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The role of obesity in diabetes mellitus, hyperlipidemia, colon cancer, sudden death and other cardiovascular diseases has confirmed in many recent research studies. In present study, it is hypothesized that obesity can serve as an independent risk factor for the decreased activities of cytoprotective antioxidants in humans and for the associated systemic oxidative stress. 150 age matched, female subjects with no history of smoking or biochemical evidence of diabetes mellitus, hypertension, hyperlipidemia, renal or liver disease or cancer were included in the study and were divided into different grades of obesity according to their body mass index (BMI). Hemoglobin and erythrocyte glutathione (GSH) concentrations were measured for each subject. The study suggests that increase BMI was found to be associated with a significant decrease in erythrocyte glutathione concentration. From these observations it is concluded that obesity even in the absence of smoking, diabetes mellitus, hyperlipidemia, renal or liver diseases can decrease the activities of body's protective antioxidants, and can enhance the systemic oxidative stress and should therefore receive the same attention as obesity with complications.
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PMID:Obesity: an independent risk factor for systemic oxidative stress. 1663 56

Nonalcoholic fatty liver disease (NAFLD) is a fatty liver disease occurring in patients without alcohol consumption. It includes a broad spectrum of liver disease, from fatty infiltration, inflammation and fibrosis, to cirrhosis, usually having obesity, hyperlipidemia, and diabetes mellitus as its etiology. NAFLD-related cirrhosis has rarely been reported in Taiwan. We herein report a 41-year-old male patient with nonalcoholic fatty liver cirrhosis (NAFLC), with the first clinical manifestation being bleeding esophageal varices (EV). The patient was obese with diabetes mellitus, but without hyperlipidemia or any history of drinking alcohol. The laboratory tests, abdominal sonography, and computed tomography revealed a typical case of liver cirrhosis. The pan-endoscopy disclosed EV with red-color sign. EV ligation was performed successfully to stop the bleeding. When the patient was in a stabilized clinical condition, a liver biopsy showed a typical histologic finding of NAFLD. Most of the cases of NAFLC reported in the literature have silent signs and symptoms. Sudden onset of the EV as the first clinical manifestation, as in this case, is rare. This case reminds us that NAFLD may indeed induce severe liver impairment, such as liver cirrhosis. Liver biochemical tests and abdominal sonography should be considered in patients with overt obesity and diabetes.
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PMID:Nonalcoholic fatty liver disease manifesting esophageal variceal bleeding. 1668

Tamoxifen is a cheap and effective estrogen-receptor antagonist, used as the adjuvant hormonal treatment of choice in women with estrogen-receptor-positive breast cancer. Tamoxifen-induced non-alcoholic steatohepatitis (NASH) may increase the demand on oncologists, not only with regard to screening for diabetes, but also for the suggested link of NASH with high incidence of coronary heart disease. At present, there is no guideline for treatment of hyperlipidaemia associated with tamoxifen-induced NASH. However, exemstane (and other aromatase inhibitors) has been shown to lower triglyceride and have a neutral effect on low-denisty lipoprotein and cholesterol levels. These may be alternative agents if severe progressive liver disease or hyperlipidaemia were encountered with tamoxifen administration. Other lipid-lowering medications may have potential benefits in the treatment of tamoxifen-induced NASH and is discussed in this article.
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PMID:Tamoxifen-induced non-alcoholic steatohepatitis: where are we now and where are we going? 1718 45

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

Nonalcoholic fatty liver disease (NAFLD) is now considered to be the most common liver disease in the United States and involves a spectrum of progressive histopathologic changes. Common risk factors associated with NAFLD include obesity, diabetes, and hyperlipidemia. Although most patients with NAFLD have simple hepatic steatosis, a significant number develop nonalcoholic steatohepatitis, which may progress to fibrosis, cirrhosis, or end-stage liver disease. There is increasing evidence that NAFLD is a common feature in patients with the cardiometabolic syndrome, a onstellation of metabolic, cardiovascular, renal, and inflammatory abnormalities in which insulin resistance is thought to play a key role in end-organ pathogenesis. NAFLD is usually diagnosed after abnormal liver chemistry results are found during routine laboratory testing. No therapy has been proven effective for treating NAFLD/nonalcoholic steatohepatitis. Expert opinion emphasizes the importance of exercise, weight loss in obese and overweight individuals, treatment of hyperlipidemia, and glucose control.
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PMID:Nonalcoholic steatohepatitis and the cardiometabolic syndrome. 1767 1

Steatosis of the liver may arise from a variety of conditions, but the molecular basis for lipid droplet formation is poorly understood. Although a certain amount of lipid storage may even be hepatoprotective, prolonged lipid storage can result in an activation of inflammatory reactions and loss of metabolic competency. Apart from drug-induced steatosis, certain metabolic disorders associated with obesity, insulin resistance, and hyperlipidemia give also rise to nonalcoholic fatty liver diseases (NAFLD). It is noteworthy that advanced stages of nonalcoholic hepatic steatosis and steatohepatitis (NASH) result ultimately in fibrosis and cirrhosis. In this regard, the lipid droplets (LDs) have been discovered to be metabolically highly active structures that play major roles in lipid transport, sorting, and signaling cascades. In particular, LDs maintain a dynamic communication with the endoplasmic reticulum (ER) and the plasma membrane via sphingolipid-enriched domains of the plasma membrane-the lipid rafts. These microdomains frequently harbor receptor tyrosine kinases and other signaling molecules and connect extracellular events with intracellular signaling cascades. Here, we review recent knowledge on the molecular mechanisms of drug and metabolically induced hepatic steatosis and its progression to steatohepatitis (NASH). The contribution of cytokines and other signaling molecules, as well as activity of nuclear receptors, lipids, transcription factors, and endocrine mediators toward cellular dysfunction and progression of steatotic liver disease to NASH is specifically addressed, as is the cross-talk of different cell types in the pathogenesis of NAFLD. Furthermore, we provide an overview of recent therapeutic approaches in NASH therapy and discuss new as well as putative targets for pharmacological interventions.
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PMID:Molecular mechanisms and therapeutic targets in steatosis and steatohepatitis. 1892 66

