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Nutrition and dietary interventions are a central component in the pathophysiology, but also a cornerstone in the management of patients with non-alcoholic fatty liver disease (NAFLD). Summarizing our rapidly advancing understanding of how our diet influences our metabolism and focusing on specific effects on the liver, we provide a comprehensive overview of dietary concepts to counteract the increasing burden of NAFLD. Specifically, we emphasize the importance of dietary calorie restriction independently of the macronutrient composition together with adherence to a Mediterranean diet low in added fructose and processed meat that seems to exert favorable effects beyond calorie restriction. Also, we discuss intermittent fasting as a type of diet specifically tailored to decrease liver fat content and increase ketogenesis, awaiting future study results in NAFLD. Finally, personalized dietary recommendations could be powerful tools to increase the effectiveness of dietary interventions in patients with NAFLD considering the genetic background and the microbiome, among others.
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Non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease, with a prevalence that is increasing in parallel with the global rise in obesity and type 2 diabetes mellitus. The pathogenesis of NAFLD is complex and multifactorial, involving environmental, genetic and metabolic factors. The role of the diet and the gut microbiome is gaining interest as a significant factor in NAFLD pathogenesis. Dietary factors induce alterations in the composition of the gut microbiome (dysbiosis), commonly reflected by a reduction of the beneficial species and an increase in pathogenic microbiota. Due to the close relationship between the gut and liver, altering the gut microbiome can affect liver functions; promoting hepatic steatosis and inflammation. This review summarises the current evidence supporting an association between NAFLD and the gut microbiome and dietary factors. The review also explores potential underlying mechanisms underpinning these associations and whether manipulation of the gut microbiome is a potential therapeutic strategy to prevent or treat NAFLD.
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Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide and affects approximately one third of adults in the United States. The disease is becoming a global epidemic as a result of the rising rates of obesity and metabolic disease. Emerging data suggest weight loss of ≥10% overall body weight is beneficial in resolving steatosis and reversing fibrosis. Prospective trials comparing various diets are limited by lack of sufficient power as well as pre- and post-treatment histopathology, and therefore no specific diet is recommended at this time. In this narrative review we examine the pathophysiology behind specific macronutrient components that can either promote or reverse NAFLD to help inform more specific dietary recommendations. Overall, the data supports reducing saturated fat, refined carbohydrates, and red and processed meats in the diet, and increasing the consumption of plant-based foods. Diets that incorporate these recommendations include plant-based diets such as the Dietary Approaches to Stop Hypertension, Mediterranean, vegetarian, and vegan diets.
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Serum milk fat globule-EGF factor 8 protein as a potential biomarker for metabolic syndrome Han Ah Lee, Jihwan Lim, Hyung Joon Joo, Young-Sun Lee, Young Kul Jung, Ji Hoon Kim, Hyunggin An, Hyung Joon Yim, Yoon Tae Jeen, Jong Eun Yeon, Do-Sun Lim, Kwan Soo Byun, Yeon Seok Seo Clinical and Molecular Hepatology.2021; 27(3): 463. CrossRef
Defining comprehensive models of care for NAFLD Jeffrey V. Lazarus, Quentin M. Anstee, Hannes Hagström, Kenneth Cusi, Helena Cortez-Pinto, Henry E. Mark, Michael Roden, Emmanuel A. Tsochatzis, Vincent Wai-Sun Wong, Zobair M. Younossi, Shira Zelber-Sagi, Manuel Romero-Gómez, Jörn M. Schattenberg Nature Reviews Gastroenterology & Hepatology.2021; 18(10): 717. CrossRef
