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Nonalcoholic fatty liver disease and obesity
Salgado Júnior, Wilson;Santos, José Sebasti?o dos;Sankarankutty, Ajith Kumar;Castro e Silva, Orlando de;
Acta Cirurgica Brasileira , 2006, DOI: 10.1590/S0102-86502006000700017
Abstract: purpose: the aim of this review is to update concepts of the nonalcoholic fatty liver disease (nafld) and to establish a relationship between this condition and obesity. methods: by means of a comprehensive literature review where special attention was devoted to articles published in the last 5 years, nafld is discussed in view of new concepts, diagnosis, staging, and treatment. results: nafld is emerging as one of the main causes of chronic liver disease and it is believed to be the hepatic component of the metabolic syndrome, whose central features include obesity, hyperinsulinemia, peripheral insulin resistance, diabetes, dyslipidemia, and hypertension. the surgical treatment of morbid obesity is one of the options available for the treatment of nafld. conclusion: nonalcoholic fatty liver disease is strongly related with obesity.
Concepts and Treatment Approaches in Nonalcoholic Fatty Liver Disease  [PDF]
Dina L. Halegoua-De Marzio,Jonathan M. Fenkel
Advances in Hepatology , 2014, DOI: 10.1155/2014/357965
Abstract: Nonalcoholic fatty liver disease (NAFLD) affects up to 30% of adults and is the most common liver disease in Western nations. NAFLD is associated with central adiposity, insulin resistance, type 2 diabetes mellitus, hyperlipidemia, and cardiovascular disease. It encompasses the entire spectrum of fatty liver diseases from simple steatosis to nonalcoholic steatohepatitis (NASH) with lobular/portal inflammation, hepatocellular necrosis, and fibrosis. Of those who develop NASH, 15–25% will progress to end stage liver disease and hepatocellular carcinoma over 10–20 years. Its pathogenesis is complex, and involves a state of lipid accumulation due to increased uptake of free fatty acids into the liver, impaired fatty acid beta oxidation, and increased incidence of de novo lipogenesis. Plasma aminotransferases and liver ultrasound are helpful in the diagnosis of NAFLD/NASH, but a liver biopsy is often required for definitive diagnosis. Many new plasma biomarkers and imaging techniques are now available that should improve the ability to diagnose NAFLD noninvasively Due to its complexity and extrahepatic complications, treatment of NAFLD requires a multidisciplinary approach with excellent preventative care, management, and treatment. This review will evaluate our current understanding of NAFLD, with a focus on existing therapeutic approaches and potential pharmacological developments. 1. Introduction Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of disorders defined by the accumulation of fat in the liver. This spectrum ranges from simple steatosis to lobular inflammation with variable degrees of fibrosis leading to cirrhosis and even hepatocellular carcinoma (HCC) [1]. It is strongly associated with the metabolic syndrome and is the leading cause of chronic liver disease worldwide, with a prevalence of 15%–30% in Western populations [2, 3]. The prevalence increases to 58% in overweight individuals and can be as high as 90% in obese individuals [4, 5]. NAFLD was historically thought to be of little importance, but recent advances have shown that NAFLD can progress to nonalcoholic steatohepatitis (NASH) in up to 25% of patients [1, 6]. NASH resembles alcoholic steatohepatitis (ASH) but occurs in individuals who do not consume excessive amounts of alcohol. Cirrhosis, which occurs in 25% of patients with NASH, can result in liver failure, portal hypertension, and hepatocellular carcinoma [7]. However, the majority of deaths among individuals with NAFLD are attributed to cardiovascular disease and malignancy [8, 9]. Unsurprisingly, these
Pathology of nonalcoholic fatty liver disease
D.G. Tiniakos, Ch. Kittas
Annals of Gastroenterology , 2007,
Abstract: Nonalcoholic fatty liver disease (NAFLD) may be the most common cause of chronic liver disease in Western countries, with an estimated prevalence of up to 24% in the general population. NAFLD is considered the hepatic manifestation of the metabolic syndrome and has been etiologically correlated with insulin resistance. The histopathological spectrum of NAFLD ranges from simple steatosis to nonalcoholic steatohepatitis (NASH), with or without fibrosis, and cirrhosis. Liver biopsy is the gold standard for diagnosing NASH in a patient with clinical features of NAFLD, image detected steatosis and chronically elevated liver enzymes. This review discusses the histopathological findings of NAFLD in adults and children, including features representing resolution of NASH following treatment and features of prognostic information. Additionally, current systems of semiquantitative assessment in NAFLD and NASH are reviewed and the concurrence of NAFLD and NASH with other chronic liver diseases, mainly hepatitis C, is discussed. Key words: steatosis, steatohepatitis, nonalcoholic, liver, pathology
Histopathology of nonalcoholic fatty liver disease  [cached]
Elizabeth M Brunt, Dina G Tiniakos
World Journal of Gastroenterology , 2010,
Abstract: Histological analysis of liver biopsies remains a standard against which other methods of assessment for the presence and amount of hepatic injury due to nonalcoholic fatty liver disease (NAFLD) are measured. Histological evaluation remains the sole method of distinguishing steatosis from advanced forms of NAFLD, i.e. nonalcoholic steatohepatitis (NASH) and fibrosis. Included in the lesions of NAFLD are steatosis, lobular and portal inflammation, hepatocyte injury in the forms of ballooning and apoptosis, and fibrosis. However, patterns of these lesions are as distinguishing as the lesions themselves. Liver injury in adults and children due to NAFLD may have different histological patterns. In this review, the rationale for liver biopsy, as well as the histopathological lesions, the microscopically observable patterns of injury, and the differential diagnoses of NAFLD and NASH are discussed.
