Relevant bibliographies by topics / Non-Alcoholic Fatty Liver Disease NASH

Academic literature on the topic 'Non-Alcoholic Fatty Liver Disease NASH'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Non-Alcoholic Fatty Liver Disease NASH.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Non-Alcoholic Fatty Liver Disease NASH"

1

Byrne, Christopher D. "Hypoxia and non-alcoholic fatty liver disease." Clinical Science 118, no. 6 (December 14, 2009): 397–400. http://dx.doi.org/10.1042/cs20090565.

Full text
Abstract:
NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic steatohepatitis)], fatty liver disease with inflammation and fibrosis (severe NASH) and cirrhosis. The molecular mechanisms contributing to NASH are the subject of considerable investigation, as a better understanding of the pathogenesis of NASH will lead to novel therapies for a condition that hitherto remains difficult to treat. In the present issue of Clinical Science, Piguet and co-workers have investigated the effects of hypoxia in the PTEN (phosphatase and tensin homologue deleted on chromosome 10)-deficient mouse, a mouse model that develops NAFLD. The authors show that a short period (7 days) of exposure to hypoxia aggravates the NAFLD phenotype, causing changes in the liver that are in keeping with NASH with increased lipogenesis and inflammation.
APA, Harvard, Vancouver, ISO, and other styles
2

Scarlat, Gabriel, Bassil Dona, Mihai Cârstea, and Marilena Stoian. "Insights into Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis." Internal Medicine 19, no. 1 (January 1, 2022): 61–77. http://dx.doi.org/10.2478/inmed-2022-0198.

Full text
Abstract:
Abstract Non-alcoholic fatty liver disease (NAFLD) constitutes a common pathological condition of the liver, the prevalence of which is currently increasing in western countries. NAFLD is frequently diagnosed in males and its incidence is higher in individuals with type 2 diabetes mellitus and obesity. Hence, the disease is considered to be the hepatic manifestation of the metabolic syndrome. A multitude of interconnected risk factors have been described over the years – genetic, hormonal and nutritional, which play important roles in the development of NAFLD. Insulin resistance is considered to be the central pathophysiological condition that promotes the disease in diabetic patients, whereas dyslipidemia and cardiovascular comorbidities (arterial hypertension, ischaemic heart disease) are frequently associated conditions. Although there are currently numerous pathophysiological mechanisms involved in NAFLD that are still unknown or poorly understood, there has been some advancements concerning the pathogenesis of the disease and its progression towards its severe form, known as non-alcoholic steatohepatitis (NASH). In the absence of a clear diagnosis and carefully controlled treatment, NAFLD/NASH may evolve towards liver cirrhosis, liver failure or hepatocellular carcinoma. However, the disease may also generate systemic effects, including the development of chronic kidney disease (CKD). The diagnosis of NAFLD/NASH is based both on its clinical manifestations, revealed by a carefully conducted patient history and physical examination of the patient, and on other investigations; histopathological findings upon liver biopsy, liver ultrasonography and the use of transient elastography (or FibroScan) are some of the most important investigations in NAFLD/NASH. The understanding of the most important risk factors and pathogenic mechanisms of the disease is fundamental for the elaboration of the most efficient treatment, to prevent chronic liver disease or the development of hepatocellular carcinoma.
APA, Harvard, Vancouver, ISO, and other styles
3

Ramai, Daryl, Antonio Facciorusso, Erika Vigandt, Bryan Schaf, Waleed Saadedeen, Aditya Chauhan, Sara di Nunzio, Aashni Shah, Luca Giacomelli, and Rodolfo Sacco. "Progressive Liver Fibrosis in Non-Alcoholic Fatty Liver Disease." Cells 10, no. 12 (December 2, 2021): 3401. http://dx.doi.org/10.3390/cells10123401.

Full text
Abstract:
Non-alcoholic steatohepatitis (NASH) is a chronic and progressive form of non-alcoholic fatty liver disease. Its global incidence is increasing and makes NASH an epidemic and a public health threat. Non-alcoholic fatty liver disease is associated with major morbidity and mortality, with a heavy burden on quality of life and liver transplant requirements. Due to repeated insults to the liver, patients are at risk for developing hepatocellular carcinoma. The progression of NASH was initially defined according to a two-hit model involving an initial development of steatosis, followed by a process of lipid peroxidation and inflammation. In contrast, current evidence proposes a “multi-hit” or “multi-parallel hit” model that includes multiple pathways promoting progressive fibrosis and oncogenesis. This model includes multiple cellular, genetic, immunological, metabolic, and endocrine pathways leading to hepatocellular carcinoma development, underscoring the complexity of this disease.
APA, Harvard, Vancouver, ISO, and other styles
4

Sadikova, D. Sh, F. A. Khaydarova, and D. M. Esimova. "CONSTRUCTION OF COMPUTER MODEL FOR DIAGNOSTICS AND MONITORING OF NON-ALCOHOLIC FATTY LIVER DISEASE." UZBEK MEDICAL JOURNAL 2, no. 2 (February 28, 2021): 9–14. http://dx.doi.org/10.26739/2181-0664-2021-2-2.

Full text
Abstract:
Timely diagnosis and treatment of non-alcoholic fatty liver disease (NAFLD) are essential to prevent the development of steatohepatitis and liver cirrhosis. This is especially true for patients with type 2 diabetes. The aim of our workwas to build a computer model for the diagnosis and monitoring of NAFLD treatment. Materials and methods. The study included more than 55 clinical and laboratory parameters of 233 patients with non-alcoholic steatosis (NAS) and 60 patients with steatohepatitis (NASH). Results. The calculations were based on the levels of systolic blood pressure, erythrocytes, ALT, AST, glutamate dehydrogenase and platelets in persons with type 2 diabetes mellitus with NAS and NASH. The model allows to differentiate NAS andNASH with a sensitivity of 82% and a specificity of 88%
APA, Harvard, Vancouver, ISO, and other styles
5

South, Kathy. "Non-Alcoholic Steatohepatitis (NASH)/Non-Alcoholic Fatty Liver Disease (NAFLD)." Gastroenterology Nursing 29, no. 2 (March 2006): 169. http://dx.doi.org/10.1097/00001610-200603000-00082.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Byrne, Christopher D., Rasaq Olufadi, Kimberley D. Bruce, Felino R. Cagampang, and Mohamed H. Ahmed. "Metabolic disturbances in non-alcoholic fatty liver disease." Clinical Science 116, no. 7 (March 2, 2009): 539–64. http://dx.doi.org/10.1042/cs20080253.

