non-alcoholic fatty liver disease/hypoxia

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Ethanol and tobacco smoke increase hepatic steatosis and hypoxia in the hypercholesterolemic apoE(-/-) mouse: implications for a "multihit" hypothesis of fatty liver disease.

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Přihlášení Registrace

Although epidemiologic studies indicate that combined exposure to cigarette smoke and alcohol increase the risk and severity of liver diseases, the molecular mechanisms responsible for hepatotoxicity are unknown. Similarly, emerging evidence indicates a linkage among hepatic steatosis and

Nocturnal Hypoxia Activation of the Hedgehog Signaling Pathway Affects Pediatric Nonalcoholic Fatty Liver Disease Severity.

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Chronic intermittent hypoxia and hedgehog (Hh) pathway dysregulation are associated with nonalcoholic fatty liver disease (NAFLD) progression. In this study, we determined the relationship between obstructive sleep apnea (OSA)/nocturnal hypoxia and Hh signaling in pediatric NAFLD. Adolescents with

[Effect of targeted inhibition of hypoxia-inducible factor-1α by 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole on the progression of non-alcoholic fatty liver disease in rats].

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Objective: To investigate the effect of targeted inhibition of hypoxia-inducible factor-1α (HIF-1α) by 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1) on the progression of non-alcoholic fat liver diseases (NAFLD) in rats. Methods: A total of 72 male Sprague-Dawley rats were randomly divided

Maternal hypoxia increases the susceptibility of adult rat male offspring to high-fat diet-induced nonalcoholic fatty liver disease.

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Exposure to an adverse intrauterine environment increases the risk for adult metabolic syndrome. However, the influence of prenatal hypoxia on the risk of fatty liver disease in offspring is unclear. The purpose of the present study was to evaluate the role of reduced fetal oxygen on the development

[Hypoxia inducible factor 1-alpha mRNA expression in alcoholic liver disease].

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OBJECTIVE To investigate the effect of hypoxia on chronic alcoholic liver disease. METHODS Twenty four male Sprague-Dawley rats were randomly into two groups. The alcohol group (n=12) was fed 56% (v/v) of ethanol once per day by gastric infusion at 8 g/kg body weight for 24 weeks. The control group

The role of hypoxia in the pathogenesis of alcoholic liver disease.

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Research on alcohol-induced liver hypoxia in experimental and clinical alcoholic liver disease (ALD) over a span of 20 years is reviewed. The data has repeatedly supported a role for hypoxia in the pathogenesis of ALD but little attention has been given to this phenomenon in a clinical setting where

Treating Obstructive Sleep Apnea and Chronic Intermittent Hypoxia Improves the Severity of Nonalcoholic Fatty Liver Disease in Children.

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OBJECTIVE To determine the effects of treating obstructive sleep apnea/nocturnal hypoxia on pediatric nonalcoholic fatty liver disease (NAFLD) severity and oxidative stress. METHODS Biopsy proven participants (n = 9) with NAFLD and obstructive sleep apnea/hypoxia were studied before and after

Hypoxia aggravates non-alcoholic steatohepatitis in mice lacking hepatocellular PTEN.

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The metabolic disorders that predispose patients to NASH (non-alcoholic steatohepatitis) include insulin resistance and obesity. Repeated hypoxic events, such as occur in obstructive sleep apnoea syndrome, have been designated as a risk factor in the progression of liver disease in such patients,

Hypoxia-regulated mechanisms in the pathogenesis of obesity and non-alcoholic fatty liver disease.

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The pandemic rise in obesity has resulted in an increased incidence of metabolic complications. Non-alcoholic fatty liver disease is the hepatic manifestation of the metabolic syndrome and has become the most common chronic liver disease in large parts of the world. The adipose tissue expansion and

Hypoxia and non-alcoholic fatty liver disease.

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NAFLD (non-alcoholic fatty liver disease) represents a spectrum of fatty liver diseases associated with an increased risk of Type 2 diabetes and cardiovascular disease. The spectrum of fatty liver diseases comprises simple steatosis, steatosis with inflammation [i.e. NASH (non-alcoholic

Association between nocturnal hypoxia and liver injury in the setting of nonalcoholic fatty liver disease.

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OBJECTIVE Obstructive sleep apnea (OSA) is suggested as a potential risk factor of nonalcoholic fatty liver disease (NAFLD). However, the underlying mechanism is still far from clear. The aim of this observational study was to investigate the influence of OSA-related hypoxia on severity of liver

The potential role of vascular alterations and subsequent impaired liver blood flow and hepatic hypoxia in the pathophysiology of non-alcoholic steatohepatitis.

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Přihlášení Registrace

Non-alcoholic fatty liver disease (NAFLD) covers a spectrum of disease ranging from steatosis to steatohepatitis (NASH) and fibrosis, but the underlying pathophysiological mechanisms remain largely unknown. As there is currently no approved pharmacological therapy and the prevalence of NAFLD keeps

Hepatocyte Hypoxia Inducible Factor-1 Mediates the Development of Liver Fibrosis in a Mouse Model of Nonalcoholic Fatty Liver Disease.

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BACKGROUND Obstructive sleep apnea (OSA) is associated with the progression of non-alcoholic fatty liver disease (NAFLD) to steatohepatitis and fibrosis. This progression correlates with the severity of OSA-associated hypoxia. In mice with diet induced obesity, hepatic steatosis leads to liver

Hypoxia: a link between fibrogenesis, angiogenesis, and carcinogenesis in liver disease.

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Liver injury causes vascular disorganization and local tissue hypoxia starting early in disease course. In this context, hypoxia acts not only as an aggravating factor of cell damage and inflammation, but also as an inhibitor of liver regeneration, a major stimulus of angiogenesis and fibrogenesis,

Obstructive sleep apnea and hypoxemia are associated with advanced liver histology in pediatric nonalcoholic fatty liver disease.

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Přihlášení Registrace

OBJECTIVE To determine whether obstructive sleep apnea (OSA) and/or nocturnal hypoxemia are associated with the severity of liver injury in patients with pediatric nonalcoholic fatty liver disease (NAFLD). METHODS Obese children aged 10-18 years with liver biopsy-proven NAFLD were enrolled.

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