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) and non-alcoholic steatohepatitis (NASH) are the hepatic manifestations of the metabolic syndrome. Since the prevalence of obesity and consequently of the metabolic syndrome is steadily increasing, the different types of NAFLD are nowadays the most common cause of liver injury in North America. The development of NASH and fatty liver cirrhosis occurs after a "two-hit-theory", in which hepatic steatosis is followed by lipid peroxidation, the production of cytokines and the induction of Fas ligand. A standardized drug based therapy does not exist so far, but glitazones have emerged as a promising treatment option. However, since the disease is related to Western lifestyle, treatment should be based on prevention and changes in lifestyle.
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PMID:[Non-alcoholic fatty liver disease and non-alcoholic steatohepatitis]. 1722 7

Essential hypertension is associated with the metabolic syndrome, insulin resistance and the development of fatty liver. Fatty liver disease is a spectrum of liver diseases ranging from simple hepatic steatosis through steato-hepatitis to cirrhosis and hepatoma. The purpose of this review is to discuss the evidence for an association between essential hypertension and non-alcoholic fatty liver disease, and to consider the diagnosis and management of non-alcoholic fatty liver disease. We conclude that it is important to consider the diagnosis of fatty liver disease in hypertensive patients, to measure the liver function tests at diagnosis and not to ignore minor elevations of serum aminotransferases. Hypertensive patients with raised liver enzymes should be referred for further assessment, particularly if risk factors for progressive liver disease, such as obesity and diabetes, are present.
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PMID:Hypertension and fatty liver: guilty by association? 1727 55

Although the vast majority of heavy drinkers and individuals with obesity, insulin resistance, and the metabolic syndrome have steatosis, only a minority ever develop steatohepatitis, fibrosis, and cirrhosis. Genetic and environmental risk factors for advanced alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) seem likely to include factors that influence the severity of steatosis and oxidative stress, the cytokine milieu, the magnitude of the immune response, and/or the severity of liver fibrosis. For ALD, the dose and pattern of alcohol intake, coffee intake, and dietary and other lifestyle factors leading to obesity are the most important environmental determinants of disease risk. For NAFLD, dietary saturated fat and antioxidant intake, small bowel bacterial overgrowth, and obstructive sleep apnea syndrome may play a role. Family studies and interethnic variations in susceptibility suggest that genetic factors are important in determining disease risk. For ALD, functional polymorphisms in the ADH and ALDH alcohol metabolizing genes play a role in determining susceptibility in Oriental populations. No genetic associations with advanced NAFLD have been replicated in large studies. Preliminary data suggest that polymorphisms in the genes encoding microsomal triglyceride transfer protein, superoxide dismutase 2, the CD14 endotoxin receptor, tumor necrosis factor alpha, transforming growth factor beta, and angiotensinogen may be associated with steatohepatitis or hepatic fibrosis or both.
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PMID:Genetics of alcoholic liver disease and nonalcoholic fatty liver disease. 1729 76

Non-alcoholic fatty liver disease has been associated with metabolic disorders, including central obesity, dyslipidemia, hypertension and hyperglycemia. Metabolic syndrome, obesity, and insulin resistance are major risk factors in the pathogenesis of non-alcoholic fatty liver disease. Non-alcoholic fatty liver disease refers to a wide spectrum of liver damage, ranging from simple steatosis to non-alcoholic steatohepatitis, advanced fibrosis and cirrhosis.
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PMID:Non-alcoholic fatty liver disease: further expression of the metabolic syndrome. 1729 57

More than 20% of Americans have nonalcoholic fatty liver disease (NAFLD), and this is, by far, the leading cause of abnormal liver enzymes in the United States. Nonalcoholic steatohepatitis (NASH), a more serious form of NAFLD, can proceed to cirrhosis and even hepatocellular carcinoma. These liver diseases represent the hepatic component of the metabolic syndrome, and this spectrum of liver disease represents a major health problem both in the United States and worldwide. Hepatic steatosis is closely linked to nutrition, including obesity, possibly high-fructose corn syrup consumption and consumption of certain types of fats. There are a variety of second insults or "hits" that appear to transform simple steatosis into NASH, with some of these second hits including certain proinflammatory cytokines, oxidative stress and possibly industrial toxins. In certain underdeveloped countries, it appears likely that industrial toxins play a role in NASH, and there is increasing interest in the potential interaction of industrial toxins and nutrients. Moreover, optimal therapy for NAFLD appears to include lifestyle modification with exercise, diet and weight loss. Certain nutrients may also be of benefit. Important areas for future research are the effect(s) of nutritional supplements on NAFLD/NASH and the effects of industrial toxins.
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PMID:Nonalcoholic fatty liver disease: predisposing factors and the role of nutrition. 1729 92