Liver regeneration in nonalcoholic fatty liver disease  [cached]
Aldo Lagomarsino
Medwave , 2012,
Abstract: Steatosis is the accumulation of fat in hepatocytes, which may be the result of liver regeneration or pathological processes such as alcoholic and nonalcoholic fatty liver disease. Despite its importance, in both cases the exact mechanism that prevails in fatty liver regeneration is poorly understood. Previous studies have shown that patients with fatty liver express dispar regeneration, possibly due to the accumulation of reactive oxygen species generated by inflammatory processes caused by activation of Kupffer cells. In this article we review several factors that affect liver regeneration, trying to understand the underlying mechanism of dispar regeneration in fatty liver as a consequence of nonalcoholic fatty liver disease.
Nonalcoholic fatty liver disease: An overview of current insights in pathogenesis, diagnosis, treatment  [cached]
Tim CMA Schreuder, Bart J Verwer, Carin MJ van Nieuwkerk, Chris JJ Mulder
World Journal of Gastroenterology , 2008,
Abstract: Estimates of people suffering from overweight (one billion) and obesity (300 million) are increasing. The accumulation of triglycerides in the liver, in the absence of excess alcohol intake, has been described in the early sixties. It was not until 1980, however, that Ludwig et al named this condition nonalcoholic steatohepatitis (NASH). Subsequently, nonalcoholic fatty liver disease (NAFLD) has been used as a general name for conditions ranging from simple steatosis through steatohepatitis to end-stage liver disease (cirrhosis). Many studies have demonstrated the significant correlation with obesity and insulin resistance. Other studies have revealed a significant correlation between hepatic steatosis, cardiovascular disease and increased intima-media thickness. WHO estimated that at least two million patients will develop cirrhosis due to hepatic steatosis in the years to come. Longitudinal cohort studies have demonstrated that those patients with cirrhosis have a similar risk to develop hepatocellular carcinoma as those with other causes of cirrhosis. Taken all together, NAFLD has become the third most important indication for liver transplantation. Therefore, training programmes in internal medicine, gastroenterology and hepatology should stress the importance of diagnosing this entity and treat properly those at risk for developing complications of portal hypertension and concomittant cardiovascular disease. This review will focus on the clinical characteristics, pathophysiology, imaging techniques and the readily available therapeutic options.
Animal models of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis  [cached]
Yoshihisa Takahashi,Yurie Soejima,Toshio Fukusato
World Journal of Gastroenterology , 2012, DOI: 10.3748/wjg.v18.i19.2300
Abstract: Nonalcoholic fatty liver disease (NAFLD) is a condition in which excess fat accumulates in the liver of a patient without a history of alcohol abuse. Nonalcoholic steatohepatitis (NASH), a severe form of NAFLD, can progress to liver cirrhosis and hepatocellular carcinoma. NAFLD is regarded as a hepatic manifestation of metabolic syndrome and incidence has been increasing worldwide in line with the increased prevalence of obesity, type 2 diabetes, and hyperlipemia. Animal models of NAFLD/NASH give crucial information, not only in elucidating pathogenesis of NAFLD/NASH but also in examining therapeutic effects of various agents. An ideal model of NAFLD/NASH should correctly reflect both hepatic histopathology and pathophysiology of human NAFLD/NASH. Animal models of NAFLD/NASH are divided into genetic, dietary, and combination models. In this paper, we review commonly used animal models of NAFLD/NASH referring to their advantages and disadvantages.
