Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interest in dissecting the genetic and environmental components of complex human disease is growing, fueled by the emerging advances in the field of genomics and related disciplines. Improved understanding of the pathogenesis of complex liver diseases such as gallbladder stones, nonalcoholic fatty liver disease, viral hepatitis, and hepatocellular carcinoma remains a goal of the clinical and experimental hepatologist alike. Despite the scientific progress and technological advancement, elucidating the underlying mechanisms of complex hepatic diseases from the genomic standpoint will be demanding. Complexity of genomic structure and function, disease heterogeneity, influence of the environment on disease development and progression, and epigenetics all contribute to the challenge. To overcome these obstacles, novel conceptual frameworks regarding biological systems and human diseases are necessary in addition to a coordinated endeavor among different scientific disciplines. Deciphering in an integrated fashion the genomic, transcriptional, and translational aspects of the pathogenesis of complex liver diseases will lead to their better prediction, diagnostics, and treatment.
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PMID:Applying genomics to the study of complex disease. 1729 73

Alcohol excess is associated with a spectrum of disease ranging from simple steatosis through steatohepatitis to cirrhosis and, in some, hepatocellular carcinoma. Alcoholic steatohepatitis itself has a variable histological picture, but a constant feature is the presence of ballooning degeneration of hepatocytes. Recent studies have emphasized the importance of apoptosis as a mechanism of cell death in this condition. It is accompanied by varying degrees of perivenular, centrilobular, and pericellular fibrosis. When severe and associated with perivenular liver cell necrosis (central sclerosing hyaline necrosis), there may be precirrhotic portal hypertension. The pattern of fibrosis may initially be diffuse with little nodule formation, but in time there is frequently the development of a micronodular cirrhosis. In approximately 15% of patients with established cirrhosis, hepatocellular carcinoma develops; several precursor lesions are now recognized which can be detected histologically. Several authors have drawn attention to additional components of the spectrum of alcoholic liver disease, including vascular changes, portal tract inflammation and fibrosis, ductular reaction, and iron overload. The morphology of alcoholic liver disease can be significantly affected by abstinence; furthermore, the clinical and morphological phenotype can be significantly influenced by the presence of comorbid conditions such as nonalcoholic fatty liver disease or viral hepatitis. Biopsy appearances can provide important prognostic information in alcoholic liver disease, and this review incorporates a proposed grading and staging schema for assessment of histological severity.
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PMID:Alcoholic liver disease. 1735 88

The aim of this study was to evaluate the relationship between apolipoprotein E gene polymorphism and nonalcoholic fatty liver disease. The study group consisted of 237 nonalcoholic fatty liver disease patients who were detected by ultrasonography and 201 controls with ultrasonographically normal livers. DNA amplifications were performed by polymerase chain reaction technique and apolipoprotein E genotypes were evaluated after digestion with CfoI restriction enzyme. Serum levels of glucose, lipids, lipoproteins, and apolipoproteins were measured in all subjects. Additionally, viral hepatitis markers, liver enzymes, and body mass index were assessed. Patients were found to have significantly higher triglyceride, glucose, aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyltransferase levels and lower high-density lipoprotein cholesterol and apolipoprotein (a) levels than controls (P<0.05). There were no statistically significant differences in genotypes and allele frequencies between all patients and controls. Comparing nonobese patients with controls, the frequencies of allele epsilon2 and genotype epsilon2epsilon3 were statistically significantly different in the controls (P=0.04 and P=0.01, respectively). In conclusion, occurrence of the epsilon2 allele and epsilon2epsilon3 genotype may be protective against development of nonalcoholic fatty liver disease.
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PMID:Apolipoprotein E gene polymorphism in nonalcoholic fatty liver disease. 1743 74

Advanced glycation end products (AGEs), e.g., carboxymethyllysine (CML) or imidazolone are involved in several age-related disorders. Concerning their accumulation, the importance of hepatic and renal function is controversially discussed. To test whether impairment of hepatic or renal function will affect their accumulation, both AGEs have been measured in various populations, such as 52 patients with liver disease [viral hepatitis C without (n = 19) and with (n = 10) fatty liver; nonalcoholic fatty liver (n = 13), nonalcoholic steatohepatitis (n = 10)]. Serum concentrations of both AGEs have been compared to those in 20 healthy controls and 24 patients with moderate renal impairment (creatinine clearance 23-55 ml/min). Concerning CML (95% C.I. 803-1200 ng/ml), no differences between the various groups could be observed. Likewise, serum levels of imidazolone (95% C.I. 1.3-5.6 units) were similar in all populations. In conclusion, moderate impairment in hepatic or in renal function did not affect serum levels of CML and imidazolone. Apparently, any increase observed in severe cirrhosis or renal failure seems to be rather a consequence than a cause of both disorders.
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PMID:Unchanged serum levels of advanced glycation endproducts in patients with liver disease. 1757 Dec 53