Hepatic iron overload conditions can be classified as genetic, mainly related to HFE haemochromatosis, and secondary, mainly associated with haematological and hepatic disorders and with metabolic syndrome. The strict affirmation of iron excess relies upon liver biopsy, MRI or calculation of the amount of iron removed through phlebotomies. Determination of its cause relies upon the assessment of transferrin saturation which, when increased, suggests the diagnosis of either haemochromatosis--implying HFE testing--or overload secondary to dysmyelopoiesis or to end-stage cirrhosis, and, when normal, suggests the diagnosis of dysmetabolic iron overload syndrome.
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PMID:[Diagnosis of iron overload]. 1741 48

There are limited data on nonalcoholic fatty liver disease (NAFLD) from India. The clinicopathological profile of Indian patients with NAFLD may be different from that of Western patients. One hundred NAFLD patients with increased liver enzymes were prospectively evaluated for clinical presentation, associated diseases, overweight/obesity, central obesity (n=54), presence of diabetes mellitus, lipid abnormalities, insulin resistance (n=39), metabolic syndrome (n=54), serum iron, serum ferritin, and transferrin saturation (n=60), and HFE gene mutations (n=30). Risk factors for the grade and stage of the disease on histology were studied in 38 biopsy-proven patients. Patients were treated with lifestyle modifications and ursodeoxycholic acid (UDCA). Seventeen nonresponder patients were treated with metformin. The majority of patients were males (n=70). Twenty percent of patients were overweight, 68% had obesity, and 78% had central obesity. Abnormal cholesterol, HDL, and triglycerides were present in 36%, 66%, and 53% of patients, respectively. Twelve percent of patients had diabetes mellitus and 16% patients had various associated diseases. All 22 (100%) patients studied by ITT and all but 1 (98%) studied by HOMA-IR were found to have reduced insulin sensitivity and 50% were found to have metabolic syndrome by the modified ATP III criteria. Two (3%) patients were found to have high serum iron, 4 (7%) patients had high ferritin, 5 (8%) patients had increased transferrin saturation, and 4 (13%) patients were found to be heterozygotes for H63D HFE gene mutation. Twenty patients of 38 (53%) had histological evidence of NASH (class 3=6, class 4=14). The other 18 (47%) qualified for class I (n=1) or class II (n=17) NAFLD. Four (10.5%) patients had bridging fibrosis and none had evidence of cirrhosis liver. Seventy-four (74%) patients achieved a biochemical response to lifestyle modification and UDCA. All 17 patients treated with metformin had a reduction in ALT level and 10 (59%) of them had normalization of their enzymes. We conclude that the clinicopathological profile of NAFLD in Indian patients is different from that in the West.
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PMID:The clinicopathological profile of Indian patients with nonalcoholic fatty liver disease (NAFLD) is different from that in the West. 1742 Sep 51

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the US, and obesity is the most common cause of NAFLD. Obesity and NAFLD are associated with hyperlipidemia, type 2 diabetes, and hypertension, all components of the metabolic syndrome. The purpose of this study was to examine the incidence of NAFLD among morbidly obese patients undergoing bariatric surgery and to determine if advanced liver disease can be predicted by demographics, comorbidities, and/or preoperative biochemical profiles. 135 nonconsecutive patients (109 female, average age 46) with mean body mass index (BMI) 50 (SD 7.6) who underwent liver biopsies during bariatric surgery were studied. Patient data including age, BMI, comorbidities, and preoperative liver function tests were analyzed against liver biopsy pathology. 86% of patients had abnormal liver biopsy results. 60% of patients had steatosis, and 27% had advanced liver disease (7% steatohepatitis, 16% fibrosis, and 4% cirrhosis). Patients were grouped according to liver biopsy pathology. Group A included patients with normal results and steatosis only. Group B included those patients with advanced liver disease:steatohepatitis, fibrosis, and cirrhosis. Of 37 patients in group B, 27% had abnormal preoperative liver function tests (LFTs) compared to 10% of patients in group A (p = 0.022). Patients in group B were more likely to have preoperative hyperlipidemia (p = 0.020) and were also found to have a significantly higher BMI (p = 0.042). Diabetes mellitus, male gender, and age were not predictive of advanced liver disease on liver biopsy, with p = 0.056, p = 0.074, p = 0.26, respectively. Liver disease is common in the morbidly obese. More than one quarter of morbidly obese patients undergoing bariatric surgery have advanced liver disease. Patients with increased preoperative LFTs, hyperlipidemia, and increased BMI are more likely to have non-alcoholic steatohepatitis, fibrosis, or cirrhosis on liver biopsy during weight loss surgery. Diabetes, male gender, and age did not predict advanced liver disease.
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PMID:Laparoscopic bariatric surgery: what else are we uncovering? Liver pathology and preoperative indicators of advanced liver disease in morbidly obese patients. 1747 22

