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Journal articles on the topic 'Alcoholic Fatty Liver'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

Korobkо, Yuriy Ivanovich. "Non-alcoholic fatty liver disease." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 7 (July 1, 2021): 20–24. http://dx.doi.org/10.33920/med-10-2107-03.

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Fatty degeneration of cells under the influence of various factors is called steatosis; most often this process is observed in the pancreas and liver. Steatosis of the liver refers to its fatty infiltration, in which fatty inclusions appear in the parenchyma of the organ, leading to dysfunction of hepatocytes. Steatosis can be focal and diffuse; in the latter case, fat cells are located over the entire surface of the liver. Until 1980, it was believed that only alcohol abuse can lead to steatosis, while fatty degeneration of the liver was noted in 90 % of alcohol abusers. Subsequently, it was found that alcoholism is not the only reason for the development of this pathological condition, after which it was proposed to divide steatosis into alcoholic and non-alcoholic. Most often, non-alcoholic steatosis develops in women over 45 years old against the background of obesity or diabetes mellitus. Also, the cause of the development of liver steatosis can be malnutrition and diseases of other digestive organs, leading to impaired absorption of nutrients, metabolic disorders, and hormonal disruptions.

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2

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

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3

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

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4

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

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5

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

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6

Diehl, Anna Mae. "Recent Events in Alcoholic Liver Disease V. Effects of ethanol on liver regeneration." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 1 (January 2005): G1—G6. http://dx.doi.org/10.1152/ajpgi.00376.2004.

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Liver regeneration is necessary to recover from alcoholic liver injury. Herein, we review evidence that ethanol interferes with liver regeneration. Briefly, alcoholic fatty livers demonstrate increased rates of hepatocyte death. The latter provides a regenerative stimulus. However, unlike mature hepatocytes in healthy adult livers, most surviving mature hepatocytes in alcoholic fatty livers cannot replicate. Therefore, less mature cells (progenitors) must differentiate to replace dead hepatocytes. Little is known about the general mechanisms that modulate the differentiation of liver progenitors in adults. Delineation of these mechanisms and clarification of how ethanol influences them might suggest new therapies for alcoholic liver disease.

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7

K.C., Geetika. "Diagnosis of Non-alcoholic fatty liver disease." Journal of Pathology of Nepal 6, no. 11 (March 17, 2016): 947–52. http://dx.doi.org/10.3126/jpn.v6i11.15679.

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Non Alcoholic Fatty Liver Disease is the deposition of fat in liver in absence of excessive of alcohol consumption. Non Alcoholic Fatty Liver Disease ranges from simple steatosis to Nonalcoholic steatohepatitis and cirrhosis. Most cases (90%) of Non Alcoholic Fatty Liver Disease have simple steatosis with benign prognosis. Ten to thirty percent of Non -Alcoholic Fatty Liver Disease progresses to NASH and 25-40% of Nonalcoholic steatohepatitis undergoes progressive liver fibrosis.Ultimately 20-30% of Nonalcoholic steatohepatitis will go into cirrhosis during their lifetime. Nonalcoholic steatohepatitis cirrhosis has higher chances of (2.6% per year) going into hepatocellular carcinoma. There are several risk factors noted for Non Alcoholic Fatty Liver Disease. Some of which includes increasing age, metabolic syndrome, dietary factors etc. Investigations regarding liver function test can be divided into invasive and noninvasive types. Under invasive procedures comes liver biopsy and non-invasive includes radiological tests and various biochemical tests. This article tries to analyze different scoring systems and their significance in diagnosing steatohepatitis and fibrosis.

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8

Venkatesan, S., Nancy W. Y. Leung, and Timothy J. Peters. "Fatty acid synthesis in vitro by liver tissue from control subjects and patients with alcoholic liver disease." Clinical Science 71, no. 6 (December 1, 1986): 723–28. http://dx.doi.org/10.1042/cs0710723.

