비알콜성 지방간 초음파 영상에 GLCM과 인공신경망을 적용한 비알콜성 지방간 질환 분류

김지율,예수영 한국방사선학회 2023 한국방사선학회 논문지 Vol.17 No.5

Non-alcoholic fatty liver disease is an independent risk factor for the development of cardiovascular disease, diabetes, hypertension, and kidney disease, and the clinical importance of non-alcoholic fatty liver disease has recently been increasing. In this study, we aim to extract feature values ​​by applying GLCM, a texture analysis method, to ultrasound images of patients with non-alcoholic fatty liver disease. By applying an artificial neural network model using extracted feature values, we would like to classify the degree of fat deposition in non-alcoholic fatty liver into normal liver, mild fatty liver, moderate fatty liver, and severe fatty liver. As a result of applying the GLCM algorithm, the parameters Autocorrelation, Sum of squares, Sum average, and sum variance showed a tendency for the average value of the feature values ​​to increase as it progressed from mild fatty liver to moderate fatty liver to severe fatty liver. The four parameters of Autocorrelation, Sum of squares, Sum average, and sum variance extracted by applying the GLCM algorithm to ultrasound images of non-alcoholic fatty liver disease were applied as inputs to the artificial neural network model. The classification accuracy was evaluated by applying the GLCM algorithm to the ultrasound images of non-alcoholic fatty liver disease and applying the extracted images to an artificial neural network, showing a high accuracy of 92.5%. Through these results, we would like to present the results of this study as basic data when conducting a texture analysis GLCM study on ultrasound images of patients with non-alcoholic fatty liver disease.

성인 여성에서 비알코올성 지방간의 중증도에 따른 대사증후군 관련성

공은희 고신대학교 의과대학 2009 고신대학교 의과대학 학술지 Vol.24 No.2

Background: The aim of this study was to elucidate the relationship between the grade of non-alcoholic fatty liver diseases diagnosed by ultrasonography and the metabolic syndrome defined by the Third Report of the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) guideline. Methods: A total of 198 women who visited a health promotion center from January, 2007 to December, 2008 were selected for this study. The ultrasound scan of the liver was performed to determine the presence and the severity of non-alcoholic fatty liver disease. The relationship between non-alcoholic fatty liver and risk categories of metabolic syndrome using NCEP-ATP III guideline were analysed. Results: The prevalence of metabolic syndrome was 19.2% in women with non-alcoholic fatty livers. When odds ratios(95% CI) for metabolic syndrome in groups with moderate and severe non-alcoholic fatty livers were compared to that of group with mild non-alcoholic fatty livers, there was an increased risk of metabolic syndrome with an odds ratio of 2.24(1.31∼4.41). Conclusion: Non-alcoholic fatty liver disease was closely related to the metabolic syndrome in healthy women and the severity classification of non-alcoholic fatty liver by ultrasound scan could be useful to predict of the severity of insulin resistance and the risk of metabolic syndrome

Protective effects of Gymnaster koraiensis extract on ethanol-induced fatty liver in rats

최수영,Yoonhee Seo,Chae Young Bang,Seok Hoon Woo,강문규 경희대학교 융합한의과학연구소 2020 Oriental Pharmacy and Experimental Medicine Vol.20 No.3

Use of chronic alcohol produces alcoholic liver disease, with relationship of the beginning of abnormal lipid metabolism. Recent studies show that abnormal cholesterol metabolism has a specific role in the pathological cause of alcoholic fatty liver disease. Gymnaster koraiensis (GK), a worthy perennial Korean wild plant has specific polyacetylene compounds. Many researches have presented that GK has many pharmacological properties, such as oxidation prevention, liver protection, and inflammation prevention. However, the conservative effect of GK on alcoholic fatty liver has not been researched so far. Male Sprague-Dawley rats were randomly separated to normal feeding (fed a normal feeding for 4 weeks) and ethanol feeding (ED) groups. Rats in the ED group were administered a Lieber-DeCarli liquid feeding (containing 6.7% ethanol) and administered GK extract (125, 250, or 500 mg/kg/day), silymarin (200 mg/kg/day), or no treatment for 4 weeks. Each treatment group contained six rats. The administration with GK decreased serum levels of triglycerides, alcohol, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase, while increased serum level of adiponectin and activity of alcohol dehydrogenase. In alcohol-triggered fatty liver, GK decreased total cholesterol and fatty acid synthase, while increased catalase and superoxide dismutase. Alterations in liver histology, as assessed by H&E staining, showed that the GK treatment decreased amass of lipids in liver. These results present that GK extract may be potential therapeutic agent for alcoholic fatty liver disease by preventing fatty acid synthesis and activating anti-oxidation enzymes, while in activating alcohol degradation in ethanol-triggered fatty liver.

