NAFLD

Noninvasive assessment of hepatic steatosis and fibrosis in patients with severe obesity

PURPOSE: In morbid obesity nonalcoholic fatty liver disease (NAFLD) is endemic. Aim of this study is to evaluate the diagnostic accuracy of the most common noninvasive methods for identify NAFLD and fibrosis in a cohort of morbid obese population. METHODS: Ninety morbid obese patients undergoing bariatric surgery (BS) and intraoperative liver biopsy were evaluated preoperatively with Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and serum biomarkers for steatosis and fibrosis and liver stiffness measurement (LSM) using acoustic radiation force impulse (ARFI) elastography.

Insulin resistance, but not insulin response, during oral glucose tolerance test (OGTT) is associated to worse histological outcome in obese NAFLD

Background and aim: Obese subjects are at high risk of nonalcoholic fatty liver disease (NAFLD) and diabetes (T2D) due to insulin resistance (IR). Since high glucose levels are as toxic as lipids for hepatic metabolism, we hypothesize that altered response to oral glucose tolerance test (OGTT) is associated to more severe NAFLD with significant/advanced liver damage.

Prevalence and Impact of Nonalcoholic Fatty Liver Disease in Atrial Fibrillation

Objective: To estimate the prevalence of nonalcoholic fatty liver disease (NAFLD) and its impact on bleeding and thrombotic events in patients with atrial fibrillation (AF). Patients and Methods: Prospective multicenter cohort study including patients with nonvalvular AF receiving vitamin K antagonists (VKAs) or non-VKA oral anticoagulants (NOACs) from February 2008 for patients on VKA and from September 2013 for patients on NOACs. NAFLD was diagnosed using the validated fatty liver index, with a cutoff score of 60 or higher.

New insight into the mechanisms of ectopic fat deposition improvement after bariatric surgery

Non-alcoholic fatty-liver disease (NAFLD) is frequent in obese patients and represents a major risk factor for the development of diabetes and its complications. Bariatric surgery reverses the hepatic features of NAFLD. However, its mechanism of action remains elusive. We performed a comprehensive analysis of the mechanism leading to the improvement of NAFLD and insulin resistance in both obese rodents and humans following sleeve-gastrectomy (SG). SG improved insulin sensitivity and reduced hepatic and monocyte fat accumulation.

Increased liver localization of lipopolysaccharides in human and experimental NAFLD

Background and Aims: Lipopolysaccharides (LPS) is increased in nonalcoholic fatty liver disease (NAFLD), but its relationship with liver inflammation is not defined. Approach and Results: We studied Escherichia coli LPS in patients with biopsy-proven NAFLD, 25 simple steatosis (nonalcoholic fatty liver) and 25 nonalcoholic steatohepatitis (NASH), and in mice with diet-induced NASH. NASH patients had higher serum LPS and hepatocytes LPS localization than controls, which was correlated with serum zonulin and phosphorylated nuclear factor-κB expression.

Reduced biliverdin reductase-a expression in visceral adipose tissue is associated with adipocyte dysfunction and nafld in human obesity

Biliverdin reductase A (BVR-A) is an enzyme involved in the regulation of insulin signalling. Knockout (KO) mice for hepatic BVR-A, on a high-fat diet, develop more severe glucose impairment and hepato-steatosis than the wild type, whereas loss of adipocyte BVR-A is associated with increased visceral adipose tissue (VAT) inflammation and adipocyte size. However, BVR-A expression in human VAT has not been investigated.

Adipose tissue remodelling in obese subjects is a determinant of presence and severity of fatty liver disease

Aims: Experimental data suggest that visceral adipose tissue (VAT) dysfunction contributes to non-alcoholic fatty liver disease (NAFLD) development in obesity, however, data on humans are limited. Aims of this study were to investigate the relationship between NAFLD and VAT morphofunctional impairment and to determine whether the extent of VAT remodelling is associated with liver damage and metabolic alterations in obesity.

Vitamin D and metabolic dysfunction-associated fatty liver disease (MAFLD): An update

Non-alcoholic fatty liver disease (NAFLD) is the first cause of chronic liver disease worldwide; it ranges from simple steatosis to steatohepatitis (NASH) and, potentially, cirrhosis and hepatocarcinoma. NAFLD is also an independent risk factor for type 2 diabetes, cardiovascular diseases, and mortality. As it is largely associated with insulin resistance and related disorders, NAFLD has been recently re-named as Metabolic dysfunction-Associated Fatty Liver Disease (MAFLD). At present, there are no approved pharmacological treatments for this condition.

Bariatric Surgery in the Setting of Liver Cirrhosis with Portal Hypertension: the Confection and Particularities of Roux-en-Y Gastric Bypass in a High-Risk Patient

Introduction: Morbid obesity is associated with the occurrence of non-alcoholic fatty liver disease, which may progress to cirrhosis. Although weight loss is the treatment of choice, surgical management can be challenging at the stage of cirrhosis. The aim of this video report is to present the confection and the features of a Roux-en-Y gastric bypass (RYGB) in the setting of liver cirrhosis. Methods: We present the case of a 60-year-old man with a weight of 115 kg and a corresponding BMI of 38.9 kg/m2, with non-alcoholic steatohepatitis (NASH)-related liver cirrhosis.

Natural modulators of nonalcoholic fatty liver disease: mode of action analysis and in silico ADME-Tox prediction

Nonalcoholic fatty liver disease (NAFLD) is considered to be the most common chronic liver disease. The discovery of natural product-based NAFLD modulators requires a more comprehensive study of their modes of action (MoAs). In this study we analysed available in the literature data for 26 naturally-derived compounds associated with experimental evidence for NAFLD alleviation and outlined potential biomolecular targets and a network of pharmacological MoAs for 12 compounds with the highest number of experimentally supported MoA key events, modulated by them.

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