Full text
Abstract:
NAFLD (non-alcoholic fatty liver disease) refers to a wide spectrum of liver damage, ranging from simple steatosis to NASH (non-alcoholic steatohepatitis), advanced fibrosis and cirrhosis. NAFLD is strongly associated with insulin resistance and is defined by accumulation of liver fat >5% per liver weight in the presence of <10 g of daily alcohol consumption. The exact prevalence of NAFLD is uncertain because of the absence of simple non-invasive diagnostic tests to facilitate an estimate of prevalence. In certain subgroups of patients, such as those with Type 2 diabetes, the prevalence of NAFLD, defined by ultrasound, may be as high as 70%. NASH is an important subgroup within the spectrum of NAFLD that progresses over time with worsening fibrosis and cirrhosis, and is associated with increased risk for cardiovascular disease. It is, therefore, important to understand the pathogenesis of NASH and, in particular, to develop strategies for interventions to treat this condition. Currently, the ‘gold standard’ for the diagnosis of NASH is liver biopsy, and the need to undertake a biopsy has impeded research in subjects in this field. Limited results suggest that the prevalence of NASH could be as high as 11% in the general population, suggesting there is a worsening future public health problem in this field of medicine. With a burgeoning epidemic of diabetes in an aging population, it is likely that the prevalence of NASH will continue to increase over time as both factors are important risk factors for liver fibrosis. The purpose of this review is to: (i) briefly discuss the epidemiology of NAFLD to describe the magnitude of the future potential public health problem; and (ii) to discuss extra- and intra-hepatic mechanisms contributing to the pathogenesis of NAFLD, a better understanding of which may help in the development of novel treatments for this condition.
APA, Harvard, Vancouver, ISO, and other styles
7

Toman, Daniel, Petr Vavra, Petr Jelinek, Petr Ostruszka, Peter Ihnat, Ales Foltys, and Jan Roman. "A review on fatty liver disease or non-alcoholic fatty liver disease and hepatocellular carcinoma." Research Journal of Biotechnology 16, no. 10 (September 25, 2021): 156–62. http://dx.doi.org/10.25303/1610rjbt156162.

Full text
Abstract:
The non-alcoholic fatty liver disease (NAFLD) is the predominant etiological factor for liver disease. There is a risk of the development of hepatocellular carcinoma (HCC) in patients suffering from NAFLD. Non-alcoholic steatohepatitis (NASH) is one of the risk factors for the development of HCC. The aim is to discuss an association of NAFLD and HCC in the adult population. HCC is one of the debilitating complications of NAFLD/NASH and obesity is a causative factor for NAFLD/NASH. Various clinical data suggest that obesity appears to be a causative factor in the progression of NAFLD/NASH to HCC. We searched data from the PubMed/Medline and Google Scholar databases including various studies and review articles. Significantly, an increased number of HCC patients with cryptogenic liver disease had well-differentiated tumors than in HCC patients with chronic viral hepatitis and alcoholism. HCC is one of the debilitating complications of NAFLD/NASH and obesity is a causative factor for NAFLD/NASH. Various preclinical and clinical data suggest that obesity appears to be an important causative factor in the progression of NAFLD/NASH to HCC.
APA, Harvard, Vancouver, ISO, and other styles
8

Doumas, Michael, Konstantinos Imprialos, Konstantinos Stavropoulos, and Vasilios G. Athyros. "What Does the Future Hold for Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis?" Current Vascular Pharmacology 17, no. 5 (August 1, 2019): 425–28. http://dx.doi.org/10.2174/157016111705190703102816.

Full text
Abstract:
: Non-Alcoholic Fatty Liver Disease (NAFLD), the most common liver disease, is characterized by accumulation of fat (>5% of the liver tissue), in the absence of alcohol abuse or other chronic liver diseases. Its prevalence is increasing because of obesity, metabolic syndrome or Type 2 Diabetes Mellitus (T2DM). NAFLD can cause liver inflammation and progress to Non-Alcoholic Steatohepatitis (NASH), fibrosis, cirrhosis or Hepatocellular Cancer (HCC). Nevertheless, Cardiovascular Disease (CVD) is the most common cause of morbidity and mortality in NAFLD/NASH patients. Current guidelines suggest the use of pioglitazone both in patients with T2DM and in those without. : The newer antidiabetic drugs such as Glucagon Like Peptide-1 Receptor Agonists (GLP-1 RA), Sodium-Glucose co- Transporter-2 inhibitors (SGLT2i), and statins plus ezetimibe, are considered safe by the guidelines, and may have a beneficial effect on NAFLD/NASH as well as Cardiovascular Disease (CVD) morbidity and mortality. : Future drugs seem to have a potential for holding down the evolution of NAFLD and reduce liver- and CVD-related morbidity and mortality, but they will take some years to be approved for routine use. : Until then pioglitazone, GLP-1 RA, SGLT2i, and statins plus ezetimibe, especially in combination might be useful for treating the huge number of patients with NAFLD/NASH.
APA, Harvard, Vancouver, ISO, and other styles
9

Bentsa, T. M. "The therapeutic aspects of non-alcoholic fatty liver disease." Medicine of Ukraine, no. 8(264) (November 22, 2022): 18–21. http://dx.doi.org/10.37987/1997-9894.2022.8(264).271835.

Full text
Abstract:
Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the developed world. NAFLD is encompasses a spectrum of liver manifestations ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), fibrosis and cirrhosis, which may ultimately progress to hepatocellular carcinoma. NASH is an aggressive form of NAFLD, associated with an increased risk of liver and non-liver-related mortality. Liver-biopsy remains the gold standard for diagnosis, but the majority of patients liver damage can be diagnosed accurately by noninvasive methods. Early identification and management of patients with intensive dietary and lifestyle modification are essential to prevent the development of advanced liver disease and its complications. Pharmacological therapy should be administered to patients with NASH purposed on the fibrosis inhibition, especially in case of the established predictors of high risk of disease progression (age ˃ 50 years, metabolic syndrome, type 2 diabetes mellitus, or ALT increase), as well as to the patients with active NASH with high inflammatory activity
APA, Harvard, Vancouver, ISO, and other styles
10

Garbuzenko, D. V. "Drug Therapy for Non-Alcoholic Steatohepatitis-Induced Liver Fibrosis." Russian Journal of Gastroenterology, Hepatology, Coloproctology 31, no. 5 (January 2, 2022): 16–24. http://dx.doi.org/10.22416/1382-4376-2021-31-5-16-24.

