Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-alcoholic fatty liver disease (NAFLD) is associated with the metabolic syndrome characterized by dislipidemia and insulin resistance. We hypothesized that ezetimibe, an inhibitor of NPC1L1, improves these metabolic disorders in Zucker obese fatty rats (ZOF). Ezetimibe significantly lowered total cholesterol and triglycerides in ZOF with prominent reduction in the remnant lipoprotein fraction and small dense low density lipoprotein fraction. Moreover, lipid deposition and fibrosis of liver were decreased by ezetimibe. Interestingly, ezetimibe improved insulin and plasma glucose response after intraperitoneal glucose injection. Further, ezetimibe enhanced insulin signaling in cultured hepatocytes. Our results indicate the potential of ezetimibe in treating the metabolic syndrome and NAFLD.
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PMID:Ezetimibe improves liver steatosis and insulin resistance in obese rat model of metabolic syndrome. 1802 91

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 a consequence of insulin resistance encompassing a spectrum that extends from simple hepatic steatosis through to nonalcoholic steatohepatitis (NASH), a condition that may progress to cirrhosis with its associated complications. A subset of nuclear receptors act as intracellular sensors for cholesterol metabolites, free fatty acids, and a range of other lipophilic molecules with pivotal roles in energy homeostasis and inflammation. These receptors represent attractive drug targets for the management of NAFLD and NASH as well as related conditions such as type 2 diabetes and the broader metabolic syndrome. To date, human studies have concentrated on peroxisome proliferator-activated receptor (PPAR) agonists, particularly those directed at PPARgamma. However, these drugs have significant limitations, so alternate approaches to nuclear receptor targeting are being explored.
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PMID:Nonalcoholic fatty liver disease: pathogenesis and potential for nuclear receptors as therapeutic targets. 1807 23

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

Nonalcoholic fatty liver disease (NAFLD) includes hepatic steatosis, nonalcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. NAFLD is the most common liver disorder in the United States and worldwide. Due to the rapid rise of the metabolic syndrome, the prevalence of NAFLD has recently dramatically increased and will continue to increase. NAFLD has also the potential to progress to hepatocellular carcinoma (HCC) or liver failure. NAFLD is strongly linked to caloric overconsumption, physical inactivity, insulin resistance and genetic factors. Although significant progress in understanding the pathogenesis of NAFLD has been achieved in years, the primary metabolic abnormalities leading to lipid accumulation within hepatocytes has remained poorly understood. Mitochondria are critical metabolic organelles serving as "cellular power plants". Accumulating evidence indicate that hepatic mitochondrial dysfunction is crucial to the pathogenesis of NAFLD. This review is focused on the significant role of mitochondria in the development of NAFLD.
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PMID:Nonalcoholic fatty liver disease and mitochondrial dysfunction. 1818 54

Nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in the United States secondary to the growing obesity epidemic. Although most patients with NAFLD do not develop progressive liver disease, the subset of NAFLD patients with nonalcoholic steatohepatitis (NASH) are at risk for progression to cirrhosis and hepatocellular carcinoma, which necessitates appropriate follow-up and management. Unfortunately, proven treatment modalities for NASH that result in complete histopathologic regression of steatosis, inflammation, and fibrosis do not exist. Many therapeutic approaches to NAFLD management have been attempted, with varying degrees of success. However, most of these studies have been limited to small, single-center, uncontrolled trials. Based on our evolving understanding of the disease's pathogenesis, it seems logical that a multidisciplinary approach addressing the underlying metabolic syndrome and the resultant intrinsic liver injury is necessary. Diet, exercise, surgical weight loss, diabetic medications, and hepatoprotective agents all have been studied and may serve as potential weapons in our armamentarium against this disease. Although most of these approaches have been studied as single-modality therapy, we believe that combination, multimodality therapy is required to treat this disease effectively.
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PMID:Current treatments in nonalcoholic steatohepatitis. 1822 3

Non-alcoholic fatty liver disease (NAFLD) is a clinicopathological entity increasingly recognized as a major health burden in developed countries. In the last decade, several studies have independently provided evidence for a strong association between NAFLD and each component of the metabolic syndrome, including central obesity, hyperglycemia, dyslipidemia, and hypertension. This article focuses on epidemiological, clinical, pathogenic and therapeutic aspects, which link these two syndromes.
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PMID:Nonalcoholic fatty liver disease and metabolic syndrome: a concise review. 1827 97

Non-alcoholic fatty liver disease (NAFLD) has been increasingly recognized as the most common pathological conditions affecting the liver. In concert with the increase in Body Mass Index in developed countries that has occurred during the last decades, more and more individuals referred for evaluation of abnormal liver tests are found to have NAFLD. In most cases, the increase in fat within the liver is not associated with impaired liver structure or function in the long-term. However, liver steatosis should be considered to be a marker of the metabolic syndrome. A minority of patients with NAFLD develop liver cirrhosis but NAFLD is probably the most common underlying cause of cryptogenic cirrhosis. Patients with NAFLD have an increased cardiovascular mortality as well as increase in liver related complications compared with matched controls. The diagnostic evaluation of a patient with suspected NAFLD depends heavily on the setting. In whom and when a liver biopsy is indicated is controversial. An adequate history is of major importance and when alcohol is suspected to be a contributing factor to the liver steatosis, several biochemical and clinical parameters may differentiate alcoholic fatty liver and NAFLD. Unfortunately, no histological gold standard is available for non-alcoholic steatohepatitis (NASH) and there is still a significant diversity among pathologist concerning the minimal requirements for the term NASH. Management of patients with NAFLD should be aimed at fighting the metabolic risk factors such as visceral obesity, hyperglycemia, type II diabetes mellitus (DM) and hypertriglyceridemia. DM has been shown to be a predictor of worsening of fibrosis. Successful lifestyle modification with increased exercise and decreased food intake is able to remove the accumulation of liver fat and can reverse insulin resistance. Unfortunately, there are no well-controlled, randomized trials of weight control as therapy for NAFLD. Some pharmacological pilot trials have been undertaken in NAFLD, but no proved treatment for all patients with NAFLD and/or NASH is available at the current time.
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PMID:The clinical aspects of non-alcoholic fatty liver disease. 1829 64

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


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