The effects of ethanol metabolites in liver and adipose tissue in acute alcohol-associated liver injury

Won Hyo Seo 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7

Alcoholic liver disease is liver damage that results from alcohol misuse. Years of alcohol abuse induces simple steatosis and steatohepatitis as early types of liver diseases, however, continuous liver damage are able to induce liver fibrosis/cirrhosis, and hepatocellular carcinoma as known as late stage of liver disease. Albeit ALD is a major personal/public health problem, the pathogenesis of ALD has not been understood very well. About 8 to 10 percent of Americans drink heavily and, 10 to 15 percent will go on to develop ALD. ALD not only generates personal health issues, but also creates a lot of social problems such as drunken driving. The pathogenesis of ALD involves complex and unclear biological processes. Interestingly, alcohol consumption can profoundly disturb the normal functions of adipose tissue by inducing adipocyte death and altering secretion of adipokines, pro-inflammatory mediators and free fatty acids from adipose tissue, which have important direct and indirect effects on the pathogenesis of alcoholic liver disease. The association of the oxidative metabolites of ethanol (acetaldehyde and reactive oxygen species) have been well studied as crucial factors to understand clinical and pathological spectrum of ALD. Especially, acetaldehyde is known to be toxic to the liver and alters lipid homeostasis. Acetaldehyde generated from lipid peroxidation induce collagen synthesis by their ability to form protein adducts that further activate transforming-growth-factor-β-dependent and independent profibrogenic pathways in activated hepatic stellate cells (HSCs). Besides of oxidative alcohol metabolite, we have investigated that non-oxidative metabolites generated during alcohol metabolism act as factors promoting liver damage. Fatty acid ethyl esters (FAEEs), nonoxidative metabolites of ethanol, are detectable in the blood after ethanol ingestion, and on that basis have been proposed as markers of ethanol intake. The investigation of the association of oxidative alcohol metabolites and non-oxidative alcohol metabolites would provide very informative clues to understand more about the pathogenesis of alcohol-mediated liver injury.

Silymarin`s Protective Effects and Possible Mechanisms on Alcoholic Fatty Liver for Rats

( Wei Zhang ),( Rutao Hong ),( Tulei Tian ) 한국응용약물학회 2013 Biomolecules & Therapeutics(구 응용약물학회지) Vol.21 No.4

Silymarin has been introduced fairly recently as a hepatoprotective agent. But its mechanisms of action still have not been well established. The aim of this study was to make alcoholic fatty liver model of rats in a short time and investigate silymarin`s protective effects and possible mechanisms on alcoholic fatty liver for rats. The model of rat`s alcoholic fatty liver was induced by intragastric infusion of ethanol and high-fat diet for six weeks. Histopathological changes were assessed by hematoxylin and eosin staining (HE). The activities of alanine transarninase (ALT) and aspartate aminotransferase (AST), the levels of total bilirubin (TBIL), total cholesterol (TC) and triglyceride (TG) in serum were detected with routine laboratory methods using an autoanalyzer. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) and the level of malondialdehyde (MDA) in liver homogenates were measured by spectrophotometry. The TG content in liver tissue was determined by spectrophotometry. The expression of nuclear factor-κB (NF-κB), intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6) in the liver were analyzed by immunohistochemistry. Silymarin effectively protected liver from alcohol-induced injury as evidenced by improving histological damage situation, reducing ALT and AST activities and TBIL level in serum, increasing SOD and GPx activities and decreasing MDA content in liver homogenates and reducing TG content in liver tissue. Additionally, silymarin markedly downregulated the expression of NF-κB p65, ICAM-1 and IL-6 in liver tissue. In conclusion, Silymarin could protect against the liver injury caused by ethanol administration. The effect may be related to alleviating lipid peroxidation and inhibiting the expression of NF-κB.

Effect of Hydrogen and Oxygen Mixed Inhalation on Non-alcoholic Fatty Liver Disease