Full text
Abstract:
Aim. An overview of current pharmacotherapy for non-alcoholic steatohepatitis (NASH)-associated liver fibrosis.Key points. In current clinical recommendations, therapeutic measures in non-alcoholic fatty liver disease should include lifestyle change, body weight normalisation, NASH-associated liver fibrosis-specific drug therapy and treatment for metabolic syndrome-related diseases. Given a lack of approved antifibrotic therapies in NASH, several drugs have nevertheless demonstrated an adequate efficacy and safety in phase 3 clinical trials, also in compensated cirrhosis, which allows their practical validation in phase 4.Conclusion. The understanding of liver fibrosis as an adverse natural consequence of non-alcoholic fatty liver disease clearly attests for an early introduction and wide use of antifibrotic therapy to improve NASH outcomes and avoid associated complications.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Non-Alcoholic Fatty Liver Disease NASH"

1

Lyall, Marcus James. "TET mediated 5’hydroxymethylation in the pathogenesis of non alcoholic fatty liver disease." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29524.

Full text
Abstract:
Non-alcoholic fatty liver disease (NAFLD) now affects around one in four adults in the human population and parallels the global increase in obesity. Within the spectrum of NAFLD, simple steatosis is associated with insulin resistance and type 2 diabetes while progression to steatohepatitis (NASH) is associated with an increased risk of liver cirrhosis and all-cause mortality. The molecular pathology of NAFLD is incompletely understood, however observational studies in human cohorts suggest the regulation of DNA methylation may play a role. 5-hydroxymethylcytosine (5hmC) is a cytosine modification generated from 5- methylcytosine (5mC) by the Ten eleven translocase isoenzymes (Tets) as part of a demethylation process. The aim of this project was to examine the role of Tet enzyme activity on the pathogenesis and progression of NAFLD. Detailed characterisation of two established murine dietary interventions allowed the selection of a NAFLD mouse model which broadly recapitulated the metabolic, histological and transcriptional features of human disease. Using DNA immunoprecipitation coupled with whole genome next generation sequencing and RNA micro expression arrays I examined the effect of high fat diet feeding (HFD) on hepatic DNA 5hmC levels within annotated gene regions. Whilst the global 5hmC profile was not altered by HFD, there was profound genic enrichment of 5hmC in upregulated mediators of cholesterol synthesis and transport (Lss, Sc4mol, Fdps, Hsd17b7, Cyp17a1, Mvd, Cyp1a2, Dhcr7 and Apoa4) with no enrichment in genes with other pathological functions (drug detoxification, inflammation, cell cycle regulation). Induced peaks of 5hmC enrichment were subsequently abolished following rescue of the NAFLD phenotype by conversion to control diet. Cross species validation was performed in vitro utilising embryonic stem cell derived hepatocytes challenged with a cocktail of high energy substrates. My in vivo findings were broadly replicated with specific 5hmC enrichment in genes synthesising lipotoxic molecules (PLIN2, CIDEC, APOA4, ACADVL, HMGCS2, APOA5, CYP2J2, IGFBP1, PPAP2C, ACSL1, APOC3, ANGPTL4, NRG1) with no enrichment in upregulated genes of alternative function. To determine whether or not the 5hmC enrichment seen is of functional relevance, I studied Tet1-/- C57BL/6J mice. Tet1-/- mice are grossly normal in appearance, however loss of Tet1 conferred a striking resistance to diet induced obesity with reduced body fat mass, improved insulin-sensitivity and near complete absence of NAFLD compared to wild type littermates. Furthermore, the HFD fed Tet1-/- liver transcriptome showed a ‘protective’ profile, with suppression of genes for lipid synthesis, inflammation and fibrosis. Thus, in multiple cross-species models of NAFLD, over nutrition induces genic hydroxymethylation specifically within activated genes driving the synthesis and transport of lipid molecules. Such changes are reversible with resolution of the NAFLD phenotype strengthening functional association. Tet1 deficiency conveys an obesity and NAFLD resistant phenotype. I therefore introduce Tet1 mediated hydroxymethylation as a novel mechanism for NAFLD pathogenesis.
APA, Harvard, Vancouver, ISO, and other styles
2

Freitas, Vinicius de Lima. "Efeitos do programa de condicionamento físico em portadores de NASH." Faculdade de Medicina de São José do Rio Preto, 2017. http://hdl.handle.net/tede/391.

