AND DEVELOPMENT OF SCIENCES. European Scientific Platform, 2021. http://dx.doi.org/10.36074/logos-29.10.2021.v2.22.

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Zou, Huixi, and Xiaoyu Yan. "Non-alcoholic Fatty Liver Disease (NAFLD) causes Erythropoietin Hyporesponsiveness." In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.188420.

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Jagtap, N., R. Kalapala, A. Katakwar, H. Kanakagiri, S. Darisetty, and DN Reddy. "Endoscopic Sleeve Gastroplasty for non-alcoholic Fatty Liver Disease." In ESGE Days 2021. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1724306.

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Shi, Ivy, and Takuya Sakaguchi. "Abstract 2111A: Molecular genetics of non-alcoholic fatty liver disease." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2111a.

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Malnick, Stephen. "5 Non-alcoholic fatty liver disease (NAFLD) -underdiagnosed but overtreated." In Preventing Overdiagnosis Abstracts, December 2019, Sydney, Australia. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/bmjebm-2019-pod.111.

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Tang, Xueyang, Chen Zhao, Kunlun Li, Baojun Li, Le Su, and Lin Zhao. "Protective Effect of Polyphenols on Non-alcoholic Fatty Liver Disease." In Conference on Artificial Intelligence and Healthcare. SCITEPRESS - Science and Technology Publications, 2021. http://dx.doi.org/10.5220/0011196700003444.

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Singh, I., V. Leone, X. Li, D. Pfister, M. Stadler, E. Kotsiliti, S. Rössler, et al. "Dysregulated epigenetic factors in non-alcoholic fatty liver disease and triggered liver cancer." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677184.

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Choi, Changhoon, Wonseok Choi, Jeesu Kim, and Chulhong Kim. "Photothermal strain imaging for diagnosis of non-alcoholic fatty liver disease." In Photons Plus Ultrasound: Imaging and Sensing 2020, edited by Alexander A. Oraevsky and Lihong V. Wang. SPIE, 2020. http://dx.doi.org/10.1117/12.2544552.

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Tirikova, O. V., N. M. Kozlova, A. YU Tarasov, S. M. Eliseev, and S. V. Lunenok. "Epidemiology of non-alcoholic fatty liver disease in the Baikal region." In Scientific achievements of the third millennium. SPC "LJournal", 2021. http://dx.doi.org/10.18411/scienceconf-03-2021-11.

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Звіти організацій з теми "Non-Alcoholic fatty liver diseases":

1

Du, Yuhan, Jiajun Li, Xinchao Huang, and shujing Wu. Association Between Serum Adiponectin And Non-alcoholic Fatty Liver Disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0080.

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2

Jin, Dachuan, Gao Peng, Shunqin Jin, Tao Zhou, Baoqiang Guo, and Guangming Li. Comparison of therapeutic effects of anti-diabetic drugs on non-alcoholic fatty liver disease patients without diabetes: A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0014.

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Анотація:
Review question / Objective: To evaluate the efficacy of different anti-diabetic drugs in the treatment of non-diabetic non-alcoholic disease by network meta-analysis, and find the best intervention. Condition being studied: Non-alcoholic fatty liver disease (NAFLD) refers to the disease in which the liver fat content exceeds 5%, and excludes the secondary causes of alcohol, infection, drugs or other specific metabolic diseases. As a spectrum of disorders, it includes hepatocyte steatosis and steatohepatitis at the initial stage, liver fibrosis at the later stage, cirrhosis at the final stage, and even liver cancer. Nowadays Non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the world with an incidence rate as high as 25% which has been rising steadily worldwide in the past 30 years. Currently there are still no approved specific therapeutic agents and global treatment guidelines for NAFLD. For non-diabetic NAFLD, there is far from a consensus, too.
3

Ismaiel, Abdulrahman, Oana Ciobanu, Mohamed Ismaiel, Daniel-Corneliu Leucuta, Stefan-Lucian Popa, Liliana David, Dilara Ensar, Nahlah Al Srouji, and Dan L. Dumitrascu. Atherogenic Index of Plasma in Non-Alcoholic Fatty Liver Disease: Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0043.