Effect of Nutrition Education in NAFLD Patients Undergoing Simultaneous Hyperlipidemia Pharmacotherapy: A Randomized Controlled Trial Won Myung Lee, Jea Hurn Bae, Young Chang, Sae Hwan Lee, Ji Eun Moon, Soung Won Jeong, Jae Young Jang, Sang Gyune Kim, Hong Soo Kim, Jeong-Ju Yoo, Young Seok Kim Nutrients.2021; 13(12): 4453. CrossRef
Reduction of Visceral Adiposity as a Predictor for Resolution of Nonalcoholic Fatty Liver in Potential Living Liver Donors Sunyoung Lee, Kyoung Won Kim, Jeongjin Lee, Taeyong Park, Hyo Jung Park, Gi‐Won Song, Sung‐Gyu Lee Liver Transplantation.2021; 27(10): 1424. CrossRef
Influence of Dietary Behaviors on Dyslipidemia in Pregnant Women and Its Effects on Physical Development of Fetuses and Infants: A Bidirectional Cohort Study Chenyang Li, Xuening Li, Dan Wu, Qi Chen, Zhe Xiao, Deliang Wen, Lingling Zhai, Lihong Jia Nutrients.2021; 13(10): 3398. CrossRef
The effects of Ramadan intermittent fasting on liver function in healthy adults: A systematic review, meta-analysis, and meta-regression MoezAlIslam Faris, Haitham Jahrami, Dana Abdelrahim, Nicola Bragazzi, Ahmed BaHammam Diabetes Research and Clinical Practice.2021; 178: 108951. CrossRef
Dieckol Decreases Caloric Intake and Attenuates Nonalcoholic Fatty Liver Disease and Hepatic Lymphatic Vessel Dysfunction in High-Fat-Diet-Fed Mice Kyung-A Byun, Seyeon Oh, Myeongjoo Son, Chul-Hyun Park, Kuk Hui Son, Kyunghee Byun Marine Drugs.2021; 19(9): 495. CrossRef
Hepatic-Metabolite-Based Intermittent Fasting Enables a Sustained Reduction in Insulin Resistance in Type 2 Diabetes and Metabolic Syndrome Markus Rohner, Robert Heiz, Simon Feldhaus, Stefan R. Bornstein Hormone and Metabolic Research.2021; 53(08): 529. CrossRef
Fasting, Nutrition and Weight Loss: An Approach to Refine Non-Alcoholic Fatty Liver Disease Galal A. AL-SAMHARI, Gaber M. AL-MUSHIKI, Rashi TAMRAKAR, Gibirima ABDULLAHI, YUE-Dong LIN, XIAN-Yan TANG Journal of Nutritional Science and Vitaminology.2021; 67(6): 366. CrossRef
KASL clinical practice guidelines: Management of nonalcoholic fatty liver disease Seong Hee Kang, Hye Won Lee, Jeong-Ju Yoo, Yuri Cho, Seung Up Kim, Tae Hee Lee, Byoung Kuk Jang, Sang Gyune Kim, Sang Bong Ahn, Haeryoung Kim, Dae Won Jun, Joon-Il Choi, Do Seon Song, Won Kim, Soung Won Jeong, Moon Young Kim, Hong Koh, Sujin Jeong, Jin-Wo Clinical and Molecular Hepatology.2021; 27(3): 363. CrossRef
The Troubling Link Between Non-alcoholic Fatty Liver Disease (NAFLD) and Extrahepatic Cancers (EHC) Ajit Venniyoor, Abdul Aziz Al Farsi, Bassim Al Bahrani Cureus.2021;[Epub] CrossRef
Kee Woon Kweon , Hong Joo Kim , Soong Hwan Lee , Yeong Jung Cho , Jong Cheol Kim , Sung Woo Kim , Hee Soo Kim , In Gyu Back , Cheol Hun Jung , Yong Hyeon Jo , Chang Woo Gham , Dong Ho
Aim s : The purpose of this study was to explore the differences of general characteristics and nutritional factors such as anthropometry and dietary intake between alcohol-related cirrhosis and virus-related liver cirrhosis and to assess the nutritional status of both of these groups. Methods : In this study, the nutritional status of 67 patients with liver cirrhosis (25 with alcohol-related and 42 with virus-related) was evaluated by using clinical assessment, anthropometric measurements, dietary intakes, and biochemical indices. Results : Although anthropometric measurements were not significantly different between alcoholic cirrhosis and viral cirrhosis, anthropometry of patients with viral cirrhosis had a higher tendency than that of alcoholic cirrhotic patients. Alcohol intake factors such as amount, duration, and frequency in alcoholic cirrhotic patients were higher than those in patients with viral cirrhosis. Energy excluding alcohol and vitamin C were significantly different between patients with alcoholic and viral cirrhosis. All subjects had lower intake of energy excluding alcohol, protein, vitamin A, thiamin, riboflavin, niacin, calcium, and iron as than recommended by the Recommended Dietary Allowances (RDA) for Koreans. Of special note was the fact that the intakes of energy excluding alcohol, vitamin A, riboflavin, and calcium were less than 75% of RDA for Koreans. Although the glucose and triglyceride levels were significantly different between alcoholic and viral cirrhotic patients, there were within normal range in both groups. There was an interaction effect in triceps skinfold thickness of the subjects according to both etiology and severity of liver disease. Conclusion : These data suggests that nutritional disorders are common in patients with both alcohol-and virus-related cirrhosis. It is necessary to educate patients with cirrhosis about the importance of a balanced dietary intake as well as its pattern, and quality of diet. (Korean J Hepatol 2000;6:59-72)