Full text
Abstract:
Submitted by Fabíola Silva (fabiola.silva@famerp.br) on 2018-01-08T16:01:25Z No. of bitstreams: 1 viniciusdelimafreitas_tese.pdf: 8494219 bytes, checksum: 35b61ce25b380b2ebf2433cf44ff18e5 (MD5)
Made available in DSpace on 2018-01-08T16:01:25Z (GMT). No. of bitstreams: 1 viniciusdelimafreitas_tese.pdf: 8494219 bytes, checksum: 35b61ce25b380b2ebf2433cf44ff18e5 (MD5) Previous issue date: 2017-05-05
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Introduction: The prevalence of hepatic steatosis and non-alcoholic fatty liver disease (NAFLD) in the Brazilian population is not known, and there are few studies about this disease in the country. Lifestyle modification, including physical activity and exercise are first line recommendation for the tratment of patients with NAFLD. Aim: To evaluate the efficacy of the Supervised physical activity and exercise program on-site and distance-supervised with duration of 12-month for patients with non-alcoholic steatohepatitis (NASH). Methods: This is a prospective, longitudinal, open cohort study including consecutive patients who had a histological diagnosis of NASH in the last 12 months and who were followed up at the outpatient NAFLD clinic. Exclusion criteria were: patients with concomitant liver diseases who could lead to steatosis; history or active significant alcohol intake such as equal or greater than 210g / week for men and 140g / week for women; drugs known to be related to NAFLD; untreated hypo or hyperthyroidism; pevious bariatric surgery; obesity equal or greater than grade III; binge eating or other uncontrolled psychiatric disorder. The patients were studied withing a pre-stated protocol study including clinical and laboratory evaluation, as well as the Baecke questionnaire and the six minute walk test (6MWT), before and after participation in the physical conditioning program. Descriptive statistics, Student's tes and the Mann-Whitney test, were performed for parametric and non-parametric variables as apropriated. The significance level adopted was p-value >0.05. Results: From the 15 included patients, three of them did not complete the multidisciplinary program during the 12-month study period. Thus, the total sample analyzed was 11 patients, that is, 73.33% of included patients. The 5% goal for body weight loss was not reached, however low density lipoprotein (LDL) presented significant reduction at the end of the study (p = 0.0130). The distance-supervised program was chosen by all patients and walking was the main physical activity (66.67%), followed by soccer. The 6-min walk distance (6MWD) was sgnificantly higher at trhee and six month when compared with basal distance at the entry of the study. Conclusion: The distancesupervised physical activity and exercise program had high adherence and was effective in improving the functional capacity for patitients with NASH. On the other hand, there was partial improvement for biochemical and antropometric variables. Aditionally, this is a distance-supervised life-style modification program with low cost and high potential cost-benefit for patients with DHGNA and NASH attended on the National Health System.
Introdução: A prevalência da Esteatose Hepática (EH) e da Doença Hepática Gordurosa Não Alcoólica (DHGNA) na população brasileira não é conhecida, e são poucos os estudos sobre esta doença no país. A mudança no estilo de vida representa a principal recomendação para o tratamento da DHGNA, assim, a atividade física e o exercício físico são ferramentas eficientes no combate à dislipidemia e acúmulo de gordura no fígado. Objetivo: Avaliar os efeitos do programa de condicionamento físico supervisionado in loco e supervisionado à distância com duração de 12 meses em pacientes com Esteatohepatite não alcoólica (NASH). Casuística e Método: Trata-se de um estudo de coorte aberto prospectivo, longitudinal, no qual foram estudados, pacientes em acompanhamento nos ambulatórios de DHGNA do Hospital de Base de São José do Rio Preto, que tiveram o diagnóstico histológico de NASH nos últimos 12 meses. Os critérios de exclusão apresentados foram: pacientes com outras doenças hepáticas concomitantes que possam cursar com esteatose; história prévia de ingestão alcoólica igual ou superior a 210g/semana para homens e 140g/semana para mulheres; medicação conhecidamente relacionada com a etiologia de DHGNA; hipotireoidismo ou hipertireoidismo não tratado; pós-operatório de cirurgia bariátrica; obesidade maior ou igual ao grau III; compulsão alimentar ou outro distúrbio psiquiátrico não controlado. Os pacientes foram analisados em protocolo de avaliação clínica e laboratorial, como o questionário de Baecke e o Teste de Caminhada de 6 minutos (TC6), antes e após a participação no programa de condicionamento físico em estudo. A estatística descritiva foi composta pelas variáveis paramétricas e não paramétricas (média, desvio padrão). As comparações entre os valores basais e, após a intervenção do programa de condicionamento físico foram efetuadas pelo teste t de Student (dados pareados) e teste não paramétrico de Mann-Whitney, com nível de significância (valores de p) inferior a 0,05. Resultados: Dos 15 pacientes incluídos no estudo, três pacientes não concluíram o programa multidisciplinar no período de 12 meses. Assim, a amostra total analisada foi de 11 pacientes, isto é, 73,33% dos incluídos no estudo. O programa supervisionado a distância foi escolhido por todos os pacientes avaliados tendo a caminhada como atividade física mais praticada (66,67%), seguido do futebol. A meta de perda de 5% do peso corporal não foi atingida ao final do estudo, e a lipoproteína plasmática de baixa densidade (LDL) apresentou redução significante (Tempo 4, p=0,0130) durante o estudo. A Distância Percorrida no Teste (DTC6) foi maior nos Tempos 1 e 2 quando comparado ao Tempo 0, com diferença significante (p < 0,05). Conclusão: O programa de condicionamento físico supervisionado à distância teve alta adesão e foi eficaz para a melhora da capacidade funcional de pacientes com NASH. A melhora foi parcial para os parâmetros bioquímicos e antropométricos. Adicionalmente, este programa de condicionamento físico, monitorado à distância, tem baixo custo e é de facil implantação no Sistema Único de Saúde, com alto potencial de custo-benefício para pacientes com DHGNA e NASH, que poderão ser maiores a longo prazo.
APA, Harvard, Vancouver, ISO, and other styles
3

Silva, Giovanna Zanelli. "Avaliação da eficácia do tratamento nutricional oferecido pelo SUS para portadores de NASH." Faculdade de Medicina de São José do Rio Preto, 2015. http://hdl.handle.net/tede/256.