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1. Percutaneous liver biopsy specimens were obtained from 11 control subjects, 24 alcoholic patients and six diabetic patients with mild to severe fatty liver and incubated in Krebs–Henseleit buffer containing 3H2O. The incorporation of 3H into fatty acid was measured and the absolute rate of fatty acid synthesis calculated. 2. Fatty acid synthesis rates were significantly lower in alcoholic fatty liver than in controls. 3. Fatty acid synthesis rates were similar in controls and patients with diabetic fatty livers. 4. Addition of 50 mmol/l ethanol did not alter the fatty acid synthesis rates in vitro. It is concluded that enhanced lipogenesis is not the major cause of fatty liver in patients with alcoholic fatty liver.

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9

Smith, Briohny W., and Leon A. Adams. "Non-alcoholic fatty liver disease." Critical Reviews in Clinical Laboratory Sciences 48, no. 3 (June 2011): 97–113. http://dx.doi.org/10.3109/10408363.2011.596521.

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10

Maurice, James, and Pinelopi Manousou. "Non-alcoholic fatty liver disease." Clinical Medicine 18, no. 3 (June 2018): 245–50. http://dx.doi.org/10.7861/clinmedicine.18-3-245.

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11

Li, Wenhao, and William Alazawi. "Non-alcoholic fatty liver disease." Clinical Medicine 20, no. 5 (September 2020): 509–12. http://dx.doi.org/10.7861/clinmed.2020-0696.

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12

Choudhari, Sahil, and Mrs A. Jothipriya. "Non-alcoholic fatty liver disease." Research Journal of Pharmacy and Technology 9, no. 10 (2016): 1782. http://dx.doi.org/10.5958/0974-360x.2016.00360.7.

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13

Della Corte, Claudia, Daniela Liccardo, Antonella Mosca, Andrea Vania, and Valerio Nobili. "Non-alcoholic fatty liver disease." Paediatrics and Child Health 23, no. 12 (December 2013): 529–34. http://dx.doi.org/10.1016/j.paed.2013.08.003.

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14

Rajwal, Sanjay, and Patricia McClean. "Non-alcoholic fatty liver disease." Paediatrics and Child Health 27, no. 12 (December 2017): 556–60. http://dx.doi.org/10.1016/j.paed.2017.07.011.

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15

Павлов, Ч. С., Е. А. Кузнецова, Ю. О. Шульпекова, and М. Ч. Семенистая. "Non-alcoholic fatty liver disease." Nauchno-prakticheskii zhurnal «Patogenez», no. 2() (June 7, 2018): 4–11. http://dx.doi.org/10.25557/2310-0435.2018.02.4-11.

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В статье освещается одна из наиболее часто встречаемых патологий печени - неалкогольная жировая болезнь печени (НАЖБП), обсуждаются современные концепции этиологии, патогенеза, принципы диагностики и новейшие походы к консервативному и хирургическому лечению данного заболевания. Описывается патофизиология инсулинорезистентности, метаболического синдрома и ряда других клинически-ассоциированных с НАЖБП состояний. Подробно рассматриваются патогенетические аспекты развития фиброза при НАЖБП и описываются современные возможности и ограничения методов визуализации в диагностике степени стеатоза и стадии фиброза печени, ультразвукового исследования и сывороточных маркеров. Обоснованы подходы к обследованию и ведению пациентов с НАЖБП на разных этапах развития заболевания. The article discusses one of the most frequent hepatic pathologies, non-alcoholic fatty liver disease, and current concepts of its etiology, pathogenesis, diagnostic principles, and the latest approaches to conservative and surgical treatment. Pathophysiology of insulin resistance, metabolic syndrome, and other conditions clinically associated with non-alcoholic fatty liver disease are described. The authors deepened the insight into mechanisms of fibrosis development, up-to-date possibilities and limitations of imaging methods in diagnosis of the degree of steatosis and the stage of liver fibrosis, ultrasound, and serum markers. Clinical substantiation of the need to create an algorithm for examining and managing patients with non-alcoholic fatty liver disease at different stages of this condition and early verification of steatosis has an undoubted merit.

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16

Collier, Jane. "Non-alcoholic fatty liver disease." Medicine 35, no. 2 (February 2007): 86–88. http://dx.doi.org/10.1016/j.mpmed.2006.11.010.

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17

Pavlides, Michael, and Jeremy F. L. Cobbold. "Non-alcoholic fatty liver disease." Medicine 43, no. 10 (October 2015): 585–89. http://dx.doi.org/10.1016/j.mpmed.2015.07.004.