The risk factors and settings for non-alcoholic fatty liver disease (NAFLD) in Asians are reviewed comprehensively. Based particularly on large community-based studies using ultrasonography, case-control series and prospective longitudinal studies, the prevalence of NAFLD in Asia is between 12% and 24%, depending on age, gender, locality and ethnicity. Further, the prevalence in China and Japan has nearly doubled in the last 10-15 years. A detailed analysis of these data shows that NAFLD risk factors for Asians resemble those in the West for age at presentation, prevalence of type 2 diabetes mellitus (T2DM) and hyperlipidemia. The apparent differences in prevalence of central obesity and overall obesity are related to criteria used to define waist circumference and body mass index (BMI), respectively. The strongest associations are with components of the metabolic syndrome, particularly the combined presence of central obesity and obesity. Non-alcoholic fatty liver disease appears to be associated with long-standing insulin resistance and likely represents the hepatic manifestation of metabolic syndrome. Not surprisingly therefore, Asians with NAFLD are at high risk of developing diabetes and cardiovascular disease. Conversely, metabolic syndrome may precede the diagnosis of NAFLD. The increasing prevalence of obesity, coupled with T2DM, dyslipidemia, hypertension and ultimately metabolic syndrome puts more than half the world's population at risk of developing NAFLD/non-alcoholic steatohepatitis/cirrhosis in the coming decades. Public health initiatives are clearly imperative to halt or reverse the global 'diabesity' pandemic, the underlying basis of NAFLD and metabolic syndrome. In addition, a perspective of NAFLD beyond its hepatic consequences is now warranted; this needs to be considered in relation to management guidelines for affected individuals.
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PMID:What are the risk factors and settings for non-alcoholic fatty liver disease in Asia-Pacific? 1756 27

Nonalcoholic fatty liver disease represents a spectrum of histopathologic abnormalities, the prevalence of which may be as high as 24% of the population of the United States. Nonalcoholic fatty liver disease will play a major role in the science and practice of gastroenterology in the near future. The fundamental derangement in nonalcoholic fatty liver disease is insulin resistance, a key component of the metabolic syndrome, which includes type 2 diabetes mellitus, hypertriglyceridemia, essential hypertension, low circulating high-density lipoprotein, and obesity. The natural history of fatty liver disease is not always benign, and causality for cirrhosis and chronic liver disease is well-founded in the literature. Treatment strategies are limited and, at present, are primarily focused on weight loss and use of insulin sensitizing agents, including the thiazolidenediones. Recent data clearly implicate hepatic insulin resistance as a culprit in accumulation of free fatty acids as triglycerides in hepatocytes. Hepatic insulin resistance is clearly exacerbated by systemic insulin resistance and impaired handling by skeletal muscle and adipose tissue of both glucose and free fatty acids. The key consequence of hepatic insulin resistance, impaired hepatocyte insulin signal transduction, results in adverse cellular and molecular changes exacerbating hepatocyte triglyceride storage. Cytokines secreted by white adipose tissue, adipokines, have emerged as key players in glucose and fat metabolism previously thought controlled largely by insulin. Modulation of adipokines may aid in further understanding of the pathophysiology and treatment of nonalcoholic fatty liver disease.
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PMID:Abnormal lipid and glucose metabolism in obesity: implications for nonalcoholic fatty liver disease. 1749 12


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