Full text
Abstract:
Submitted by Natalia Vieira (natalia.vieira@famerp.br) on 2016-05-20T17:39:42Z No. of bitstreams: 1 giovannazanellisilva_dissert.pdf: 2457622 bytes, checksum: 3faf263a6839bd66d93d3bcefc887385 (MD5)
Made available in DSpace on 2016-05-20T17:39:42Z (GMT). No. of bitstreams: 1 giovannazanellisilva_dissert.pdf: 2457622 bytes, checksum: 3faf263a6839bd66d93d3bcefc887385 (MD5) Previous issue date: 2015-11-27
Introduction: Nonalcoholic Fatty Liver Disease (NAFLD) is characterized by an increase in intracellular content of triglycerides; its prevalence worldwidely is nearly 20-30% of the population. This disease has spectral nature that includes steatosis and nonalcoholic steatohepatitis (NASH) in the absence of significant alcohol consumption. Although NAFLD may remain as a stable disease for longer periods, this condition may progress to advanced stages of cirrhosis and liver cancer. Diabetes Mellitus Type 2, insulin resistance and obesity are important risk factors, among others, for development of NAFLD, and are directly related to sedentary lifestyle and inappropriate eating habits. Thus, alteration in lifestyle, changes in eating habits and regular physical activity play a fundamental role in treating this disease. Aim: To evaluate the effectiveness of hypocaloric diet for the treatment of NASH as well as adherence to treatment. Methods: This is a prospective longitudinal open cohort study, in which 26 NASH patients were divided into 2 group: 15 patients in the control group and 11 patients in the treatment group which were followed up for 6 months. Both groups were diagnosed by liver biopsy. The treatment group was a given lifestyle change program with supervised low-calorie diet (20-25 kcal / kg actual weight / day), monitored exercise, standard treatment of metabolic syndrome and drug maintenance treatment with metformin and N- acetylcysteine. The control group received general guidelines on diet and weight loss, encouragement to practice physical exercise, standard treatment of metabolic syndrome and maintenance of drug treatment with metformin. Criteria for inclusion: patients with at least one of the component of metabolic syndrome; BMI ≥ 25 and ≤ 40 kg /m² and sedentary for at least three months. Criteria for exclusion: other concomitant liver diseases, alcohol intake greater than or equal to 21 drinks / week, or 140 g / day for men and 14 drinks / week or 70g / day for women, medication known to be associated with NAFLD, untreated hypothyroidism or hyperthyroidism, previous bariatric surgery, or uncontrolled psychiatric disorder. Diagnostic criteria: the diagnosis of NASH was done by liver biopsy in patients with steatosis on ultrasound or MRI and at least one risk factor for advanced fibrosis into the period up to one year before entering the study. The lifestyle change program in the treatment group had a weight loss goal of 5% or more of their initial weight within six months. Evaluation criteria: a monthly basis applied the clinical evaluation protocol and on a quarterly basis the laboratorial, according to the following variables: weight, height, body mass index, waist circumference, hip circumference, aminotransferase levels, gamma GT, total cholesterol and fractions, triglycerides. Statistical analysis: the descriptive variables were expressed as frequency, mean or median, standard deviation and variation as applicable. The Student t test and Mann-Whitney test were used for comparative analysis. It was admitted confidence interval of 95% and a significance level of P <0.05. Results: Of the 15 patients enrolled with a diagnosis of NASH who were submitted to nutritional treatment, 12 patients completed the six month follow-up of the study. The average age was 51.42 years ± 8.50, being 08 (66%) women and 04 (33%) men. Of this total, only one patient refused to carry out physical activity. Two (17%) among the 12 participants who completed the six month follow-up reached the percentage of expected weight loss. The average percentage of adaptation to the proposed diet was 82.93% ± 13.51%. Conclusion: The lifestyle change program tested for six months associated with NASH treatment, was not effective for clinical and biochemical improvement even with satisfactory adherence by most patients. Our data point out to the potential role of more restrictive diets and intensive supervision in this context combined with multidisciplinary team for the treatment of NASH. This real-life study produced crucial information for readjustment of the multidisciplinary treatment protocol for patients followed up in the service.
Introducao: A doenca hepatica gordurosa nao alcoolica (DHGNA) e caracterizada pelo aumento do conteudo intracelular de triglicerideos, com prevalencia mundial de aproximadamente 20 a 30% da populacao. Esta doenca tem natureza espectral que engloba esteatose e esteatohepatite nao-alcoolica (NASH), na ausencia de consumo significante de alcool. Embora DHGNA possa permanecer como uma doenca estavel por longos periodos, esta condicao pode progredir para estagios avancados de cirrose e cancer de figado. O Diabetes Mellitus Tipo 2, resistencia a insulina e obesidade sao importantes fatores de risco, dentre outros, para desenvolvimento da DHGNA, e estao diretamente relacionadas ao estilo de vida sedentario e habitos alimentares inapropriados. Dessa forma, alteracao no estilo de vida, mudancas nos habitos alimentares e atividade fisica regular tem papel fundamental no tratamento desta doenca. Objetivo: Avaliar a eficacia da dieta hipocalorica durante o tratamento do NASH, assim como, a adesao ao tratamento instituido. Metodo e Casuistica: Trata-se de um estudo de coorte aberto prospectivo, longitudinal, no qual foram incluidos consecutivamente 26 pacientes, divididos em dois grupos: 15 pacientes no grupo tratamento e 11 pacientes no grupo controle acompanhados durante 6 meses. Ambos tinham diagnostico de NASH por biopsia. O grupo tratamento recebeu programa de mudanca no estilo de vida com dieta hipocalorica supervisionada (20 - 25 kcal/kg de peso atual/dia), exercicio fisico supervisionado, tratamento padrao dos componentes da sindrome metabolica e manutencao de tratamento medicamentoso com metformina e N-acetilcisteina. O grupo controle recebeu orientacoes gerais de dieta e perda de peso, estimulo a pratica de exercicio fisico, tratamento padrao dos componentes da sindrome metabolica e manutencao do tratamento medicamentoso com metformina. Criterios de inclusao: portadores de pelo menos uma caracteristica de sindrome metabolica, IMC . 25 e . 40kg/m2, e sedentarios por no minimo tres meses. Criterios de exclusao: outras doencas hepaticas concomitantes, ingestao alcoolica igual ou superior a 21 doses/semana ou 140g/dia para homens e 14 doses/semana ou 70g/dia para mulheres, medicacao conhecidamente relacionada com DHGNA, hipotireoidismo ou hipertireoidismo nao tratados, pos operatorio de cirurgia bariatrica, compulsao alimentar ou outro disturbio psiquiatrico nao controlado. Criterios diagnosticos: o diagnostico de NASH foi feito por biopsia de figado em pacientes portadores de esteatose ao ultrassom ou ressonancia magnetica e pelo menos um fator de risco para fibrose avancada, no periodo de ate 1 ano antes da entrada no estudo. Programa de mudanca no estilo de vida no grupo tratado teve como meta a reducao minima ou superior a 5% de seu peso inicial no periodo de seis meses. Criterios de avaliacao: aplicado mensalmente o protocolo de avaliacao clinica e trimestralmente o laboratorial, de acordo com as seguintes variaveis: peso, altura, indice de massa corporal, circunferencia abdominal, circunferencia do quadril, niveis de aminotransferases, gama GT, colesterol total e fracoes, triglicerideos. Analise estatistica: as variaveis descritivas foram expressas em frequencia, media ou mediana, desvio padrao e variacao conforme aplicaveis. Foram utilizados os testes t de Student e teste de Mann-Whitney para analises comparativas. Foi admitido intervalo de confianca de 95% e nivel de significancia para P<0,05. Resultados: Dos 15 pacientes incluidos com diagnostico de NASH que foram submetidos ao programa de mudanca no estilo de vida, 12 pacientes concluiram o acompanhamento de 6 meses do estudo. A idade média foi de 51,42 anos ± 8,50, sendo 08 (66%) pessoas do gênero feminino e 04(33%) do gênero masculino. Deste total, apenas um paciente negou a realização de atividade física. Dois (17%) participantes dentre os 12 que concluíram os seis meses de acompanhamento atingiram a porcentagem de perda de peso esperada. A média da porcentagem de adequação à dieta proposta dos participantes do estudo encontrada foi de 82,93% ± 13,51%. Conclusão: O programa de mudança no estilo de vida testado durante seis meses associado ao tratamento do NASH, não foi eficaz para a melhora clínica e bioquímica mesmo com adesão satisfatória pela maioria dos pacientes. Este estudo de vida real produziu informações de fundamental importância para readequação do protocolo de atendimento multidisciplinar dos pacientes em acompanhamento no serviço.
APA, Harvard, Vancouver, ISO, and other styles
4

Yenilmez, Batuhan O. "DEVELOPMENT OF AN RNAi THERAPEUTIC STRATEGY AGAINST NON-ALCOHOLIC STEATOHEPATITIS (NASH)." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1158.

