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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-alcoholic steatohepatitis (NASH), the metabolic syndrome of the liver, characterised by the consequences of obesity (insulin resistance, production of free radicals, chronic inflammation) has become a new epidemic in the United States as in Europe. Diagnosis is suspected in patients with obesity, denying alcohol abuse, having typical co-morbitities (Hypertension, Diabetes mellitus, Hyperlipidemia). Liver histology confirms the diagnosis of NASH. Fatty liver without inflammation bears a good prognosis. Liver fibrosis, however, in NASH patients signalizes progression to liver cirrhosis and even HCC. Treatment modalities are limited. Reduction of body weight, physical activity, treatment of co-morbitities, specially Hypertension and Diabetes are of paramount importance. At the moment it remains unclear whether glitazone treatment could be introduced in the therapeutic armentarium.
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PMID:[Non-alcoholic steatohepatitis--a new epidemic]. 1806 58

Nonalcoholic fatty liver disease (NAFLD) is systematically associated with insulin resistance and the metabolic syndrome, where behavior therapy remains the primary treatment, simultaneously addressing all the clinical and biochemical defects. However, very few studies have tested the effectiveness of intensive behavior therapy in NAFLD, aimed at lifestyle modifications to produce stable weight loss by reduced calorie intake and increased physical activity. Searching the literature for studies testing weight loss and lifestyle modifications for the treatment of NAFLD, only 14 reports were traced where the entry assessment satisfied well-defined criteria. The final effectiveness was based on hard histological outcomes in 5 cases. All but 1 were pilot, uncontrolled studies or limited case series, and in general the details of treatment were scanty. In only 3 cases treatment was carried out along the guidelines of behavior treatment to reduce excess nutrition and increase exercise; in these cases, a remarkable effect on weight loss and an improvement in liver histology were reported. The principles of behavior therapy are presented in detail, to help physicians change their prescriptive attitude into a more empowerment-based approach. A brief section is also included on the practical aspects and public policies to be implemented at societal level to obtain the maximum effects in lifestyle changes. There is a need for multidisciplinary teams including dietitians, psychologists, and physical activity supervisors caring for patients with NAFLD. Alternatively, general practitioners and physicians working in gastrointestinal units should limit their intervention to engage patients with NAFLD before referral to specialized teams set up for the treatment of diabetes and obesity.
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PMID:Behavior therapy for nonalcoholic fatty liver disease: The need for a multidisciplinary approach. 1809 21

Raised liver enzymes are common in type 2 diabetes (T2DM) but often considered benign. Non-alcoholic fatty liver was the cause in 65% of cases but other causes included alcoholic liver disease and viral hepatitis. Cirrhosis was identified in 11 patients. There is a significant burden of advanced liver diseases from a variety of aetiologies in patients with T2DM.
Diabetes Res Clin Pract 2008 Apr
PMID:Should patients with type 2 diabetes and raised liver enzymes be referred for further evaluation of liver disease? 1818 26

Nonalcoholic fatty liver disease (NAFLD) is a group of diseases with excess fat in liver in the absence of a poorly defined limit of alcohol consumption. Most common variety, a universal public health problem, is associated with insulin resistance caused by a host of genetic and epigenetic defects modulated by life style and environmental factors. In fact the term NAFLD is loose to incorporate so many etiologies except alcoholism and few other etiologies, presenting as fat in liver. However as a sign fatty liver is very important in predicting the risk of diabetes, cardiovascular disease, stroke, cirrhosis and cancer. Abnormal fat accumulation can result from several defects in nuclear receptors associated with lipid sensing, synthesis and oxidation like LXR, FXR, SREBP, ChREBP and PPAR; defects in the lipid influx-efflux channels, insulin signaling, proteins involved in fatty acid catabolism, defects in adipose tissue development and function, inappropriate nutrition and finally defects in neural regulatory mechanisms. The progress of the disease is determined by the basic defects which results in fat accumulation, an individual's immunological response to the accumulated fat and its derivatives and the oxidant stress response. Congregation of unrelated genetic defects under same diagnosis 'NAFLD' can result in inefficient patient management. Further studies are required to understand the molecular basis of fatty liver to enable a personalized management of diseases presenting as fatty liver in the absence of alcohol abuse.
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PMID:The blind men 'see' the elephant-the many faces of fatty liver disease. 1824 Mar 40

Non-alcoholic fatty liver disease (NAFLD) is now the commonest liver disorder in the developed world affecting up to a third of individuals. It is closely associated with features of the metabolic syndrome, particularly obesity and diabetes. It can progress to cirrhosis, hepatocellular carcinoma and liver failure and is an increasing indication for transplantation. Dietary and genetic factors determine susceptibility to NAFLD and its progression. NAFLD may also be involved in the pathogenesis of cardiovascular disease. Most patients present with incidentally found abnormal liver blood tests. Diagnosis is usually one of exclusion. Liver biopsy is required for disease staging, but new imaging modalities and biomarkers are emerging which may eventually fulfil this role. There is, as yet no firm evidence-based treatment for NAFLD. Therapy is currently directed at treating components of the metabolic syndrome which may also be beneficial for the liver. The recent elucidation of the mechanisms leading to progressive disease suggests a variety of novel targets worthy of testing in animal models of NAFLD and subsequently in pilot studies in humans.
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PMID:Non-alcoholic fatty liver disease: the mist gradually clears. 1830 79