Understanding mechanisms of the pathogenesis of nonalcoholic fatty liver disease  [cached]
Metin Basaranoglu, Serra Kayacetin, Nevin Yilmaz, Ertugrul Kayacetin, Orhan Tarcin, Abdullah Sonsuz
World Journal of Gastroenterology , 2010,
Abstract: A central issue in the understanding of the pathogenesis of nonalcoholic fatty liver disease is the problem of the underlying mechanisms which are not fully understood. In the setting of excessive central adiposity, insulin resistance is the major underlying cause of fat accumulation in hepatocytes. Because of the difficulties with human trials, several animal models have been developed for this purpose mainly characterized as follows: genetically disturbed or murine fatty liver, methionine-choline deficient diet fed or murine steatohepatitis, and high-fat or sucrose diet fed models. Although these animal models have provided useful information, none of them accurately reflect genetic, metabolic and biochemical characteristics of the human disease.
Rodent Models of Nonalcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis  [PDF]
Kento Imajo,Masato Yoneda,Takaomi Kessoku,Yuji Ogawa,Shin Maeda,Yoshio Sumida,Hideyuki Hyogo,Yuichiro Eguchi,Koichiro Wada,Atsushi Nakajima
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms141121833
Abstract: Research in nonalcoholic fatty liver disease (NAFLD), including nonalcoholic steatohepatitis (NASH), has been limited by the availability of suitable models for this disease. A number of rodent models have been described in which the relevant liver pathology develops in an appropriate metabolic context. These models are promising tools for researchers investigating one of the key issues of NASH: not so much why steatosis occurs, but what causes the transition from simple steatosis to the inflammatory, progressive fibrosing condition of steatohepatitis. The different rodent models can be classified into two large groups. The first includes models in which the disease is acquired after dietary or pharmacological manipulation, and the second, genetically modified models in which liver disease develops spontaneously. To date, no single rodent model has encompassed the full spectrum of human disease progression, but individual models can imitate particular characteristics of human disease. Therefore, it is important that researchers choose the appropriate rodent models. The purpose of the present review is to discuss the metabolic abnormalities present in the currently available rodent models of NAFLD, summarizing the strengths and weaknesses of the established models and the key findings that have furthered our understanding of the disease’s pathogenesis.
Nuclear Receptors in Nonalcoholic Fatty Liver Disease  [PDF]
Jorge A. López-Velázquez,Luis D. Carrillo-Córdova,Norberto C. Chávez-Tapia,Misael Uribe,Nahum Méndez-Sánchez
Journal of Lipids , 2012, DOI: 10.1155/2012/139875
Abstract: Nuclear receptors comprise a superfamily of ligand-activated transcription factors that are involved in important aspects of hepatic physiology and pathophysiology. There are about 48 nuclear receptors in the human. These nuclear receptors are regulators of many hepatic processes including hepatic lipid and glucose metabolism, bile acid homeostasis, drug detoxification, inflammation, regeneration, fibrosis, and tumor formation. Some of these receptors are sensitive to the levels of molecules that control lipid metabolism including fatty acids, oxysterols, and lipophilic molecules. These receptors direct such molecules to the transcriptional networks and may play roles in the pathogenesis and treatment of nonalcoholic fatty liver disease. Understanding the mechanisms underlying the involvement of nuclear receptors in the pathogenesis of nonalcoholic fatty liver disease may offer targets for the development of new treatments for this liver disease. 1. Introduction Liver diseases are a serious problem throughout the world. In Mexico, since 2000, cirrhosis and other chronic liver diseases have become among the main causes of mortality [1]. The incidence and prevalence of liver diseases are increasing along with changes in lifestyle and population aging, and these diseases were responsible for 20,941 deaths in 2007 [2]. In Mexico, the incidence of metabolic syndrome is also increasing. The metabolic syndrome has recently been associated with nonalcoholic fatty liver disease (NAFLD), and about 90% of patients with NAFLD have more than one feature of the metabolic syndrome [3]. The severity of NAFLD is one factor contributing to the development of nonalcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma [4, 5]. The growing obesity epidemic requires a better understanding of the genetic networks and signal transduction pathways that regulate the pathogenesis of these conditions. A clear definition of the mechanisms responsible for metabolic control may provide new knowledge for the development of new drugs, with novel mechanisms of action, for the treatment of chronic liver diseases. The ability of individual nuclear receptors (NRs) to regulate multiple genetic networks in different tissues and their own ligands may represent a new class of potential drugs targets. To elucidate the challenges involved in developing such drugs, this paper focuses on the role of hepatic NRs in lipid metabolism and the possible effects on the physiopathology of NAFLD. 2. Nonalcoholic Fatty Liver Disease NAFLD is defined by the accumulation of triglycerides in
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