Full text
Abstract:
Nonalcoholic steatohepatitis (NASH) is a severe liver disorder characterized by triglyceride accumulation, severe inflammation, and fibrosis. With the recent increase in prevalence, NASH is now the leading cause of liver transplantation, with no approved therapeutics available. Despite years of research, the exact molecular mechanism of NASH progression is not well understood, but fat accumulation is believed to be the primary driver of the disease. Therefore, diacylglycerol O-acyltransferase 2 (DGAT2), a key enzyme in triglyceride synthesis, has been explored as a NASH target. RNAi-based therapeutics is revolutionizing the treatment of liver diseases, with recent chemical advances supporting long term gene silencing with single subcutaneous administration. Here we identified a hyper-functional, fully chemically stabilized GalNAc conjugated siRNA targeting DGAT2 (Dgat2-1473) that upon injection elicits up to three months of DGAT2 silencing (>80-90%, p<0.0001) in wild-type and NSG-PiZ “humanized” mice. Using an obesity-driven mouse model of NASH (ob/ob-GAN), Dgat2-1473 administration prevents and reverses triglyceride accumulation (> 50%, p:0.0008), resulting in significant improvement of the fatty liver phenotype. However, surprisingly, the reduction in liver fat didn’t translate into a similar impact on inflammation and fibrosis. Thus, while Dgat2-1473 is a practical, long-lasting silencing agent for potential therapeutic attenuation of liver steatosis, combinatorial targeting of a second pathway may be necessary for therapeutic efficacy against NASH.
APA, Harvard, Vancouver, ISO, and other styles
5

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

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Cavallari, Karelin Alvisi. "Influência da vitamina D sérica na adiponectina, visfatina e resistina nas alterações histológicas no fígado de pacientes com doença hepática gordurosa não alcoólica." Botucatu, 2016. http://hdl.handle.net/11449/137757.

Full text
Abstract:
Orientador: Sergio Alberto Rupp de Paiva
Resumo: A doença hepática gordurosa não alcoólica (DHGNA) é um conjunto de desordens caracterizado pela esteatose macrovesicular no consumo de álcool insuficiente para causar lesão hepática. A disfunção do tecido adiposo e a alteração no padrão de citocinas têm de destacado no desenvolvimento da doença, especialmente a adiponectina, visfatina e resistina. Além disso, a vitamina D parece modular a expressão de citocinas, podendo influenciar o desenvolvimento da doença. O objetivo do presente estudo foi avaliar a associação das alterações histológica com a concentração sérica de adiponectina, visfatina, resistina e vitamina D em pacientes com DHGNA. Foram recrutados 82 pacientes com DHGNA. Foi realizada anamnese clinica e nutricional, avaliação antropométrica e de composição corporal, consumo alimentar, biomarcadores da DHGNA, dosagens séricas de adiponectina, visfatina, resistina, 25hidrovitamina D e biópsia hepática em todos os pacientes no intervalo de no máximo 3 meses. Foi observado na amostra 83% dos pacientes do sexo feminino, maioria branco,s 79% sedentários e 96% obesos. Verificamos associação da adiponectina como fator protetor para fibrose (OR:0,88; 95% CI0,78-1; p=0,05) e da visfatina como fator de risco para fibrose perisinusoidal (OR:2,66; 95% CI:1,3-5,44; p=0,007) e fibrose (OR:2,96; 95% CI1,19-7,35; p=0,02). Em relação à VD, observamos a presença de hipovitaminose D em 60% dos pacientes; com influência da concentração sérica de VD na visfatina como fator de proteção par... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Non-alcoholic fatty liver disease (NAFLD) is a spectrum of disorders characterized by macrovesicular steatosis without enough alcohol to cause liver damage. The adipose tissue dysfunction and the adipokines pattern changes have been emphasized in non-alcoholic fatty liver disease development, especially adiponectin, resistin and visfatin. In addition, vitamin D may modulate the expression of adipokines, therefore influencing the disease development. The aim of the study was to evaluate the association of serum adiponectin, visfatin, resistin and vitamin D with histological changes in NAFLD patients. Thus, 82 NAFLD patients were enrolled. Nutritional and clinical anamneses, diet, physical activity, anthropometric parameters, a set of biomarkers related to NAFLD were evaluated within a range of 3 months. Out of the 82 patients, 83% were female, most of then whites, 79% sedentary and 96% obese. Adiponectin has been associated as a protective factor for fibrosis (OR: 0.88; 95% CI0,78-1; p = 0.05); while visfatin as a risk factor for perisinusoidal fibrosis (OR: 2.66; 95% CI : 1.3 to 5.44; p = 0.007) and fibrosis (OR: 2.96; 95% CI1,19-7,35; p = 0.02). Vitamin D deficiency was observed in 60% of patients. Vitamin D influences visfatin as a protective factor for non-alcoholic steato-hepatitis (NASH) (OR: 0.84; 95% CI: 0.73 to 0.979; p = 0.025) and resistin as a risk factor for lobular inflammation (OR: 1 13, 95% CI: 1-1.28; p = 0.051). Adipokines are associated with NAFLD hepatic... (Complete abstract click electronic access below)
Mestre
APA, Harvard, Vancouver, ISO, and other styles
7

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

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
8

Coilly, Audrey. "Marqueurs diagnostiques et pronostiques de la stéatohépatite métabolique Metabolism dysregulation induces a specific lipid signature of nonalcoholic steatohepatitis in patients MMP9 Identified as predictive factors of poor prognosis in patients with nonalcoholic fatty liver using data mining approaches and gene expression analysis Recent Insights into Treatment of Non-Alcoholic Steatohepatitis International Liver Transplantation Consensus Statement on End-stage Liver Disease Due to Nonalcoholic Steatohepatitis and Liver Transplantation. Quantitative assessment of triglycerides by Fourier Transform InfraRed (FTIR) spectroscopy of donor liver helps predicting outcome after liver transplantation." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS211.

