ArticleHepatology international2013
Hepatic angiogenesis and fibrosis are common features in morbidly obese patients.
Article in Hepatology international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed.
- Protective Effects of Berberine on Nonalcoholic Fatty Liver Disease in db/db Mice via AMPK/SIRT1 Pathway Activation.Current medical science · 2024Article
- Microarray-based Detection of Critical Overexpressed Genes in the Progression of Hepatic Fibrosis in Non-alcoholic Fatty Liver Disease: A Protein-protein Interaction Network Analysis.Current medicinal chemistry · 2024Article
- Mast Cells Promote Nonalcoholic Fatty Liver Disease Phenotypes and Microvesicular Steatosis in Mice Fed a Western Diet.Hepatology (Baltimore, Md.) · 2021Observational
- Non-alcoholic fatty liver disease: A major challenge in type 2 diabetes mellitus (Review).Experimental and therapeutic medicine · 2020Review
- An Overview of Lipid Metabolism and Nonalcoholic Fatty Liver Disease.BioMed research international · 2020Review
- Natural History of Nonalcoholic Fatty Liver Disease: Implications for Clinical Practice and an Individualized Approach.Canadian journal of gastroenterology & hepatology · 2020Review
- Article
- Metformin modulates innate immune-mediated inflammation and early progression of NAFLD-associated hepatocellular carcinoma in zebrafish.Journal of hepatology · 2019Article
- Article
- Underrated enemy - from nonalcoholic fatty liver disease to cancers of the gastrointestinal tract.Clinical and experimental hepatology · 2018Review
- Serum levels of vascular endothelial growth factor in non-alcoholic fatty liver disease.Annals of gastroenterology · 2017Article
- Role of MicroRNAs in NAFLD/NASH.Digestive diseases and sciences · 2016Review
- Obesity and renovascular disease.American journal of physiology. Renal physiology · 2015Review
- Angiogenesis and liver fibrosis.World journal of hepatology · 2015Review
- [Evaluation methods of angiogenesis in experimental liver fibrosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2015Article
- Article
- Non-alcoholic fatty liver disease and obesity: biochemical, metabolic and clinical presentations.World journal of gastroenterology · 2014Review
- Angiogenesis: a phenomenon which aggravates chronic liver disease progression.Hepatology international · 2013Article
- Hepatic fibrosis developing in morbid obesity independent of steatohepatitis: new mechanism or the Rube Goldberg machine?Hepatology international · 2013Article
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7 authors.
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Abstract
backgroundA mass of visceral adipose tissue is one of the most important determinants of progressive liver injury in nonalcoholic fatty liver disease (NAFLD). In accordance, nonalcoholic steatohepatitis (NASH) and fibrosis are believed to occur more commonly in morbidly obese patients compared with nonobese NAFLD patients. AIM OF THE STUDY: Comparative analysis of NAFLD histopathologic features and angiogenesis activity in morbidly obese and nonobese subjects. MATERIALS AND
methodsBiopsy samples from 40 severely obese (BMI ≥40 kg m(-2)) and 30 nonobese (BMI ≤30 kg m(-2)) NAFLD patients were examined. Kleiner's classification was used to diagnose NASH by grading steatosis, cytoplasmatic ballooning of hepatocytes, and lobular inflammation. The severity of fibrosis was evaluated according to the liver fibrosis staging system. Qualitative and quantitative immunohistochemical analyses of VEGF A, Flk-1, and CD34 were performed to study angiogenesis and the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) method was used to study hepatocyte apoptosis.
resultsSeverely obese patients did not differ from nonobese patients with respect to age and sex distribution. NASH was diagnosed in nine (22.5%) severely obese patients and in seven (23.3%) nonobese patients. Fibrosis was more common in morbidly obese patients (82.5 vs. 43.5%, χ(²) = 11.71, p = 0.003) and was not associated with NASH. Moreover, the severity of fibrosis was greater in obese patients, as advanced fibrosis (bridging fibrosis and cirrhosis) occurred in six (15%) severely obese patients and in two (6.7%) nonobese patients. In morbidly obese individuals, angiogenesis was independent of NASH and was activated at the stage of simple steatosis. In severe obesity, there was a positive relationship between the stage of fibrosis and angiogenic activity.
conclusionIn severely obese patients, fibrosis is probably promoted by mechanisms independent of NASH. In these patients, angiogenesis is activated early in the natural history of NAFLD and correlates with the severity of fibrosis.
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