Recent studies have shown that dietary phospholipids, especially phosphatidylcholine and phosphatidylserine, have various beneficial biological effects. However, there are not enough data concerning the physiological function of dietary phosphatidylinositol (PI). The metabolic syndrome, a cluster of metabolic abnormalities such as dyslipidemia, diabetes mellitus, and hypertension, is a widespread and increasingly prevalent disease in industrialized countries. Nonalcoholic fatty liver disease (NAFLD) is often associated with features of the metabolic syndrome. NAFLD describes the spectrum of liver damage ranging from hepatic steatosis to steatohepatitis, liver fibrosis, and cirrhosis, and it is emerging as the most common liver disease worldwide. The present study examined whether dietary PI protects Zucker ( fa/ fa) rats from the metabolic syndrome. For 4 weeks, rats were fed semisynthetic diets containing either 7% soybean oil or 5% soybean oil plus 2% PI. Dietary PI markedly prevented the development of hepatomegaly and hepatic steatosis and lowered hepatic injury markers in serum. Additionally, hyperinsulinemia was relieved by the feeding of dietary PI in Zucker rats. These effects were attributable to an increase in serum adiponectin, enhancement of fatty acid beta-oxidation, and suppression of mRNA expression of inflammatory genes in the liver. This is the first report that dietary PI increases serum adiponectin level and prevents the development of NAFLD in a rat model of the metabolic syndrome.
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PMID:Dietary phosphatidylinositol prevents the development of nonalcoholic fatty liver disease in Zucker (fa/fa) rats. 1832 72

Nonalcoholic fatty liver disease is an increasingly prevalent disorder that spans a range of conditions from hepatic steatosis to cirrhosis. It is commonly associated with obesity and diabetes, two components of the metabolic syndrome. Although hepatic steatosis may be reversible, disease progression appears to be triggered by overproduction of reactive oxygen species and mitochondrial injury in hepatocytes. Evolving treatments are focused on reversing insulin resistance, which underlies many of the metabolic derangements in this disease.
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PMID:Nonalcoholic fatty liver disease: diagnosis and relation to metabolic syndrome and approach to treatment. 1836 95

It is unknown whether chronic kidney disease (CKD) is associated with nonalcoholic fatty liver disease among patients with type 2 diabetes. We followed 1760 outpatients with type 2 diabetes and normal or near-normal kidney function and without overt proteinuria for 6.5 yr for the occurrence of CKD (defined as overt proteinuria and/or estimated GFR <60 ml/min per 1.73 m(2)). During follow-up, 547 participants developed incident CKD. Nonalcoholic fatty liver disease, diagnosed by liver ultrasound and exclusion of other common causes of chronic liver disease, was associated with a moderately increased risk for CKD (hazard ratio 1.69; 95% confidence interval 1.3 to 2.6; P < 0.001). Adjustments for gender, age, body mass index, waist circumference, BP, smoking, diabetes duration, glycosylated hemoglobin, lipids, baseline estimated GFR, microalbuminuria, and medications (hypoglycemic, lipid-lowering, antihypertensive, or antiplatelet drugs) did not appreciably attenuate this association (hazard ratio 1.49; 95% confidence interval 1.1 to 2.2; P < 0.01). In conclusion, our findings suggest that nonalcoholic fatty liver disease is associated with an increased incidence of CKD in individuals with type 2 diabetes, independent of numerous baseline confounding factors.
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PMID:Increased risk of CKD among type 2 diabetics with nonalcoholic fatty liver disease. 1838 24

Nonalcoholic fatty liver disease (NAFLD) is considered to be a hepatic manifestation of metabolic syndrome. The clinicopathologic spectrum ranges from simple steatosis to nonalcoholic steatohepatitis (NASH). Simple steatosis has a relatively benign clinical course, but NASH can progress to cirrhosis and hepatocellular carcinoma. As yet there is no convincingly effective treatment for NAFLD and the best option for these patients might be a multimodal treatment plan targeting obesity, insulin resistance, diabetes mellitus, hyperlipidemia and hypertension.
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PMID:[Treatment of fatty liver disease]. 1840 89

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disease in Western World and frequently associated with insulin resistance and overweight and occurs often with type 2 diabetes. Interestingly, NAFLD is not only regarded as a hepatic component of the metabolic syndrome but also as an independent risk factor and a marker for increase in cardiovascular disease (CVD). Significantly, NAFLD is associated with an increased risk of all-cause mortality and predicts future CVD events independent of age, sex, LDL-cholesterol and features of metabolic syndrome. Although there was initial concern about drug toxicity with NAFLD, increasing evidence suggests that commonly used drugs such as metformin and statins do not cause harm and the thiazolidinediones (TZDs) may even confer a therapeutic benefit in NAFLD. Interestingly, medical and surgical treatments of obesity show potential benefit in treating NAFLD. In this review, we have focused on the safety and therapeutic impact of TZDs, statins, metformins and obesity medications in NAFLD. The potential benefit of bariatric surgery and the role of weight loss per se in treating NAFLD are also discussed.
Diabetes Obes Metab 2009 Mar
PMID:Current treatment of non-alcoholic fatty liver disease. 1856 73


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