Full text
Abstract:
L’obésité est un problème majeur de santé publique en France puisque 50% de la population est en surpoids ou obèse. Plusieurs complications hépatiques de l’obésité existent dont la NASH, pathologie caractérisée par l’association de lésions de stéatose et d’hépatite, d’anomalies des tests hépatiques. Chez un tiers des patients, la NASH conduit à l’apparition d’une fibrose puis d’une cirrhose. Elle favorise l’apparition du carcinome hépatocellulaire.La physiopathologie de la NASH est caractérisée par une dérégulation du métabolisme lipidique qui conduit à l’accumulation de lipides au niveau des hépatocytes. Celle-ci est toxique. La composition et le rôle des lipides comme promoteur de la NASH est de plus en plus étudié.Le premier volet de la thèse concerne la mise en évidence de marqueurs diagnostiques de la NASH. Dans cette étude, nous avons établi pour la première fois une signature lipidique de la NASH sur la base de la quantification de 32 lipides. Aucun des lipides identifiés ne permettait par lui-même de discriminer la stéatose de la NASH.En revanche, la signature lipidique globale permettait de distinguer les témoins patients des NAFL et des NASH. Nous avons également mis en évidence une dérégulation de la voie métabolique impliquée dans la synthèse des acides gras dans la NASH.Le deuxième volet avait pour objectif l’identification de nouveaux marqueurs pronostiques de la NASH. L'analyse par microarray d'expression de gènes a montré 1549 gènes discriminant les patients ayant une stéatopathie, NAFL ou NASH, des obèses sains ou des contrôle. Parmi eux, 58 gènes discriminaient la NASH de la stéatose simple. Ces gènes étaient impliqués dans le remodelage de la matrice extracellulaire et l'inflammation. Le gène le plus discriminant était FABP4. Parmi les gènes fortement associés à une expression élevée de FABP4, la métalloprotéinase MMP9 était surexprimée chez 55% des patients NASH. Nous avons identifié un total de 330 gènes régulés de manière différentielle, dont 229 gènes étaient surexprimés chez des patients NASH présentant un niveau d'expression élevé de MMP9. En utilisant les niveaux d'expression génique des gènes FABP4 et MMP9 hépatiques comme indicateurs de la progression de la maladie dans une cohorte indépendante de patients atteints de NAFLD, nous avons identifié les patients atteints de NAFL et NASH susceptibles d'avoir un mauvais pronostic.Enfin, dans le troisième volet, nous nous sommes intéressés à la valeur diagnostique et pronostique de la stéatose des greffons hépatiques, mesurée par FTIR. En effet, la stéatose en particulier lorsqu’elle dépasse 60% et macrovacuolaire, est connue pour impacter significativement la fonction et la survie des greffons hépatiques. Dans notre étude, parmi 58 prélèvements de greffons, le pourcentage moyen de stéatose macrovacuolaire et de stéatose microvésiculaire, évalué par le pathologiste, était de 2% à 30%, respectivement. La concentration moyenne en triglycérides hépatiques mesurée par chromatographie couplée en phase gazeuse à la spectrométrie était de 214 nmol/mg de tissu hépatique. L'estimation de la teneur en triglycérides obtenue par FTIR était significativement corrélée (r2 = 0,812) avec les résultats de la concentration moyenne en triglycérides hépatiques mesurée par chromatographie couplée en phase gazeuse à la spectrométrie. Trente-quatre (58%) patients ont présenté des complications définies par un stade Dindo-Clavien ≥2, dont 2 non-fonction primaire du greffon et 5 décès. Le seuil le plus discriminant entre le niveau de triglycérides et l’échec de la TH était de 54,02 nmol/mg de tissu hépatique obtenu par FTIR. La quantification du contenu hépatique en triglycérides par GC/MS était significativement associée à la survie du patient à la fin du suivi (p<0,0001) et à un échec de la transplantation (p <0,0001). L'estimation du contenu hépatique en triglycérides à l'aide de FTIR était significativement associée à la survie après greffe d'un an (p<0,0001)
Obesity is a major public health problem in France since 50% of the population has overweight. Several hepatic complications of obesity exist including NASH, pathology characterized by the combination of histological lesions of hepatic steatosis and hepatitis, liver test abnormalities and the absence of known liver disease, particularly toxic (alcohol) or virus. In one third of patients, NASH leads to fibrosis and then cirrhosis. It also promotes the development of hepatocellular carcinoma.The pathophysiology of NASH is characterized by a deregulation of lipid metabolism that leads to the accumulation of lipids in the hepatocytes. This accumulation of lipids is toxic and one of the causes of insulin resistance and the development of diabetes mellitus. All stages of lipid metabolism are affected by an accumulation of triglycerides, an increase in hepatic lipogenesis and a decrease in ß-oxidation. The composition and the role of lipids as a promoter of NASH is being increasingly studied.The first part of the thesis concerns the detection of diagnostic markers of NASH. In this study, we established for the first time a lipid signature of nonalcoholic steatohepatitis by quantification of 32 lipids. The overall lipid signature allowed distinguishing controls from NAFL and NASH. We have also demonstrated a deregulation of the metabolic pathway involved in the synthesis of fatty acids in NASH. This deregulation has been observed in both humans and animal models in our study.The second part aimed to identify new hepatic prognostic markers of NASH. Microarray analysis of gene expression showed 1549 genes discriminating patients with NAFL or NASH, healthy obese or controls. Among them, 58 genes discriminated NASH from simple steatosis. These genes were involved in extracellular matrix remodeling and inflammation. The most discriminating gene was FABP4 (fatty acid binding protein 4). Among genes strongly associated with high expression of FABP4, matrix metalloproteinase-9 (MMP9) was overexpressed in 55% of NASH patients. We identified a total of 330 differentially regulated genes, of which 229 genes were overexpressed in NASH patients with high levels of MMP9 expression. Using the gene expression levels of the liver FABP4 and MMP9 genes as indicators of disease progression in an independent cohort of NAFLD patients, we identified patients with NAFL and NASH who may have a poor prognosis.Finally, in the third part, we looked at the diagnostic and prognostic value of steatosis of liver grafts, measured by FTIR (Infrared Fourier Transform Microspectroscopy). Indeed, steatosis, when it exceeds 60% and is macrovacuolar, is known to significantly impact the function and survival of liver grafts. In our study, among 58 graft samples, the average percentage of macrovacuolar steatosis and microvesicular steatosis assessed by the pathologist was 2% to 30%, respectively. The average concentration of liver triglycerides measured by gas chromatography-spectrometry was 214 [10-1045] nmol/mg liver tissue. The FTIR triglyceride content estimate was significantly correlated (r2=0.812) with the results of the average hepatic triglyceride concentration measured by gas chromatography-spectrometry. Thirty-four (58%) patients had complications defined by a Dindo-Clavien stage ≥2, including 2 non-primary graft function and 5 deaths. The most discriminating threshold between triglyceride level and TH failure was 59.29 and 54.02 nmol/mg hepatic tissue obtained by spectrometry and FTIR, respectively. Quantification of hepatic triglyceride content by GC/MS was significantly associated with patient survival at the end of follow-up (p <0.0001) and failure of transplantation (p <0.0001). Estimating hepatic triglyceride content using FTIR was significantly associated with one-year post-transplant survival (p <0.0001)
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

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

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Non-Alcoholic Fatty Liver Disease NASH"

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Beattie, R. Mark, Anil Dhawan, and John W.L. Puntis. Fatty liver disease in children. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569862.003.0055.