Xue Yazhuo,Zhang Guangjie,Song Guohua,Qin Shucun 한국물학회 2019 한국물학회지 Vol.7 No.1

Non-alcoholic fatty liver disease is closely related to insulin resistance and genetic susceptibility, and it is a metabolic stress liver injury. As a result of the multifactorial pathological development in vivo, endogenous reactive oxygen species (ROS) increase, leading to inflammatory necrosis of hepatocytes. In recent years, many studies have confirmed that hydrogen is not a physiological inert gas. It has reliable therapeutic properties for some diseases, such as type 2 diabetes, Parkinson's disease, atherosclerosis and so on. It can be said that hydrogen is a gas with great potential medical value. We used nitrogen-oxygen mixture as control, and inhaled hydrogen-oxygen mixture (66% hydrogen and 33% oxygen) to non-alcoholic fatty liver patients. We found that hydrogen can improve the blood lipid level, reduce the plasma total cholesterol level and low density lipoprotein level, and increase the liver/spleen CT ratio in patients with non-alcoholic fatty liver. At the same time, hydrogen can improve the anti-inflammatory and anti-oxygen ability of plasma in patients with non-alcoholic fatty liver. It can reduce plasma glutamic oxaloacetic transaminase and alanine transaminase levels in patients with nonalcoholic fatty liver disease. The results showed that hydrogen could protect hepatocytes and alleviate the degree of nonalcoholic fatty liver.

Correlation of Clinical and Histopathologic Parameters with Ultrasonographic Grades in Pediatric Non-Alcoholic Fatty Liver Disease

강보경,김미미,신수진,김용주 대한의학회 2019 Journal of Korean medical science Vol.34 No.47

Background: Liver biopsy is the gold standard for diagnosing non-alcoholic steatohepatitis (NASH), but liver biopsy in children is not available in many institutes and many parents are reluctant to agree with the procedure. We investigated the correlation of clinical and pathologic parameters with the severity of non-alcoholic fatty liver disease (NAFLD) in pediatric patients using ultrasonographic examination methods and measured the prevalence of fatty pancreas in pediatric NAFLD. Methods: Liver biopsy and abdominal ultrasound (US) examinations were performed in 58 children (42 boys, 16 girls; mean age, 12 years; age range, 4–19 years) between March 2006 and August 2017. Fatty liver and fatty pancreas were evaluated by two independent radiologists using US according to 4- and 3-point scales, respectively. We then analyzed the correlations of clinical, laboratory, and histopathologic parameters with the ultrasonographic grade of steatosis. Results: Forty-two children showed simple steatosis (NAFLD activity score [NAS] ≤ 5) while 16 showed NASH (NAS > 5). Higher body mass index (BMI) percentile, waist circumference, hematocrit, insulin resistance, and lower insulin sensitivity index were significantly positively correlated with the grade of fatty liver. NAFLD activity score, amount of steatosis, and fibrosis significantly worsened as the fatty liver grade increased. Higher BMI, lower insulin sensitivity index, and boy were significantly positively correlated with the fatty pancreas grade. Conclusion: Altogether, ultrasonographic severity of fatty liver shows good correlation with that of clinical parameters and hepatic pathology.

Schisandra chinensis Prevents Alcohol-Induced Fatty Liver Disease in Rats

박형준,이수정,송윤오,장선희,고응규,강석남,정병엽,김홍덕,김곤섭,조재현 한국식품영양과학회 2014 Journal of medicinal food Vol.17 No.1

Schisandra chinensis (SC), a traditional herbal medicine, has been prescribed for patients suffering from various liver diseases, including hepatic cancer, hypercholesterolemia, and CCl4-induced liver injury. We investigated whether SC extract has a protective effect on alcohol-induced fatty liver and studied its underlying mechanisms. Rats were fed with ethanol by intragastric administration every day for 5 weeks to induce alcoholic fatty liver. Ethanol treatment resulted in a significant increase in alanine aminotransferase, aspartate aminotransferase, and hepatic triglyceride (TG) levels and caused fatty degeneration of liver. Ethanol administration also elevated serum TG and total cholesterol (TC) and decreased highdensity lipoprotein (HDL) cholesterol levels. However, after administration of ethanol plus SC extracts, the ethanol-induced elevation in liver TC and TG levels was reversed. Elevation in serum TG was not observed after treatment with SC. Moreover, compared with the ethanol-fed group, the rats administered ethanol along with SC extracts for 5 weeks showed attenuated fatty degeneration and an altered lipid profile with decreased serum TC and TG, and increased HDL cholesterol levels. Chronic ethanol consumption did not affect peroxisome proliferator-activated receptor c (PPARc) levels, but it decreased PPARa and phospho-AMP-activated protein kinase (AMPK) levels in the liver. However, SC prevented the ethanol-induced decrease in PPARa expression and induced a significant decrease in sterol regulatory element-binding protein-1 expression and increase in phospho-AMPK expression in rats with alcoholic fatty liver. SC administration resulted in a significant decrease in intracellular lipid accumulation in hepatocytes along with a decrease in serum TG levels, and it reversed fatty liver to normal conditions, as measured by biochemical and histological analyses. Our results indicate that the protective effect of SC is accompanied by a significant increase in phospho-AMPK and PPARa expression in hepatic tissue of alcoholic rats, thereby suggesting that SC has the ability to prevent ethanol-induced fatty liver, possibly through activation of AMPK and PPARa signaling.