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Review question / Objective: P - Non-alcoholic fatty liver disease (NAFLD) I - Atherogenic index of plasma (AIP) C - Imaging and histopathology O - Mean difference and Area Under the Curve S - Observational studies. Condition being studied: Non-alcoholic fatty liver disease (NAFLD), is a common liver disease characterized by the presence of excessive fat build up within hepatocytes, in the absence of other conditions that result in hepatic steatosis and with little to no alcohol consumption. It refers to a broad range of conditions including steatosis, non-alcoholic steatohepatitis (NASH) and cirrhosis.
4

Ismaiel, Abdulrahman, Ayman Jaaouani, Daniel-Corneliu Leucuta, Stefan-Lucian Popa, and Dan-Lucian Dumitrascu. The Visceral Adiposity Index in Non-Alcoholic Fatty Liver Disease and Liver Fibrosis — Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0056.

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Review question / Objective: The objective of the study was to compare the mean difference and AUROC of Visceral Adiposity Index (VAI) in NAFLD/NASH/liver fibrosis patients and controls in observational studies. Condition being studied: Nonalcoholic fatty liver disease (NAFLD) is a multi-system disease, being mainly a liver pathology involving excessive hepatic fat accumulation unrelated to alcohol consumption or other secondary causes of hepatic steatosis. It is an emerging cause of concern and increasing clinical burden, imposing a public health challenge. NAFLD is the most common chronic liver disease and is predicted to be the most common indication for a liver transplant in Western countries by 2030, owing to a prevalence of 25% worldwide. The visceral adiposity index (VAI) is a scoring system based on body mass index, triglycerides, high-density lipoproteins (HDLs), and waist circumferences (WCs).
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LIAO, JiaQian, GuoRong WANG, Tian ZHANG, XiaoYuan DENG, Yao LIU, and NaiFang XING. Prevalence of Non-Alcoholic Fatty Liver Disease in Chinese Adults:a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0111.

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Zhang, Tiefeng, Duan Han, Tianqi Zhang, Cai Jing, and Jianguang Sun. Complementary and alternative therapies for non-alcoholic fatty liver disease: A Bayesian network meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2020. http://dx.doi.org/10.37766/inplasy2020.12.0136.

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Chen, Hui, Xinyu Liu, Zhenzhen Meng, Xiaoqiang Huang, Shanghua Piao, and Jiao Guo. Effectiveness of Chaihu-Shugan-San in treatment of Non-alcoholic Fatty Liver Disease: A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0074.

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Moskalenko, O. L., O. V. Smirnova, E. V. Kasparov, and I. E. Kasparova. STRUCTURE OF PSYCHOLOGICAL DISORDERS IN PATIENTS WITH METABOLIC SYNDROME AND NON-ALCOHOLIC FAT LIVER DISEASE. Science and Innovation Center Publishing House, 2021. http://dx.doi.org/10.12731/2658-4034-2021-12-4-2-340-348.

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The article is devoted to the study of the psychological characteristics of the behavior of patients with non-alcoholic fatty liver disease (NAFLD). The manifestations of NAFLD are a powerful frustrating factor for patients, negatively affect the quality of life, hinder psychosocial adaptation and serve as the basis for the formation of chronic stress from the disease, which blocks the actual needs of the individual. Psychological factors are an important component in the clinical assessment of patients in connection with the individualization of the treatment process and secondary psychoprophylaxis, including methods of somato-centered and personality-centered psychotherapy.
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Zhang, Jing, Yiting Wang, and Xinyi Xia. Incidence of Breast cancer among Non-alcoholic fatty liver disease patients: a systematic review and meta-analysis protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2020. http://dx.doi.org/10.37766/inplasy2020.10.0046.

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Zhang, Qiuyi, Lihong Fu, Fengjie Qiao, and Zhenhua Zhou. Meta-analysis of the clinical efficacy of Lingguizhugan decoction in the treatment of non-alcoholic fatty liver disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0039.

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