Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease associated with insulin resistance, obesity and type 2 diabetes. Excessive accumulation of triglycerides (TG) is a hallmark of NAFLD and therefore, a better understanding of the steps involved in regulating hepatic TG synthesis might yield novel information regarding the prevention and treatment of NAFLD. In the recent years, the transcription factor ChRepsilonBP has emerged as a major mediator of glucose action on lipogenic genes and as a key determinant of lipid synthesis in vitro. More importantly, this factor has been described to play a central role in hepatic steatosis and insulin resistance physiopathology. Although its implication in human disease has not yet been demonstrated, ChRepsilonBP could be an interesting therapeutic target against metabolic syndrome components.
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PMID:[Can the hyperactivity of lipogenesis cause hepatic steatosis? A role for ChREBP]. 1895 May 80

Nonalcoholic fatty liver disease (NAFLD) is an increasingly recognized cause of liver disease in the United States and worldwide. With obesity being an important risk factor universally, NAFLD is now receiving greater attention and is regarded as a public health issue. In addition, as a result of an aging population and the improving control of other major causes of chronic liver disease, such as hepatitis C and hepatitis B, the burden of NAFLD is expected to increase in years to come. Prevalence estimates of this disease vary widely across populations because of differences in methods for diagnosis and/or definition. New strategies for the prevention, diagnosis, and management will be required to alter the course of this disease.
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PMID:The epidemiology of nonalcoholic fatty liver disease: a global perspective. 1895 90

Hepatic fibrosis is an integral part in the progression of chronic liver disease, ultimately leading to cirrhosis and hepatocellular carcinoma. Globally, alcohol consumption, hepatitis B (HBV) and hepatitis C (HCV) have been the main causes of cirrhosis. More recently, the increasing prevalence of obesity and the metabolic syndrome has resulted in increasing incidence of cirrhosis secondary to nonalcoholic fatty liver disease (NAFLD), especially in developed countries. Chronic liver disease and cirrhosis are important causes of morbidity and mortality in the world. Moreover, the burden of chronic liver disease is projected to increase, due in part to the increasing prevalence of end-stage liver disease and HCC secondary to NAFLD and HCV.
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PMID:The global impact of hepatic fibrosis and end-stage liver disease. 1898 63

It is well established that the consumption of alcohol is implicated in both the cause and progression of chronic liver disease. The quantity of drink that is consumed, the pattern of drinking and type of alcoholic beverages consumed are all possible factors in disease aetiology. The impact of specific dietary components on the cause and progression of chronic liver disease is unclear although it is known that obesity, and hence the over-consumption of energy, is a predictor of fatty liver. Work to elucidate the role of both diet and alcohol in the aetiology of liver disease is hindered by the methods currently available to measure dietary (including alcohol) intake. The validity and reliability of retrospective methods of assessing diet are limited by their reliance on memory and, for the 24 h recall, the short-time period of intake assessed and its inability to assess variability across the week. Prospective methods which measure food and drink intake at the time of consumption, and include weighed or estimated food diaries, are useful for prospective cohort studies but are expensive and have a high respondent burden. For estimation of alcohol intake retrospectively, the Cognitive Lifetime Drinking questionnaire, which prompts responses using a lifetime calendar, is a useful tool but still depends on memory. More work is required to develop valid, reliable and easily administered tools for measurement of both diet and alcohol.
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PMID:Measurement of food and alcohol intake in relation to chronic liver disease. 1903 8

Minimal encephalopathy was originally associated with chronic liver disease but is increasingly associated with most other chronic diseases and particularly with diabetes and also chronic disorders in other organs: kidneys, lungs, thyroid and with obesity. It is increasingly with dramatically increased and more or less permanent increase in systemic inflammation, most likely a result of Western lifestyle. Frequent physical exercise and intake of foods rich in vitamins, antioxidants, fibres, lactic acid bacteria etc in combination with reduction in intake of refined and processed foods is known to reduce systemic inflammation and prevent chronic diseases. Some lactic acid bacteria, especially Lb paracasei, lb plantarum and pediococcus pentosaceus have proven effective to reduce inflammation and eliminate encephalopathy. Significant reduction in blood ammonia levels and endotoxin levels were reported in parallel to improvement of liver disease. Subsequent studies with other lactic acid bacteria seem to demonstrate suppression of inflammation and in one study also evidence of clinical improvement.
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PMID:Bio-ecological control of chronic liver disease and encephalopathy. 1910 22

About 30% of patients with cirrhosis have diabetes mellitus (DM). Nowadays, it is a matter for debate whether type 2 DM in the absence of obesity and hypertriglyceridemia may be a risk factor for chronic liver disease. DM, which develops as a complication of cirrhosis, is known as "hepatogenous diabetes". Insulin resistance in muscular and adipose tissues and hyperinsulinemia seem to be the pathophysiologic bases of diabetes in liver disease. An impaired response of the islet beta-cells of the pancreas and hepatic insulin resistance are also contributory factors. Non-alcoholic fatty liver disease, alcoholic cirrhosis, chronic hepatitis C (CHC) and hemochromatosis are more frequently associated with DM. Insulin resistance increases the failure of the response to treatment in patients with CHC and enhances progression of fibrosis. DM in cirrhotic patients may be subclinical. Hepatogenous diabetes is clinically different from that of type 2 DM, since it is less frequently associated with microangiopathy and patients more frequently suffer complications of cirrhosis. DM increases the mortality of cirrhotic patients. Treatment of the diabetes is complex due to liver damage and hepatotoxicity of oral hypoglycemic drugs. This manuscript will review evidence that exists in relation to: type 2 DM alone or as part of the metabolic syndrome in the development of liver disease; factors involved in the genesis of hepatogenous diabetes; the impact of DM on the clinical outcome of liver disease; the management of DM in cirrhotic patients and the role of DM as a risk factor for the occurrence and exacerbation of hepatocellular carcinoma.
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PMID:Liver cirrhosis and diabetes: risk factors, pathophysiology, clinical implications and management. 1914 Feb 27

Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in developed countries and is increasing in prevalence with the rise of diabetes and obesity. In addition to obesity and age, gender may also influence the prevalence and severity of NAFLD. However, mechanisms underlying gender-based differences in NAFLD have not been clearly defined. Furthermore, alterations in body composition, fat distribution and/or hormonal or metabolic changes that occur following menopause and in the setting of polycystic ovary syndrome may influence the development and progression of NAFLD. In this article, we will summarize known gender differences as well as the proposed mechanisms for gender differences in NAFLD, review two women-specific issues that may influence the prevalence and severity of NAFLD, menopause and polycystic ovary syndrome, and discuss potential therapeutic options for women with NAFLD who are postmenopausal or have polycystic ovary syndrome.
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PMID:Nonalcoholic fatty liver disease in women. 1924 56

Hepatitis C virus (HCV) infection is a major cause of chronic liver disease and can lead to hepatocellular carcinoma and end-stage liver disease. The current FDA-approved treatment for HCV (pegylated interferon-alpha (IFNalpha) with ribavirin) is effective in only about 50% of patients. Epidemiological evidence suggests that obesity, alcohol, smoking, and environmental pollutants may contribute to resistance to IFNalpha therapy in HCV. Acrolein, a ubiquitous environmental pollutant and major component of cigarette smoke, is also generated endogenously by cellular metabolism and lipid peroxidation. This study examines the effects of acrolein on (i) IFNalpha-mediated signaling and antiviral gene expression in cultured and primary human hepatocytes and (ii) HCV replication in an HCV-replicon system. Our data demonstrate that nontoxic concentrations of acrolein significantly inhibited IFNalpha-induced tyrosine phosphorylation of both cytoplasmic and nuclear STAT1 and STAT2, without altering the total levels. Also, acrolein down-regulated IFNalpha-stimulated gene transcription, resulting in reduced expression of antiviral genes. Importantly, acrolein abolished the IFNalpha-mediated down-regulation of HCV viral expression in the HCV-replicon system. This study defines mechanisms involved in resistance to IFNalpha and identifies the pathogenic role of acrolein, and potentially other environmental pollutants, in suppressing IFNalpha antiviral activity and establishes their adverse impact on HCV therapy.
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PMID:Acrolein, a ubiquitous pollutant and lipid hydroperoxide product, inhibits antiviral activity of interferon-alpha: relevance to hepatitis C. 1934 60

Liver dysfunction is a prominent entity in Western medicine that has historically affected patients suffering from chronic viral or alcoholic hepatitis. The incidence of these conditions has not changed dramatically in recent years but the overall number of patients with liver dysfunction has increased considerably with the emergence of the obesity epidemic. Nonalcoholic fatty liver disease (NAFLD) has become increasingly recognized as the most common cause of chronic liver disease in the United States. Although the rate of progression of NAFLD to overt cirrhosis is low, the high prevalence of this condition, combined with the moderate degree of liver dysfunction it engenders, has resulted in a significant increase in the number of patients with liver disease that can be encountered by a surgical practice. Any degree of clinically evident liver disease in a prospective surgical patient should raise concern for the entire surgical team. This particularly applies to intraabdominal surgery whereby the presence of hepatomegaly, portal hypertension, variceal bleeding, and ascites can turn even the most routine operation into a morbid and life-threatening procedure. Nonabdominal surgery avoids some of the technical challenges presented by liver disease but the anesthetic management of a cirrhotic patient still makes any operation potentially more dangerous. In this article, approaches to minimize the risk when surgery becomes necessary in the presence of liver disease are discussed.
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PMID:Surgery in the patient with liver disease. 1994 76

Obesity appears to be a risk factor for hepatic steatosis, which has been implicated in the development of hepatic fibrosis in patients with hepatitis C virus infection. We conducted the current study to examine whether obesity is associated with hepatic steatosis among patients with chronic hepatitis C identified from a population-based cohort. Study participants were persons with chronic hepatitis C who had had a liver biopsy, identified from a population-based study of persons with newly identified chronic liver disease conducted in gastroenterology practices. Data were collected through patient interviews, medical record abstraction, and review of previously performed liver biopsies. The outcome variable of interest was significant steatosis, defined as steatosis grade > or =2 determined from liver biopsy samples. Univariate and multivariate analyses were performed using logistic regression techniques. The analysis included 450 patients with chronic hepatitis C with available liver biopsy slides. Overall, only 15.8% of subjects had significant hepatic steatosis (grade > or =2), while 35.9% of obese subjects had significant steatosis. In multivariate analysis, significant fibrosis (defined as > or = grade 2) (odds ratio [OR], 3.43; 95% confidence interval [CI], 1.59-7.37), obesity (OR, 3.32; 95% CI, 1.84-5.98), genotype 3 (OR, 2.5; 95% CI, 1.09-5.75), and the presence of multiple metabolic comorbidities (OR, 1.91; 95% CI, 0.88-4.11) were independently associated with steatosis. In this unique United States cohort of patients with newly diagnosed chronic liver disease due to hepatitis C, obesity was independently associated with hepatic steatosis. The results of this study provide additional evidence that obesity worsens liver damage in patients with chronic hepatitis C, and suggest a role for weight loss as a treatment modality in these patients.
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PMID:Prevalence and predictors of hepatic steatosis in adults with newly diagnosed chronic liver disease due to hepatitis C. 1974 89


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