Excessive weight gain, hypertension, hyperlipidemia, and diabetes are frequently observed in patients having undergone liver transplantation (LTx). These alterations are probably multifactorial in origin, and cluster to generate a metabolic syndrome (MS), increasing the risk of cardiovascular events. We assessed the prevalence of MS (National Cholesterol Education Program-Adult Treatment Panel III criteria) in 296 LTx patients in the course of regular follow-up, at least 6 months after transplantation (median, 38 months). Several pre-LTx and post-LTx data were collected to identify the factors associated with the presence of MS. In a subset of 99 patients, insulin resistance was measured by the homeostasis model assessment. High blood pressure was present in 53% of cases, hyperlipidemia in 51%, high glucose in 37%, and enlarged waist circumference in 32%. Overall, MS (defined as 3 or more of the above features) was present in 44.5% of cases. Insulin resistance (homeostasis model assessment > 2.7) was observed in 41% of cases. Hypertension and hyperlipidemia were more frequent in subjects on cyclosporine than in tacrolimus-treated cases, whereas the type of immunosuppressive drug had no effect on the prevalence of diabetes, enlarged waist, and MS. In a logistic regression analysis, only pre-LTx body mass index (odds ratio, 1.20), body mass index increase (odds ratio, 1.18), and pre-LTx diabetes (odds ratio, 2.36) predicted MS; age, gender, etiology of liver disease, time from LTx, type of immunosuppressive drug, and previous hepatocellular carcinoma were removed from the model. Disorders related to MS are frequent in LTx patients, and are related to both pre-LTx conditions and to weight gain. Weight control is mandatory in LTx patients to prevent risk factors of premature atherosclerosis.
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PMID:Metabolic syndrome in liver transplantation: relation to etiology and immunosuppression. 1897 73

Adipose tissue is a massive source of bioactive substances known as adipocytokines, including tumor necrosis factor (TNF)-alpha, resistin, leptin, and adiponectin. Recent advances in medical research view obesity as a chronic low-grade inflammatory state. Hypertrophied adipocytes in obesity release chemokines that induce macrophage accumulation in adipose tissue. Accumulated macrophages in obese adipose tissue produce proinflammatory cytokines and nitric oxide, and these inflammatory changes induce adipocytokine dysregulation. The latter is characterized by a decrease in insulinsensitizing and anti-inflammatory adipocytokines, and an increase in proinflammatory adipocytokines. Adipocytokine dysregulation induces obesity-related metabolic disorders, the so-called metabolic syndrome. Metabolic syndrome is a cluster of metabolic abnormalities, including diabetes mellitus, hypertension, hyperlipidemia, and nonalcoholic steatohepatitis (NASH). Recent studies have revealed that obesity is an independent risk factor for chronic liver diseases, such as NASH, alcoholic liver disease, chronic hepatitis C, and hepatocellular carcinoma. A common mechanism underlying these hepatic clinical states is thought to be adipocytokine dysregulation. In this review, we discuss the association of adipocytokines, especially leptin, adiponectin, TNF-alpha, and resistin, with liver diseases.
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PMID:Adipocytokines and liver disease. 1901 34

Lipid metabolism in dogs can be divided into exogenous and endogenous pathways and exhibits some unique characteristics compared to other species. Hyperlipidemia is common in dogs, and can be either primary or secondary to other diseases. Secondary hyperlipidemia is the most common form and can be a result of endocrine disorders, pancreatitis, cholestasis, protein-losing nephropathy, obesity, and high fat diets. Primary hyperlipidemia is less common and usually associated with certain breeds. Hypertriglyceridemia of Miniature Schnauzers is the most common type of primary hyperlipidemia in dogs in the United States, and appears to have a genetic basis although its etiology remains unknown. Possible complications of canine hyperlipidemia include pancreatitis, liver disease, atherosclerosis, ocular disease, and seizures. Management is achieved by administration of low fat diets with or without the administration of lipid-lowering agents such as omega-3 fatty acids, gemfibrozil, and niacin.
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PMID:Lipid metabolism and hyperlipidemia in dogs. 1916 16

Biliary stasis can occur in many different diseases. Pruritus, metabolic bone disease, deficiencies of fat-soluble vitamins, steatorrhea, hyperlipidemia and fatigue represent the major extra-hepatic manifestations of cholestatic liver disease that considerably affect the patient's quality of life. The present article reviews pathogenetic and clinical aspects of and current therapeutic approaches to extra-hepatic manifestations of cholestatic liver disease.
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PMID:[Under-evaluated extrahepatic manifestations of cholestasis]. 1929 75


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