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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the absence of significant research, we performed a prospective study to examine the association between nonalcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD). The study cohort comprised a total of 8329 healthy men, with normal baseline kidney functions and no proteinuria, working in a semiconductor manufacturing company and its 13 affiliates. Alcohol intake was assessed with a self-reported questionnaire. Biochemical tests for liver and metabolic function and abdominal ultrasonography were done. Chronic kidney disease was defined as either the presence of proteinuria or a glomerular filtration rate (GFR) of <60 mL/min per 1.73 m(2). Cox proportional hazards model was used to estimate hazard ratios in the model for CKD. During 26717.1 person-years of follow-up, 324 men developed CKD. Nonalcoholic fatty liver disease was associated with the development of CKD (crude relative risk, 2.18; 95% confidence interval [CI], 1.75-2.71); and this relationship remained significant even after adjustment for age, GFR, triglyceride, and high-density lipoprotein cholesterol (adjusted relative risk [aRR], 1.55; 95% CI, 1.23-1.95). The association between NAFLD and incident CKD was evident in the NAFLD group with elevated serum gamma-glutamyltransferase (GGT) (aRR, 2.31; 95% CI, 1.53-3.50), even after adjustment for age, GFR, triglyceride, and high-density lipoprotein cholesterol, but not in the NAFLD group without elevated GGT (aRR, 1.09; 95% CI, 0.79-1.50) (P = .008 for interaction). To summarize, NAFLD with elevated GGT concentration was associated with an increased CKD risk among nondiabetic, nonhypertensive Korean men, irrespective of metabolic syndrome.
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PMID:Nonalcoholic fatty liver disease predicts chronic kidney disease in nonhypertensive and nondiabetic Korean men. 1832 62

Obesity has become epidemic in the United States, in Europe, and in many urban areas in the developing world. The globalization of certain 'fast foods' and 'soft drinks' may, in part, be contributing to this epidemic. Diets high in saturated fatty acids and trans fats as well as drinks that have high fructose corn syrup levels may be particularly harmful. Recent research suggests that fat is a dynamic endocrine organ and that visceral fat is associated with the metabolic syndrome. Central obesity leads to organ steatosis and altered serum adipokines including reduced adiponectin and markedly elevated leptin. This abnormal adipokine milieu results in increased tissue infiltration of monocytes and macrophages which produce proinflammatory cytokines that alter organ function. Over many years, the combination of steatosis and local inflammation leads to fibrosis and eventually to cancer. Nonalcoholic fatty liver disease (NAFLD) is a precursor for nonalcoholic steatohepatitis (NASH). NAFLD and NASH (1) lead to cirrhosis and hepatocellular carcinoma, (2) increase the risk of liver resection, and (3) compromise the outcome of liver transplantation. Similarly, in the pancreas nonalcoholic fatty pancreas disease (NAFPD) may lead to nonalcoholic steatopancreatitis (NASP). NAFPD and NASP may (1) promote the development of chronic pancreatitis and pancreatic cancer, (2) exacerbate the severity of acute pancreatitis, and (3) increase the risk of pancreatic surgery. In the gallbladder nonalcoholic fatty gallbladder disease (NAFGBD, cholecystosteatosis) may lead to steatocholecystitis. Cholecystosteatosis may be an explanation for (1) the increased incidence of chronic acalculous cholecystitis and (2) the increased number of cholecystectomies.
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PMID:Hepato-pancreato-biliary fat: the good, the bad and the ugly. 1833 22

Nonalcoholic fatty liver disease (NAFLD) is a growing problem that is associated with the metabolic syndrome. The goal of the present study was to evaluate for ethnic differences in NAFLD and clinical correlates of NAFLD. The study population consisted of 567 patients seen at an urban obesity clinic. Elevated aminotransferase levels were used as a surrogate marker for NAFLD. The prevalence of elevated aminotransferases was highest in Hispanics (39%), followed by Caucasians (28%), and African Americans (12%). In univariate analysis, elevated aminotransferase levels were associated with ethnicity (Hispanic > African American, P < 0.001, and Caucasian > African American P = 0.030), hypertriglyceridemia (P < 0.001), and male gender (P < 0.001). The pattern of results was confirmed in multivariate analysis, except that the differences between Caucasians and African Americans was no longer significant. In conclusion, in an obesity clinic population, elevated aminotransferase levels and hypertriglyceridemia were most common in Hispanics and least common in African Americans.
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PMID:Ethnicity and nonalcoholic fatty liver disease in an obesity clinic: the impact of triglycerides. 1834 82

Nonalcoholic fatty liver disease (NAFLD), hypertriglyceridemia, and elevated free fatty acids are present in the majority of patients with metabolic syndrome and type 2 diabetes mellitus and are strongly associated with hepatic insulin resistance. In the current study, we tested the hypothesis that an increased rate of fatty acid oxidation in liver would prevent the potentially harmful effects of fatty acid elevation, including hepatic triglyceride (TG) accumulation and elevated TG secretion. Primary rat hepatocytes were transduced with adenovirus encoding carnitine palmitoyltransferase 1a (Adv-CPT-1a) or control adenoviruses encoding either beta-galactosidase (Adv-beta-gal) or carnitine palmitoyltransferase 2 (Adv-CPT-2). Overexpression of CPT-1a increased the rate of beta-oxidation and ketogenesis by approximately 70%, whereas esterification of exogenous fatty acids and de novo lipogenesis were unchanged. Importantly, CPT-1a overexpression was accompanied by a 35% reduction in TG accumulation and a 60% decrease in TG secretion by hepatocytes. There were no changes in secretion of apolipoprotein B (apoB), suggesting the synthesis of smaller, less atherogenic VLDL particles. To evaluate the effect of increasing hepatic CPT-1a activity in vivo, we injected lean or obese male rats with Adv-CPT-1a, Adv-beta-gal, or Adv-CPT-2. Hepatic CPT-1a activity was increased by approximately 46%, and the rate of fatty acid oxidation was increased by approximately 44% in lean and approximately 36% in obese CPT-1a-overexpressing animals compared with Adv-CPT-2- or Adv-beta-gal-treated rats. Similar to observations in vitro, liver TG content was reduced by approximately 37% (lean) and approximately 69% (obese) by this in vivo intervention. We conclude that a moderate stimulation of fatty acid oxidation achieved by an increase in CPT-1a activity is sufficient to substantially reduce hepatic TG accumulation both in vitro and in vivo. Therefore, interventions that increase CPT-1a activity could have potential benefits in the treatment of NAFLD.
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PMID:A moderate increase in carnitine palmitoyltransferase 1a activity is sufficient to substantially reduce hepatic triglyceride levels. 1834 15

