non-alcoholic fatty liver disease

Synergistic interaction of fatty acids and oxysterols impairs mitochondrial function and limits liver adaptation during nafld progression

The complete mechanism accounting for the progression from simple steatosis to steatohepatitis in nonalcoholic fatty liver disease (NAFLD) has not been elucidated. Lipotoxicity refers to cellular injury caused by hepatic free fatty acids (FFAs) and cholesterol accumulation. Excess cholesterol autoxidizes to oxysterols during oxidative stress conditions. We hypothesize that interaction of FAs and cholesterol derivatives may primarily impair mitochondrial function and affect biogenesis adaptation during NAFLD progression.

Poor adherence to mediterranean diet and serum lipopolysaccharide are associated with oxidative stress in patients with non-alcoholic fatty liver disease

Oxidative stress plays a pivotal role in non-alcoholic fatty liver disease (NAFLD). Factors inducing oxidative stress in NAFLD may be several; however, a relationship with the adherence to Mediterranean Diet (Med-diet) and with serum lipopolysaccharide (LPS) has been poorly investigated in this setting. The aim was to investigate factors associated with impaired oxidative stress in NAFLD, focusing on the potential role of LPS and Med-diet.

Non-alcoholic fatty liver disease and heart valve disease: a neglected link

Non-alcoholic fatty liver disease (NAFLD ) occurs when fatty infiltration affects more than 5% of liver tissue, in the presence of less than 20 g (2.5 U) of alcohol consumption per day, after ruling out other causes of liver affections. NAFLD is a slowly progressive condition including a wide range of liver diseases with varying degrees of severity (from simple steatosis to coexistent inflammation with hepatocyte necrosis and fibrosis, to cirrhosis). Non-alcoholic steatohepatitis (NASH) is a more advanced stage of NAFLD disease, i.e.

Baseline homa IR and circulating FGF21 levels predict NAFLD improvement in patients undergoing a low carbohydrate dietary intervention for weight loss: a prospective observational pilot study

Background: Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver disease. Very low-calorie ketogenic diets (VLCKD) represent a feasible treatment as they induce profound weight loss and insulin resistance (IR) improvement. Despite the recognized benefits on NAFLD deriving from pharmacological administration of fibroblast growth factor 21 (FGF21), whose endogenous counterpart is a marker of liver injury, little is known about its physiology in humans.

Overview of studies of the vitamin D/vitamin D receptor system in the development of non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world. NAFLD is known to be associated with obesity, type 2 diabetes, metabolic syndrome and increased cardiovascular events: for these reasons, it is becoming a global public health problem and represents an important challenge in terms of prevention and treatment. The mechanisms behind the pathogenesis of NAFLD are multiple and have not yet been completely unraveled; consequently, at moment there are not effective treatments.

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