Focal fatty change of the liver is a nodular lesion which is a rarely described and poorly characterized entity. The hepatic nodule measured 1.4cm at its maximum diameter, was subcapsular in location and occurred adjacent to the falciform ligament. Microscopically it was composed of hepatic tissue with a preserved lobular architecture. The central venous structures and portal tracts with their triads were regularly placed. The cytoplasm of almost all of the hepatocytes within the nodule was replaced by macrovesicular fat vacuoles with the nuclei displaced. Several large abnormal vessels were found at the margin of the nodule. The nodule was discovered incidentally on postmortem examination of a female infant who proved, at autopsy, to have multiple cardiac anomalies and bronchopneumonia. The possible inadequate local tissue perfusion due to abnormal intrahepatic vessels at this particular location could be augmented by multiple cardiac anomalies culminating in focal ischemia and focal fatty change. When encountered in surgery or on gross examination, it could be confused with other space occupying lesions such as liver cell adenoma, abscess and metastatic lesions.
Fatty Liver/complications ; Fatty Liver/pathology* ; Female ; Heart Defects, Congenital/complications ; Hepatic Artery/abnormalities ; Human ; Infant

Atherosclerosis ; complications ; Fatty Liver ; complications ; Humans ; Non-alcoholic Fatty Liver Disease

Metabolic (dysfunction) associated fatty liver disease (MAFLD), previously known as non-alcoholic fatty liver disease, is the most common cause of chronic liver disease worldwide. Many risk factors contribute to the pathogenesis of MAFLD with metabolic dysregulation being the final arbiter of its development and progression. MAFLD poses a substantial economic burden to societies, which based on current trends is expected to increase over time. Numerous studies have addressed various aspects of MAFLD from its risk associations to its economic and social burden and clinical diagnosis and management, as well as the molecular mechanisms linking MAFLD to end-stage liver disease and hepatocellular carcinoma. This review summarizes current understanding of the pathogenesis of MAFLD and related diseases, particularly liver cancer. Potential therapeutic agents for MAFLD and diagnostic biomarkers are discussed.
Carcinoma, Hepatocellular/complications* ; Humans ; Liver Neoplasms/complications* ; Non-alcoholic Fatty Liver Disease/complications* ; Risk Factors

Fatty Liver ; prevention & control ; therapy ; Humans ; Obesity ; complications ; Weight Loss

OBJECTIVES: The pathogenesis of nonalcoholic fatty liver in non-obese persons is poorly understood. We aimed to elucidate whether hyperinsulinemia and glucose intolerance are associated with development of fatty liver in patients with normal body weight. METHODS: Forty-seven patients with fatty liver were divided into non-obese (n = 25) and obese groups (n = 22) according to age adjusted body mass index. Inclusion criteria were as follows: (1) elevated transaminase levels during more than 3 months of follow up period, (2) no detectable HBsAg or anti-HCV in the serum, (3) alcohol consumption less than 40 gm/week, (4) no use of potential hepatotoxic drugs within 3 months and (4) sonographic evidence of fatty liver(moderate to severe degree). Baseline insulin levels and oral glucose tolerance test using 75gm of glucose were performed and the results were compared in each group of patients. RESULTS: Mean baseline insulin levels were elevated in both groups above the reference value, 9.3 +/- 3.5 microU/L in non-obese group and 9.9 +/- 3.5 microU/L in obese group (p = 0.26). Seventeen of non-obese patients (68%) had elevated basal insulin level and 16 of obese patients (73%) had elevated basal insulin level (p = 0.39). In oral glucose tolerance test, there was no difference in glucose level between non-obese and obese groups from O minute to 180 minutes (p > 0.05). Eleven patients from the non-obese group (44%) and 8 patients from the obese group (36%) had either impaired glucose tolerance or diabetes (p = 0.29). CONCLUSION: Our data suggest that hyperinsulinemia and glucose intolerance may play a role in the pathogenesis of fatty liver in patients with normal body weight as well as in patients with obesity.
Adult ; Body Weight ; Fatty Liver/pathology ; Fatty Liver/etiology* ; Fatty Liver/blood ; Female ; Glucose Intolerance/complications* ; Human ; Insulin/blood* ; Insulin Resistance ; Male ; Middle Age ; Obesity/complications

Fatty Liver ; complications ; epidemiology ; therapy ; Female ; Humans ; Insulin Resistance ; Non-alcoholic Fatty Liver Disease ; Polycystic Ovary Syndrome ; complications ; epidemiology ; therapy

Humans ; Non-alcoholic Fatty Liver Disease/complications* ; Cardiovascular Diseases/complications* ; Risk Factors ; Liver

Nonalcoholic fatty liver disease (NAFLD) is a type of metabolic stress liver injury that is closely associated with insulin resistance and genetic susceptibility. The continuum of liver injury in NAFLD can range from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH) and even lead to cirrhosis and liver cancer. The pathogenesis of NAFLD is complicated. Pro-inflammatory cytokines, lipotoxicity, and gut bacterial metabolites play a key role in activating liver-resident macrophages (Kupffer cells, KCs) and recruiting circulating monocyte-derived macrophages (MoDMacs) to deposit fat in the liver. With the application of single-cell RNA-sequencing, significant heterogeneity in hepatic macrophages has been revealed, suggesting that KCs and MoDMacs located in the liver exert distinct functions in regulating liver inflammation and NASH progression. This study focuses on the role of macrophage heterogeneity in the development and occurrence of NAFLD and NASH, in view of the fact that innate immunity plays a key role in the development of NAFLD.
Humans ; Non-alcoholic Fatty Liver Disease/pathology* ; Liver/pathology* ; Macrophages/metabolism* ; Liver Cirrhosis/complications* ; Disease Progression

Fatty Liver ; complications ; epidemiology ; Hepatitis B, Chronic ; complications ; epidemiology ; Hepatitis C, Chronic ; complications ; epidemiology ; Humans

Nonalcoholic and alcoholic rabbit models of fatty liver were established by feeding on high-fat diet and alcohol, respectively, and fatty liver stiffness at different pathological stages was assessed with real-time shear-wave elastography (SWE), so as to investigate the fibrosis process during the development of fatty liver. The fatty liver stiffness of rabbit in nonalcoholic and alcoholic groups was higher than that in the control group, and that in alcohol group was higher than that in the nonalcoholic group (P<0.01). The elasticity modulus of liver in fatty liver rabbits of nonalcoholic and alcoholic groups showed a positive correlation with progression of liver fibrosis (P<0.01). Real-time SWE, as a noninvasive diagnostic method, can objectively reflect the liver stiffness change and progression of liver fibrosis during the development of fatty liver.
Animals ; Elasticity ; Elasticity Imaging Techniques ; methods ; Fatty Liver, Alcoholic ; complications ; diagnostic imaging ; Liver Cirrhosis ; diagnostic imaging ; etiology ; Male ; Non-alcoholic Fatty Liver Disease ; complications ; diagnostic imaging ; Rabbits