Nonalcoholic fatty liver disease (NAFLD) is closely associated with several metabolic syndrome features, including obesity, dyslipidemia, insulin resistance, and increased cardiovascular risk. The present study was undertaken to assess whether NAFLD in children is associated with increased carotid artery intima-media thickness (IMT), a marker of early-generalized atherosclerosis. We analyzed carotid IMT along with serum triglycerides, total, low-density lipoprotein and high-density lipoprotein cholesterol, glucose, insulin, insulin resistance index (as homeostasis model assessment of insulin resistance), aminotransferases, leptin, and adiponectin in 29 obese children with NAFLD, 33 obese children without liver involvement, and 30 control children. The diagnosis and severity of NAFLD was based on ultrasound scan, after exclusion of infectious and metabolic disorders. Obese children with NAFLD had significantly increased carotid IMT [mean 0.58 (95% confidence intervals 0.54-0.62 mm)] than obese children without liver involvement [0.49 (0.46-0.52) mm; p = 0.001] and control children [0.40 (0.36-0.43) mm; p < 0.0005]. In a stepwise multiple regression model, after adjusting for age, gender, Tanner stage, and cardiovascular risk factors, the severity of fatty liver was significantly associated with maximum IMT (b = 0.08; p < 0.0005). Our results suggest that NAFLD is strongly associated with carotid atherosclerosis even in childhood.
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PMID:Nonalcoholic fatty liver disease and carotid atherosclerosis in children. 1835 51

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

Nonalcoholic fatty liver disease (NAFLD) is a major form of chronic liver disease in adults and children. It is one of the consequences of the current obesity epidemic, and can progress to nonalcoholic steatohepatitis (NASH), characterized by steatosis, inflammation, and progressive fibrosis, ultimately leading to cirrhosis and end-stage liver disease. The factors implicated in this progression are poorly understood. NASH is closely associated with obesity and the metabolic syndrome. Recent studies emphasize the role of insulin resistance, oxidative stress, lipid peroxidation, and cytokine release in the development of NASH. This review summarizes the current knowledge on the etiology and pathomechanism of NASH and the role of the metabolic syndrome in NASH development.
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PMID:Nonalcoholic steatohepatitis and the metabolic syndrome. 1837 Aug 30

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

Nonalcoholic fatty liver disease (NAFLD) is an important cause of liver-related morbidity and mortality. The association between NAFLD and the metabolic syndrome is well established: the presence of the metabolic syndrome signifies advanced histology in NAFLD patients. Emerging data indicate that patients with NAFLD have a significantly higher prevalence of cardiovascular disease. This article reviews the definitions of the two syndromes, their association, and the cardiovascular risk conferred by both when they occur separately and together. This review also discusses management options for the syndromes, including treating the individual components of the metabolic syndrome in NAFLD patients.
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PMID:Nonalcoholic fatty liver disease as a component of the metabolic syndrome. 1841 46

Non-alcoholic steatohepatitis (NASH) is a hepatic manifestation of the metabolic syndrome that can progress to liver cirrhosis. The major aim of this study was to establish a novel NASH mouse model accompanied by obesity and insulin resistance, then explore the molecular mechanisms of NASH and evaluate the effects of both the peroxisome proliferator-activated receptor alpha (PPARalpha) agonist fenofibrate and the PPARgamma agonist rosiglitazone in this established NASH model. The novel model was induced in C57BL/6 mice by 23 weeks of ad libitum feeding of a modified high-fat diet (mHFD), with lower methinione and choline and higher fat content. In comparison to the controls, the model animals developed pronounced obesity, dyslipidemia and insulin resistance. Marked liver lesions characterized by severe steatosis, inflammation, fibrosis, increased hepatic triglyceride content, and elevated serum alanine aminotransferase (ALT) levels were observed in the models. In this novel model, treatment with fenofibrate or rosiglitazone significantly improved insulin sensitivity and corrected dyslipidemia; however, fenofibrate was more effective than rosiglitazone in improving hepatic morphology and ALT levels. Further study showed that long-term feeding of mHFD significantly increased expression of mRNA for hepatic PPARgamma, adipose fatty acid binding protein (ap2) and CD36 and suppressed expression of mRNA for hepatic PPARalpha and carnitine palmitoyl transferase-1a (CPT-1a). These results showed the successful establishment of the combined NASH and obese-insulin resistance mouse model. Additionally, aberrant expressions of hepatic PPARalpha and PPARgamma may play a major role in the pathogenesis of NASH by affecting hepatic lipogenesis and fatty acid oxidation in this novel model.
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PMID:The establishment of a novel non-alcoholic steatohepatitis model accompanied with obesity and insulin resistance in mice. 1841 55


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