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18

Pavlides, Michael, and Jeremy Cobbold. "Non-alcoholic fatty liver disease." Medicine 47, no. 11 (November 2019): 728–33. http://dx.doi.org/10.1016/j.mpmed.2019.08.007.

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19

ANGULO, PAUL, and KEITH D. LINDOR. "Non-alcoholic fatty liver disease." Journal of Gastroenterology and Hepatology 17 (February 2002): S186—S190. http://dx.doi.org/10.1046/j.1440-1746.17.s1.10.x.

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20

Farrell, Geoffrey C., Rebecca Wardell, Narci Teoh, and Shiv Chitturi. "Non‐alcoholic fatty liver disease." Internal Medicine Journal 49, no. 5 (May 2019): 681–83. http://dx.doi.org/10.1111/imj.14283.

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21

Méndez-Sánchez, Nahum. "Non alcoholic fatty liver disease." Annals of Hepatology 8 (2009): S3. http://dx.doi.org/10.1016/s1665-2681(19)31819-8.

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22

Bhala, N., T. Usherwood, and J. George. "Non-alcoholic fatty liver disease." BMJ 339, jul16 1 (July 16, 2009): b2474. http://dx.doi.org/10.1136/bmj.b2474.

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23

TUYAMA, Ana C., and Charissa Y. CHANG. "Non-alcoholic fatty liver disease." Journal of Diabetes 4, no. 3 (August 17, 2012): 266–80. http://dx.doi.org/10.1111/j.1753-0407.2012.00204.x.

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24

Gaglio, Paul J. "Non-Alcoholic Fatty Liver Disease." Clinics in Liver Disease 20, no. 2 (May 2016): i. http://dx.doi.org/10.1016/s1089-3261(16)30018-6.

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25

Alhadyan, Roula Hadyan Mohammed, Albader Abdulhameed Y. Khojah, and Abdulaziz Ghareeb Abdullah Alanazi. "Non-Alcoholic Fatty Liver Disease." Egyptian Journal of Hospital Medicine 70, no. 4 (January 2018): 570–76. http://dx.doi.org/10.12816/0043808.

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26

Björnsson, Einar, and Paul Angulo. "Non-alcoholic fatty liver disease." Scandinavian Journal of Gastroenterology 42, no. 9 (January 2007): 1023–30. http://dx.doi.org/10.1080/00365520701514529.

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27

Tan, Hui-Hui, and Jason Pik-Eu Chang. "Non-Alcoholic Fatty Liver Disease." Proceedings of Singapore Healthcare 19, no. 1 (March 2010): 36–50. http://dx.doi.org/10.1177/201010581001900106.

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28

Alba, L. M., and K. Lindor. "Non-alcoholic fatty liver disease." Alimentary Pharmacology & Therapeutics 17, no. 8 (April 2003): 977–86. http://dx.doi.org/10.1046/j.1365-2036.2003.01493.x.

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29

Godlee, F. "Non-alcoholic fatty liver disease." BMJ 343, jul20 3 (July 20, 2011): d4652. http://dx.doi.org/10.1136/bmj.d4652.

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30

Sattar, N., E. Forrest, and D. Preiss. "Non-alcoholic fatty liver disease." BMJ 349, sep19 15 (September 19, 2014): g4596. http://dx.doi.org/10.1136/bmj.g4596.

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31

Cua, Ian Homer Y., and Jacob George. "Non-alcoholic fatty liver disease." British Journal of Hospital Medicine 66, no. 2 (February 2005): 106–11. http://dx.doi.org/10.12968/hmed.2005.66.2.17559.

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32

Pearce, Lynne. "Non-alcoholic fatty liver disease." Nursing Standard 30, no. 52 (August 24, 2016): 15. http://dx.doi.org/10.7748/ns.30.52.15.s16.

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33

Powell, Elizabeth E., Vincent Wai-Sun Wong, and Mary Rinella. "Non-alcoholic fatty liver disease." Lancet 397, no. 10290 (June 2021): 2212–24. http://dx.doi.org/10.1016/s0140-6736(20)32511-3.

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34

Brůha, Radan. "Non-Alcoholic Fatty Liver Disease." Vnitřní lékařství 65, no. 9 (September 1, 2019): 571–75. http://dx.doi.org/10.36290/vnl.2019.098.

