Plasma total and free fatty acids composition in human non-alcoholic steatohepatitis

Almeida, Isabel Tavares de; Cortez‐Pinto, Helena; Fidalgo, Gina; Rodrigues, Débora F.; Camilo, M.

doi:10.1054/clnu.2001.0529

Cited by 211 publications

(154 citation statements)

References 19 publications

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“…In order to understand the impact of NAFL/NASH risk factors on liver cells, the system was exposed to a lipotoxic milieu composed of elevated glucose (25 mM), insulin (6,900 pM), and FFAs including oleic (65 μM) and palmitic (45 μM) acid, at concentrations derived from the differences between the plasma levels of healthy and NASH patients (14,15). These factors were present for the duration of the experiment (10 days).…”

Section: Resultsmentioning

confidence: 99%

Development of an in vitro human liver system for interrogating nonalcoholic steatohepatitis

et al. 2016

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Section: Resultsmentioning

confidence: 99%

Development of an in vitro human liver system for interrogating nonalcoholic steatohepatitis

et al. 2016

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“…LRP is important for lipid and lipoprotein uptake to cells [27] . Lipid profiles of steatohepatitis patients were found disturbed [28] . It was shown that midkine takes part in the inflammatory and repair processes after partial hepatectomy.…”

Section: Discussionmentioning

confidence: 99%

Midkine secretion protects Hep3B cells from cadmium induced cellular damage

Yazıhan¹,

Ataoglu²,

Akçıl³

et al. 2008

WJG

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AIM:To evaluate role of midkine secretion during Cadmium (Cd) exposure in the human hepatocyte cell line Hep3B cells. METHODS:Different dosages of Cd (0.5-1-5-10 μg/mL) were applied to Hep3B cells and their effects to apoptosis, lactate dehydrogenase (LDH) leakage and midkine secretion were evaluated as time dependent m a n n e r. S a m e e x p e r i m e n t s w e re re p e a t e d w i t h exogenously applied midkine (250-5000 pg/mL) and/or 5 μg/mL Cd.

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“…Patients carrying variant alleles of acyl-CoA dehydrogenases may result in the progression of steatohepatitis, because of aberrant fatty acid oxidation (7). In addition, the following undoubtedly contribute to lipid storage within the liver (5,(8)(9)(10): Insufficient synthesis and inhibition of apolipoproteins; Inhibition of newly synthesized VLDL transportation from the endoplasmic reticulum to the Golgi complex; Dysfunction of the Golgi-endoplasmic reticulum-lysosome complex; Reduction of saccharification or secretory vesicles of newly synthesized VLDL; Interference with exocytosis of newly synthesized VLDL as a result from malfunction of secretory vesicles migrating to hepatocyte serosa; Chronic hunger, poor digestion and absorption, low protein diet leading to the deficiency of 'anti-fatty liver factors' (including methionine, choline and phosphatidylcholine), bringing about insufficient synthesis of apolipoproteins, in particular apoB and VLDL. It has been demonstrated that lipid metabolism disturbance is regulated insufficiently by vital transcription factors that are indispensable for lipogenesis, such as the activation of AMP-activated protein kinase (AMPK), Jun N-terminal kinase (JNK), protein kinase C and nuclear factor (NF)-κB (11).…”

Section: Pathogeneisismentioning

confidence: 99%

“…Excessive oxidative stress derives from mitochondrial dysfunction and iron overload. The unceasingly increased ROS, and the product of oxidative stress, results in the rapid depletion of ATP, DNA injury, instability of protein and release of inflammatory factors, sequentially break cellular completeness of structure and function, which promotes the development of NAFLD (6,10).…”

Section: Gene Polymorphisms In Mediators Of Oxidative Stressmentioning

confidence: 99%

Development of gene polymorphisms in meditators of nonalcoholic fatty liver disease

Wang

Gong

2017

Biomedical Reports

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Abstract. Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease worldwide, the morbidity of which closely correlates with diversity of ethnicity, minority, family and location. Its histology spans from simple steatosis, to nonalcoholic steatohepatitis, which ultimately results in fibrosis, cirrhosis and hepatocellular carcinoma. The accelerating prevalence of NAFLD is due to an incremental incidence of metabolic syndrome that is distinguished by dyslipidemia, glucose impairment, obesity, excessive oxidative stress and adipocytokine impairment. Additionally, the pathogenesis of NAFLD is thought to be a multifactorial and complicated disease associated with lifestyle habits, nutritional factors and genetics. However, the pathogenesis and underlying mechanism in the development of NAFLD caused by genetics remains unclear. People have been increasingly emphasizing on the relationship between NAFLD and gene polymorphisms in recent years, with the aim of having a comprehensive elucidation of associated gene polymorphisms influencing the pathogenesis of the disease. In the current article, the authors attempted to critically summarize the most recently identified gene polymorphisms from the facets of glucose metabolism, fatty acid metabolism, oxidative stress and related cytokines in NAFLD that contribute to promoting the progression of the disease.

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Plasma total and free fatty acids composition in human non-alcoholic steatohepatitis

Cited by 211 publications

References 19 publications

Development of an in vitro human liver system for interrogating nonalcoholic steatohepatitis

Development of an in vitro human liver system for interrogating nonalcoholic steatohepatitis

Midkine secretion protects Hep3B cells from cadmium induced cellular damage

Development of gene polymorphisms in meditators of nonalcoholic fatty liver disease

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