Renal hyperfiltration, fatty liver index, and the hazards of all-cause and cardiovascular mortality in Finnish men

Mounir Ould Setti,Ari Voutilainen,Tomi-Pekka Tuomainen 한국역학회 2021 Epidemiology and Health Vol.43 No.-

OBJECTIVES: Renal hyperfiltration (RHF) and fatty liver are separately associated with adverse health outcomes. In this study, we investigated the mortality hazard of coexisting RHF and fatty liver. METHODS: Middle-aged men from the Kuopio Ischaemic Disease Risk Factor Study (n=1,552) were followed up for a median of 29 years. Associations among RHF, fatty liver index (FLI) score, age, body mass index, smoking status, alcohol consumption, and hypertension status were assessed using logistic regression. Cox proportional hazards models were used to determine the hazard ratios (HRs) for all-cause and cardiovascular disease (CVD) mortality with respect to RHF and fatty liver. RESULTS: Of the men, 5% had RHF (n=73), whereas a majority had fatty liver (n=848). RHF was associated specifically with smoking, and fatty liver was associated specifically with overweight. The all-cause mortality hazard was highest (HR, 1.96; 95% confidence interval [CI], 1.27 to 3.01) among men with RHF and fatty liver (n=33). Among men with RHF but normal FLI (n=40), the HR of all-cause mortality was 1.67 (95% CI, 1.15 to 2.42). Among men with fatty liver but a normal estimated glomerular filtration rate (n=527), the HR of all-cause mortality was 1.35 (95% CI, 1.09 to 1.66). CVD mortality hazard was associated with RHF, but not fatty liver. We detected no interaction effect between RHF and fatty liver for all-cause (synergy index, 0.74; 95% CI, 0.21 to 2.67) or CVD (synergy index, 0.94; 95% CI, 0.34 to 2.60) mortality. CONCLUSIONS: RHF and fatty liver are independently associated with all-cause and CVD mortality.

Estrogen-related receptor γ controls sterol regulatory element-binding protein-1c expression and alcoholic fatty liver

Kim, Don-Kyu,Kim, Yong-Hoon,Lee, Jae-Ho,Jung, Yoon Seok,Kim, Jina,Feng, Rilu,Jeon, Tae-Il,Lee, In-Kyu,Cho, Sung Jin,Im, Seung-Soon,Dooley, Steven,Osborne, Timothy F.,Lee, Chul-Ho,Choi, Hueng-Sik Elsevier 2019 Biochimica et biophysica acta, Molecular and cell Vol.1864 No.12

<P><B>Abstract</B></P> <P>Although SREBP-1c regulates key enzymes required for hepatic <I>de novo</I> lipogenesis, the mechanisms underlying transcriptional regulation of SREBP-1c in pathogenesis of alcoholic fatty liver is still incompletely understood. In this study, we investigated the role of ERRγ in alcohol-mediated hepatic lipogenesis and examined the possibility to ameliorate alcoholic fatty liver through its inverse agonist. Hepatic ERRγ and SREBP-1c expression was increased by alcohol-mediated activation of CB<SUB>1</SUB> receptor signaling. Deletion and mutation analyses of the <I>Srebp-1c</I> gene promoter showed that ERRγ directly regulates <I>Srebp-1c</I> gene transcription <I>via</I> binding to an ERR-response element. Overexpression of ERRγ significantly induced SREBP-1c expression and fat accumulation in liver of mice, which were blocked in <I>Srebp-1c</I>-knockout hepatocytes. Conversely, liver-specific ablation of <I>ERRγ</I> gene expression attenuated alcohol-mediated induction of SREBP-1c expression. Finally, an ERRγ inverse agonist, GSK5182, significantly ameliorates fatty liver disease in chronically alcohol-fed mice through inhibition of SREBP-1c-mediated fat accumulation. ERRγ mediates alcohol-induced hepatic lipogenesis by upregulating SREBP-1c expression, which can be blunted by the inverse agonist for ERRγ, which may be an attractive therapeutic strategy for the treatment of alcoholic fatty liver disease in human.</P> <P><B>Highlights</B></P> <P> <UL> <LI> ERRγ is induced by alcohol-mediated activation of CB<SUB>1</SUB> receptor signaling. </LI> <LI> ERRγ increases hepatic SREBP-1c expression and alcohol-mediated hepatic lipogenesis </LI> <LI> An ERRγ inverse agonist inhibits SREBP-1c-induced hepatic <I>de novo</I> lipogenesis. </LI> <LI> An ERRγ inverse agonist ameliorates alcohol fatty liver disease. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>