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35

Ajmo, Joanne M., Xiaomei Liang, Christopher Q. Rogers, Brandi Pennock, and Min You. "Resveratrol alleviates alcoholic fatty liver in mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 4 (October 2008): G833—G842. http://dx.doi.org/10.1152/ajpgi.90358.2008.

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Alcoholic fatty liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of alcoholic liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of fatty acid oxidation and prevented alcoholic liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human alcoholic fatty liver disease.

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36

Mahmood, Kawa Abdullah. "PREVALENCE OF FATTY PANCREAS AMONG PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE IN SULAIMANI." Journal of Sulaimani Medical College 6, no. 2 (December 1, 2016): 107–15. http://dx.doi.org/10.17656/jsmc.10094.

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37

Eaton, S., A. M. Zaitoun, C. O. Record, and K. Bartlett. "β-Oxidation in Human Alcoholic and Non-Alcoholic Hepatic Steatosis." Clinical Science 90, no. 4 (April 1, 1996): 307–13. http://dx.doi.org/10.1042/cs0900307.

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1. The CoA and carnitine ester intermediates of mitochondrial β-oxidation have not previously been quantified in liver disease, although there is some evidence that β-oxidation is inhibited in alcoholic fatty liver. Mitochondria were isolated from needle liver biopsies from normal subjects, from patients with alcoholic fatty liver and patients with fatty liver of other aetiologies, incubated with 60 μmol/l [U-14C]hexadecanoate and the resultant CoA and carnitine esters were measured. 2. Although there was no significant difference in β-oxidation flux between the patient groups, there was a significant rise in the proportion of 3-hydroxyacyl-CoA and 2-enoyl-CoA esters in patients with alcoholic fatty liver compared with normal subjects, and in patients with non-alcoholic fatty liver, suggesting an inhibition at the level of 3-hydroxyacyl-CoA dehydrogenase activity. 3. In alcoholic patients this difference could not be accounted for on the basis of the measured activity of short and long-chain 3-hydroxyacyl-CoA dehydrogenases, and it is suggested that either an inhibition of complex I activity or diminished amounts of ubiquinone are likely to be responsible for the observed accumulation of CoA and carnitine esters, which may contribute to the accumulation of triacylglycerols in alcoholic steatosis. In fatty liver of other aetiologies, short- and long-chain 3-hydroxyacyl-CoA dehydrogenase activities were decreased.

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38

Khambu, Bilon, Shengmin Yan, Nazmul Huda, Gang Liu, and Xiao-Ming Yin. "Autophagy in non-alcoholic fatty liver disease and alcoholic liver disease." Liver Research 2, no. 3 (September 2018): 112–19. http://dx.doi.org/10.1016/j.livres.2018.09.004.

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39

Milroy, Christopher M. "Fatty Liver and the Forensic Pathologist." Academic Forensic Pathology 8, no. 2 (June 2018): 296–310. http://dx.doi.org/10.1177/1925362118782061.

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Fatty liver is a common finding in clinical practice and at autopsy. It is most commonly seen associated with alcohol abuse and in non-alcoholic fatty liver disease (NAFLD). It may also be seen in many other conditions in both adults and children. It is now recognized that NAFLD, like alcoholic liver disease, may lead to end stage liver disease. Nonalcoholic fatty liver disease is associated with increased mortality from other disorders, particularly cardiovascular diseases. Fatty liver may be seen in many conditions that concern autopsy pathologists, including drug toxicity, anorexia, hepatic ischemia, and heatstroke. In infants, steatosis is common in sudden unexpected deaths. Fatty liver has been associated with sudden death and this review examines the pathology and role of fatty liver in sudden death. Acad Forensic Pathol. 2018 8(2): 296-310

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40

Tompa, Anna, Anna Biró, Péter Balázs, and Mátyás Jakab. "A nem alkoholos zsírmáj befolyásoló hatása olajipari munkások perifériás lymphocytáinak gén- és immuntoxikológai paramétereire." Orvosi Hetilap 157, no. 35 (August 2016): 1394–402. http://dx.doi.org/10.1556/650.2016.30533.

