No abstract available.
Aging* ; Non-alcoholic Fatty Liver Disease*

No abstract available.
Fibrosis* ; Liver Diseases* ; Liver* ; Non-alcoholic Fatty Liver Disease*

No abstract available.
Non-alcoholic Fatty Liver Disease* ; Sitagliptin Phosphate* ; Synbiotics*

No abstract available.
Coronary Disease/*diagnosis ; Fatty Liver, Alcoholic/*diagnosis ; Female ; Humans ; Male ; Non-alcoholic Fatty Liver Disease/*diagnosis/*epidemiology

Non-alcoholic fatty liver disease (NAFLD) includes a wide spectrum of diseases that range from simple steatosis to non-alcoholic steatohepatitis (NASH) and cirrhosis. In addition, the burden of NAFLD is rapidly growing. Previously, NAFLD was regarded as a hepatic manifestation of metabolic syndrome, which is a traditional cardiovascular disease (CVD) risk factor. However, there has been an increasing evidence that suggest NAFLD to be an independent risk factor of CVD. Therefore, currently, NAFLD should be reconsidered as not only a simple manifestation of metabolic syndrome, but also a systemic disease that contribute to CVD. There are some reasonable hypotheses about the relationship between NAFLD and CVD. Moreover, many studies have been performed to better understand this relationship. Nonetheless, the underlying mechanisms and pathogenesis of NAFLD that contribute to CVD have not yet been fully elucidated to date. This review focuses on the underlying mechanisms and relationship between NAFLD and CVD.
Cardiovascular Diseases ; Fatty Liver ; Fibrosis ; Humans ; Non-alcoholic Fatty Liver Disease* ; Risk Factors

Despite the rapidly increasing prevalence of non-alcoholic fatty liver disease (NAFLD) in type 2 diabetes (T2D), few treatment modalities are currently available. We investigated the hepatic effects of the novel thiazolidinedione (TZDs), lobeglitazone (Duvie) in T2D patients with NAFLD. We recruited drug-naïve or metformin-treated T2D patients with NAFLD to conduct a multicenter, prospective, open-label, exploratory clinical trial. Transient liver elastography (Fibroscan®; Echosens, Paris, France) with controlled attenuation parameter (CAP) was used to non-invasively quantify hepatic fat contents. Fifty patients with CAP values above 250 dB/m were treated once daily with 0.5 mg lobeglitazone for 24 weeks. The primary endpoint was a decline in CAP values, and secondary endpoints included changes in components of glycemic, lipid, and liver profiles. Lobeglitazone-treated patients showed significantly decreased CAP values (313.4 dB/m at baseline vs. 297.8 dB/m at 24 weeks; P = 0.016), regardless of glycemic control. Lobeglitazone improved HbA1C values (7.41% [57.5 mM] vs. 6.56% [48.2 mM]; P < 0.001), as well as the lipid and liver profiles of the treated patients. Moreover, multivariable linear regression analysis showed that hepatic fat reduction by lobeglitazone was independently associated with baseline values of CAP, liver stiffness, and liver enzymes, and metformin use. Lobeglitazone treatment reduced intrahepatic fat content, as assessed by transient liver elastography, and improved glycemic, liver, and lipid profiles in T2D patients with NAFLD. Further randomized controlled trials using liver histology as an end point are necessary to evaluate the efficacy of lobeglitazone for NAFLD treatment (Clinical trial No. NCT02285205).
Elasticity Imaging Techniques ; Humans ; Linear Models ; Liver ; Metformin ; Non-alcoholic Fatty Liver Disease* ; Prevalence ; Prospective Studies

No abstract available.
Carcinoma, Hepatocellular/*diagnosis ; Female ; Humans ; Liver Neoplasms/*diagnosis ; Male ; Non-alcoholic Fatty Liver Disease/*diagnosis

The liver lies at the intersection of multiple metabolic pathways and consequently plays a central role in lipid metabolism. Pathological disturbances in hepatic lipid metabolism are characteristic of chronic metabolic diseases, such as obesity-mediated insulin resistance, which can result in nonalcoholic fatty liver disease (NAFLD). Tissue damage induced in NAFLD activates and recruits liver-resident and non-resident immune cells, resulting in nonalcoholic steatohepatitis (NASH). Importantly, NASH is associated with an increased risk of significant clinical sequelae such as cirrhosis, cardiovascular diseases, and malignancies. In this review, we describe the immunopathogenesis of NASH by defining the known functions of immune cells in the progression and resolution of disease.
Cardiovascular Diseases ; Fatty Liver ; Fibrosis ; Insulin Resistance ; Lipid Metabolism ; Liver ; Metabolic Diseases ; Metabolic Networks and Pathways ; Non-alcoholic Fatty Liver Disease*

Nonalcoholic steatohepatitis (NASH) is becoming common chronic liver disease because of the increasing global prevalence of obesity and consequently Nonalcoholic fatty liver disease (NAFLD). However, the mechanism for progression of NAFLD to NASH and then cirrhosis is not completely understood, yet. The triggering of these hepatic diseases is thought from hepatocyte injury caused by over-accumulated lipid toxicity. Injured hepatocytes release damage-associated molecular patterns (DAMPs), which can stimulate the Kupffer cells (KCs), liver-resident macrophages, to release pro-inflammatory cytokines and chemokines, and recruit monocyte-derived macrophages (MDMs). The increased activation of KCs and recruitment of MDMs accelerate the progression of NAFLD to NASH and cirrhosis. Therefore, characterization for activation of hepatic macrophages, both KCs and MDMs, is a baseline to figure out the progression of hepatic diseases. The purpose of this review is to discuss the current understanding of mechanisms of NAFLD and NASH, mainly focusing on characterization and function of hepatic macrophages and suggests the regulators of hepatic macrophages as the therapeutic target in hepatic diseases.
Chemokines ; Cytokines ; Fatty Liver* ; Fibrosis ; Hepatocytes ; Kupffer Cells ; Liver Diseases ; Macrophages* ; Non-alcoholic Fatty Liver Disease* ; Obesity ; Prevalence

PURPOSE: Insulin resistance (IR) has an important role in the development of non-alcoholic steatohepatitis (NASH). We aimed to analyze the association between liver histopathology and IR in pediatric patients with NASH. MATERIALS AND METHODS: In 24 children with non-alcoholic fatty liver disease (NAFLD), we investigated whether the hepatic pathologic characteristics have relations with following three biochemical indices; IR index including homeostasis model assessment of IR (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and insulin sensitivity indices-free fatty acid (ISI-FFA). RESULTS: Among 24 patients, 16 (66.6%) had a high NAFLD activity score (NAS), which is diagnostic of NASH. Higher serum triglyceride level was significantly correlated with a high NAS. Higher steatosis grades were significantly associated with low insulin sensitivity (p=0.023). In addition, severe lobular inflammation was associated with higher IR: HOMA-IR (p=0.014) and QUICKI (p=0.023). Severe fibrosis correlated with low insulin sensitivity and high IR indexes: ISI-FFA (p=0.049), HOMA-IR (p=0.028), and QUICKI (p=0.007). CONCLUSION: Patients with high IR had more severe lobular inflammation and hepatic fibrosis. Analyses of biochemical and endocrine parameters can be applied to determine the severity of the hepatic pathologic status in patients with NASH, especially in children who cannot undergo a liver biopsy.
Biopsy ; Child ; Fatty Liver* ; Fibrosis ; Homeostasis ; Humans ; Inflammation ; Insulin Resistance* ; Insulin* ; Liver* ; Non-alcoholic Fatty Liver Disease ; Triglycerides