Liver fibrosis results from chronic damage to the liver in conjunction with the progressive accumulation of fibrillar extracellular matrix proteins. Fibrosis progression in patients with chronic viral hepatitis is a dynamic process where hepatic stellate cells, the most important contributor cell type, respond to a variety of host genetic factors and viral proteins. The abuse of alcohol, superimposed fatty liver disease, and age at the time of viral infection are some of the factors that accelerate liver fibrosis. Liver biopsy remains the gold standard to diagnose fibrosis and significant advances have been made to develop noninvasive markers for liver fibrosis.
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PMID:Liver fibrosis and chronic viral hepatitis. 1761 56

In recent years, there has been an increasing prevalence of obesity and related diseases. This epidemiological change has increased the interest of researchers in the molecular and biochemical pathways involved in the pathogenesis of hepatic and biliary diseases. Insulin resistance is considered the major mechanism involved in the hepatic and biliary manifestations of obesity. Epidemiological, clinical, and basic research demonstrates that insulin resistance is associated with gallstone disease, nonalcoholic fatty liver disease, and poor outcomes in viral hepatitis C treatments. Fascinating experimental evidence demonstrates that fat-induced hepatic insulin resistance may result from the activation of kinases leading to impaired insulin signaling. The insulin-resistant state is characterized by a failure to suppress hepatic glucose production and glycogenolysis, with enhanced fat accumulation in hepatocytes because of increased lipolysis, increased free fatty acid uptake by hepatocytes, and increased hepatic synthesis of triglycerides. This molecular signaling induces a low-grade chronic inflammatory state, characterized by increased levels of proinflammatory molecules and acute-phase proteins. This review summarizes the most important molecular and biochemical issues in the hepatic and biliary diseases associated with insulin resistance.
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PMID:Hepatobiliary diseases and insulin resistance. 1769 41

The prevalence of type 2 diabetes is higher in patients who have liver diseases, such as nonalcoholic fatty liver disease, chronic viral hepatitis, hemochromatosis, alcoholic liver disease, and cirrhosis. The development of diabetes in patients with cirrhosis is well recognized, but evidence is emerging that the development of chronic liver disease and progression to cirrhosis may occur after the diagnosis of diabetes and that diabetes plays a role in the initiation and progression of liver injury. This article provides an overview of the evidence for an increased prevalence of diabetes in a range of liver diseases; the effect of diabetes on the severity of disease; the potential mechanisms whereby coexistent diabetes exacerbates progression of hepatic fibrosis; and the impact of obesity, insulin resistance, and type 2 diabetes on clinical outcomes.
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PMID:Impact of diabetes on the severity of liver disease. 1790 49

Although per capita alcohol consumption, and thus the prevalence of alcoholic liver disease, decreases generally with age in Europe and in the United States, recently an increase in alcohol consumption has been reported in individuals over 65 years. Reasons explaining this observation may include an increase in life expectancy or a loss of life partners and, thus, loneliness and depression. Although ethanol metabolism and ethanol distribution change with age, and an elderly person's liver is more susceptible to the toxic effect of ethanol, the spectrum of alcoholic liver diseases and their symptoms and signs is similar to that seen in patients of all ages. However, prognosis of alcoholic liver disease in the elderly is poor. In addition, chronic alcohol consumption may enhance drug associated liver disease and may also act as a cofactor in other liver diseases, such as viral hepatitis and nonalcoholic fatty liver disease.
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PMID:Alcoholic liver disease in the elderly. 1792 45

The pregnancy supposes a deep change in the human physiology. Such changes can entail the appearance of diseases that secondarily affect the liver, like the hipermesis gravidica, HELLP syndrome, the cholestasis of pregnancy and the acute hepatic steatosis of the pregnancy. Within the acquired diseases, viral hepatitis are the first cause of jaundice in the pregnant. Hepatitis E can display a particularly aggressive course and also the Herpes simple virus. In relation to hepatitis C during the pregnancy, their presence does not affect the pregnancy, childbirth or perinatal health of the mother and Newborn. The main concern of the heath workers is to diminish the risk of transmission of the disease from the mother to newborn.
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PMID:[Hepatitis c and pregnancy]. 1793 34

Endoplasmic reticulum stress, initiated by protein overload or malfolding, activates a complex network of interacting and parallel responses that dampen the stress. However, when the protective response is insufficient, a set of responses leads to apoptosis. Coupled with the latter are promotion of lipid synthesis and proinflammatory responses. Evidence has been mounting for an important role of the endoplasmic reticulum (ER) stress response in the pathogenesis of chronic viral hepatitis, insulin resistance and nonalcoholic fatty liver disease, ischemia-reperfusion injury, genetic disorders of protein malfolding, and alcoholic liver disease. In the latter, a key candidate for inducing ER stress is hyperhomocysteinemia. Betaine treatment promotes removal of homocysteine and prevents ER stress, fatty liver, and apoptosis in a mouse model of alcohol-induced liver disease. With increasing interest in the potential role of ER stress in liver disease, greater understanding of pathophysiology, prevention, and treatment of liver disease is anticipated.
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PMID:Endoplasmic reticulum stress and liver injury. 1797 73


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