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Introduction: More than half of the Hungarian population is overweight or obese, therefore, non-alcoholic fatty liver is a common problem. According to clinical experience, 20–30% of fatty liver cases is not related to alcohol, but can be linked to diabetes, obesity or metabolic syndrome. Aim: The authors studied the correlation between genotoxicity, immuntoxicity and non-alcoholic fatty liver among oil refinery workers. Method: During this genotoxicological monitoring study the data of 107 exposed were compared to 67 controls. Results: 36% of oil refinery workers had non-alcoholic fatty liver, while none of the selected, non-exposed controls had this abnormality. Chromosomal aberrations were elevated from 1.6% to 3.75% in the exposed group, immunotoxicological parameters were also changed, and CD71 positive B-cell ratio increased especially among subjects having non-alcoholic fatty liver. Conclusions: Non-alcoholic fatty liver can negatively influence the genotoxic effects of environmental hazards in workplaces. In the future this condition should be considered during risk assessment. Orv. Hetil., 2016, 157(35), 1394–1402.

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41

You, Min, and David W. Crabb. "Recent Advances in Alcoholic Liver Disease II. Minireview: molecular mechanisms of alcoholic fatty liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 1 (July 2004): G1—G6. http://dx.doi.org/10.1152/ajpgi.00056.2004.

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Alcohol has long been thought to cause fatty liver by way of altered NADH/NAD+ redox potential in the liver, which, in turn, inhibits fatty acid oxidation and the activity of tricarboxylic acid cycle reactions. More recent studies indicate that additional effects of ethanol both impair fat oxidation and stimulate lipogenesis. Ethanol interferes with DNA binding and transcription-activating properties of peroxisome proliferator-activated receptor-α (PPARα), as demonstrated with cultured cells and in ethanol-fed mice. Treatment of ethanol-fed mice with a PPARα agonist can reverse fatty liver even in the face of continued ethanol consumption. Ethanol also activated sterol regulatory element binding protein 1, inducing a battery of lipogenic enzymes. These effects may be due in part to inhibition of AMP-dependent protein kinase, reduction in plasma adiponectin, or increased levels of TNF-α in the liver. The understanding of these ethanol effects provides new therapeutic targets to reverse alcoholic fatty liver.

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42

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

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43

Bush, Haley, Pegah Golabi, and Zobair M. Younossi. "Pediatric Non-Alcoholic Fatty Liver Disease." Children 4, no. 6 (June 9, 2017): 48. http://dx.doi.org/10.3390/children4060048.

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44

Bhattacharya, Ishan. "Deconstructing non-alcoholic fatty liver disease." Lancet 355, no. 9219 (June 2000): 1975. http://dx.doi.org/10.1016/s0140-6736(05)72913-5.

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45

Nobili, V., and M. Pinzani. "Paediatric non-alcoholic fatty liver disease." Gut 59, no. 5 (April 28, 2010): 561–64. http://dx.doi.org/10.1136/gut.2009.187039.

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46

Ngu, JH, GB Goh, Z. Poh, and R. Soetikno. "Managing non-alcoholic fatty liver disease." Singapore Medical Journal 57, no. 07 (July 2016): 368–71. http://dx.doi.org/10.11622/smedj.2016119.

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47

Purohit, Vishnudutt, Bin Gao, and Byoung-Joon Song. "Molecular Mechanisms of Alcoholic Fatty Liver." Alcoholism: Clinical and Experimental Research 33, no. 2 (February 2009): 191–205. http://dx.doi.org/10.1111/j.1530-0277.2008.00827.x.

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48

Ahmed, Mohamed H., and Christopher D. Byrne. "Treating non-alcoholic fatty liver disease." Practice Nursing 18, no. 3 (March 2007): 120–26. http://dx.doi.org/10.12968/pnur.2007.18.3.23284.

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49

In-chief, Editor. "Non-alcoholic fatty liver disease – 2019." Sri Lanka Journal of Diabetes Endocrinology and Metabolism 9, no. 2 (December 12, 2019): 64. http://dx.doi.org/10.4038/sjdem.v9i2.7402.

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50

Zhang, Jinxiang, Yong Lin, and Lanjing Zhang. "Trends in Alcoholic Fatty Liver Disease." JAMA 322, no. 10 (September 10, 2019): 979. http://dx.doi.org/10.1001/jama.2019.10347.

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