Background/Aims The experimental production of cholesterol gallstone suggests that alteration of the nature of gallbladder mucus may be a factor in the induction of gallbladder stones. This study was designed to clarify the changes of the gallbladder epithelia and the role of a high cholesterol-cholic acid diet (CCD) in the formation of the gallstones. Method: Forty mice were fed on a diet of natural 1% high-cholesterol egg yolk and 2.5% cholic acid for 8 weeks. The mice were sacrificed biweekly and followed up for 8 weeks. The gallbladder tissues and bile were prepared for electron microscopic examination. We observed the ultrastructural changes of the epithelia and the sediments of the gallbladder bile with scanning and transmission electron microscopic observation. Results: 1) Process of Gallstone formation in bile: At the 2nd week in mice fed with CCD, the crystals grew up by appositional layering into monoliths and then by aggregation into mulberry-shaped stones. At the 8th week many stones and numerous concrements were observed. 2) Scanning electron microscopic findings: In mice fed with CCD, the scattered whitish patches of epithelial cell surfaces exhibited the cauliflower-like apical protrusion secreting mucin. These protrusions appeared to be swellings of the apical plasmalemma and they were mixed with the mucus and microvilli. 3) Transmission electron microscope findings: At the 2nd week, numerous electron lucent secretory granules were observed in the apical zone of the epithelial cells. Increased numbers of fat vacuoles were also observed in the basal area of epithelium. Two types of cells were observed in the lining epithelium: dark and light cells. Conclusion: This study suggests that long-term administration of CCD, and the resultant increased secretion of glycoprotein from gallbladder epithelial cells, could be a factor in the induction of the gallstones.
Background/Aims ErbB receptor proteins are transmembrane tyrosine kinase receptors; when they are
activated by interaction with ligands, they generate diverse cellular responses, especially during lesion
development and progression to cancer. In this study the expression of ErbB receptors and TGF-α were
investigated using an experimental cirrhosis rat model giving rise to hepatocellular neoplasms, similar to human
liver diseases. Methods: Fifty three male rats received intraperitoneal injection of diethylnitrosamine (DEN, 50
mg/kg), weekly for 18 weeks. Until the eighth week, two rats were sacrificed every two weeks and from the
tenth to the eighteenth week, five rats were sacrificed weekly. Grossly, dyschromatic and dysmorphic nodules
were counted and categorized into three groups: N1/N2/N3: 3 mm≤x<5 mm/5 mm≤x<10 mm/x≥10 mm in
diameter. All nodules were examined, histologically. Antibodies for GSTp, TGF-α, EGF-R, ErbB2, ErbB3 and
ErbB4 were used for immunohistochemistry. Results: The onset of cirrhoses was noted from the twelfth week.
Preneoplastic foci, hepatocellular adenomas (HCA) and hepatocellular carcinomas (HCC) were noted from the
second, eleventh and fifteenth week, respectively. The nodules (N1/N2/N3: 397/258/64) included regenerating
nodule; RN (N1/N2/N3: 72.3%/15.9%/0%), HCA (N1/N2/N3: 27.2%/82.2%/7.6%) and HCC (N1/N2/N3: 0.5%/
1.9%/92.4%). EGF-R was expressed in 12.5% of RN, 64.7% HCA and 75.2% HCC. TGF-α was expressed in
92.4% of RN, 91.3% HCA and 93.2% HCC. Sixty eight percent of TGF-α expressing nodules showed
concurrent EGF-R expression. ErbB2 was expressed in 83.6% of RN, 72.9% HCA and 88.7% HCC. ErbB4 was
expressed in 95.2% of RN, 86.3% HCA and 62.5% HCC. Conclusions: Increased expression of EGF-R and
decreased expression of ErbB4, might be related with tumor progression during DEN-induced
hepatocarcinogenesis. (Korean J Hepatol 2007;13:70-80)