Full text
Abstract:
Demographics 406Pathophysiology 406Differential diagnoses 407Presenting features 407Investigation 408Management 409Fatty liver disease is now increasingly recognized in children, particularly in the setting of obesity.The term non-alcoholic steatohepatitis (NASH) was first coined in 1980 by Ludwig to describe a pattern of liver injury in adults in which the liver histology was consistent with alcoholic hepatitis, but in whom significant alcohol consumption was denied. NASH can be considered as part of a broader spectrum of non-alcoholic fatty liver disease that extends from simple steatosis through steatohepatitis that is characterized by the potential to progress to fibrosis, cirrhosis and subsequent end stage liver disease....
APA, Harvard, Vancouver, ISO, and other styles
8

McNiff, Pil, and Diana Jo Rossano. Non Alcoholic Fatty Liver Disease: Recipes That Improve NASH, NAFLD, and Silent Liver Disease. Independently Published, 2019.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

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

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

Khanna, Sudeep. Non-Alcoholic Fatty Liver Disease. Elsevier - Health Sciences Division, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Non-Alcoholic Fatty Liver Disease NASH"

1

Stern, Christiane, and Vlad Ratziu. "Pharmacological Options for NASH." In Non-Alcoholic Fatty Liver Disease, 309–27. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6_17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Patrono, Damiano, Silvia Martini, and Renato Romagnoli. "Liver Transplantation and NAFLD/NASH." In Non-Alcoholic Fatty Liver Disease, 343–62. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6_19.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Pastore, Mirella, Alessandra Gentilini, and Fabio Marra. "Mechanisms of Fibrogenesis in NASH." In Non-Alcoholic Fatty Liver Disease, 97–127. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Tincopa, Monica A., and Stephen A. Harrison. "Noninvasive Diagnostic Approach to NASH: Radiological Diagnostics." In Non-Alcoholic Fatty Liver Disease, 257–69. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Castagneto-Gissey, Lidia, James R. Casella-Mariolo, and Geltrude Mingrone. "Bariatric Surgery and NASH: A Feasible Option." In Non-Alcoholic Fatty Liver Disease, 329–42. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Miele, Luca, Marco Biolato, Caterina Conte, Francesca Mangiola, Antonio Liguori, Antonio Gasbarrini, and Antonio Grieco. "Etiopathogenesis of NAFLD: Diet, Gut, and NASH." In Non-Alcoholic Fatty Liver Disease, 73–95. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Maher, Jacquelyn J. "Pathogenesis of NAFLD and NASH." In Alcoholic and Non-Alcoholic Fatty Liver Disease, 71–101. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-20538-0_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Petta, Salvatore, and Aurora Giannetti. "Non-invasive Diagnostic Approach to NASH: Biological Markers." In Non-Alcoholic Fatty Liver Disease, 235–56. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-95828-6_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Siddiqui, Mohammad S., and Arun J. Sanyal. "Drug Therapy for NASH: Insulin-Sensitizing Agents (Metformin and Thiazolidinediones)." In Non-Alcoholic Fatty Liver Disease, 271–83. Oxford, UK: Wiley-Blackwell, 2013. http://dx.doi.org/10.1002/9781118556153.ch24.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Musso, Giovanni, Federica Molinaro, Elena Paschetta, Roberto Gambino, and Maurizio Cassader. "Lipid Modifiers and NASH: Statins, Ezetimibe, Fibrates, and Other Agents." In Non-Alcoholic Fatty Liver Disease, 293–307. Oxford, UK: Wiley-Blackwell, 2013. http://dx.doi.org/10.1002/9781118556153.ch26.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Non-Alcoholic Fatty Liver Disease NASH"

1

Yin, Chong, Siqi Liu, Vincent Wai-Sun Wong, and Pong C. Yuen. "Learning Sparse Interpretable Features For NAS Scoring From Liver Biopsy Images." In Thirty-First International Joint Conference on Artificial Intelligence {IJCAI-22}. California: International Joint Conferences on Artificial Intelligence Organization, 2022. http://dx.doi.org/10.24963/ijcai.2022/220.

Full text
Abstract:
Liver biopsy images play a key role in the diagnosis of global non-alcoholic fatty liver disease (NAFLD). The NAFLD activity score (NAS) on liver biopsy images grades the amount of histological findings that reflect the progression of NAFLD. However, liver biopsy image analysis remains a challenging task due to its complex tissue structures and sparse distribution of histological findings. In this paper, we propose a sparse interpretable feature learning method (SparseX) to efficiently estimate NAS scores. First, we introduce an interpretable spatial sampling strategy based on histological features to effectively select informative tissue regions containing tissue alterations. Then, SparseX formulates the feature learning as a low-rank decomposition problem. Non-negative matrix factorization (NMF)-based attributes learning is embedded into a deep network to compress and select sparse features for a small portion of tissue alterations contributing to diagnosis. Experiments conducted on the internal Liver-NAS and public SteatosisRaw datasets show the effectiveness of the proposed method in terms of classification performance and interpretability. regions containing tissue alterations. Then, SparseX formulates the feature learning as a low-rank decomposition problem. Non-negative matrix factorization (NMF)-based attributes learning is embedded into a deep network to compress and select sparse features for a small portion of tissue alterations contributing to diagnosis. Experiments conducted on the internal Liver-NAS and public SteatosisRaw datasets show the effectiveness of the proposed method in terms of classification performance and interpretability.
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Miette, V., C. Fournier, L. Adara, and L. Sandrin. "P1C-2 Liver Stiffness Measurement Using Transient Elastography in Patients with Non-Alcoholic Fatty Liver (NAFLD) and Non-Alcoholic Steatohepatitis (NASH)." In 2007 IEEE Ultrasonics Symposium Proceedings. IEEE, 2007. http://dx.doi.org/10.1109/ultsym.2007.335.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Non-Alcoholic Fatty Liver Disease NASH"

1

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
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).
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Non-Alcoholic Fatty Liver Disease NASH' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography