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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

NAFLD (non-alcoholic fatty liver disease) encompasses the spectrum of fatty liver disease in insulin-resistant individuals who often display T2DM (Type 2 diabetes mellitus) and obesity. The present review highlights the pathophysiological basis and clinical evidence for a possible causal linkage between NAFLD and CVD (cardiovascular disease). The role of traditional and non-traditional CVD risk factors in the pathophysiology of NAFLD is considered in the first part of the review, with the basic science shared by atherogenesis and hepatic steatogenesis discussed in depth in the second part. In conclusion, NAFLD is not an innocent bystander, but a major player in the development and progression of CVD. NAFLD and CVD also share similar molecular mechanisms and targeted treatment strategies. On the research side, studies should focus on interventions aimed at restoring energy homoeostasis in lipotoxic tissues and at improving hepatic (micro)vascular blood supply.
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PMID:Is liver fat detrimental to vessels?: intersections in the pathogenesis of NAFLD and atherosclerosis. 1901 56

Non-alcoholic fatty liver disease includes a broad spectrum of liver abnormalities ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), which can progress to cirrhosis and hepatocellular carcinoma. Patients with primary NASH have the metabolic (or insulin resistance) syndrome, condition typically associated with obesity, diabetes, hyperlipidemia and hypertension. To understand the mechanisms implicated in development of NASH, animal models of non-alcoholic fatty liver disease have been generated. These have greatly improved our understanding of some of the aspects of this disease. The challenge now is to identify the common mechanisms between the animal models and humans, which could eventually lead to a better prognosis and development of novel therapeutic strategies.
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PMID:Non-alcoholic steatohepatitis and animal models: understanding the human disease. 1902 69

In view of the epidemic obesity in childhood, facing the disease and its associated morbidities early at this age becomes crucial for public health researchers and care givers. The present review focuses on pediatric Non Alcoholic Fatty Liver Disease (NAFLD) among co-morbidities, being the disease yet under diagnosed and under treated despite a prevalence growing exponentially. Evidences suggest that the environmental background for the development of NAFLD may be established in early life, and that the duration of the disease affects probably the likelihood of progression to more severe disease (necro-inflammation or Non Alcoholic SteatoHepatitis, also termed, NASH; fibrosis and cirrhosis). NAFLD associates with abdominal obesity, insulin resistance and features of metabolic syndrome. In genetically prone individuals, malnutrition (i.e., excessive consumption of saturated fats and refined sugars) leads to the derangement of the adipose tissue architecture and homeostasis, the peripheral and hepatic resistance to insulin-stimulated glucose uptake, thus favoring a condition of chronic low-grade inflammation. Excessive nutrients cannot be stored in the adipose tissue and overflow elsewhere, mainly to the muscle tissue and liver. Fat deposition in both sites enhances insulin resistance and further deposition of fats in a vicious manner. What is of special interest comparing NAFLD in children and adults is that the histological appearance of the disease differs significantly, likely representing a yet physiological response to environmental stressors in children and a long-term adaptation in adults. In this article, we review the current concepts about paediatric NAFLD, its pathogenesis, diagnosis and treatment, with particular regard to lifestyle and foods habits.
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PMID:Nonalcoholic fatty liver disease in children. 1915 26

Obesity is currently a worldwide epidemic and public health burden that increases the risk for developing insulin resistance and several chronic diseases such as diabetes, cardiovascular diseases and non-alcoholic fatty liver disease. The multifactorial causes of obesity include several genetic, dietary and lifestyle variables that together result in an imbalance between energy intake and energy expenditure. Dietary approaches to limit fat intake are commonly prescribed to achieve the hypocaloric conditions necessary for weight loss. But dietary fat restriction is often accompanied by increased carbohydrate intake, which can dramatically increase endogenous fatty acid synthesis depending upon carbohydrate composition. Since both dietary and endogenously synthesized fatty acids contribute to the whole-body fatty acid pool, obesity can therefore result from excessive fat or carbohydrate consumption. Stearoyl-Coenzyme A desaturase-1 (SCD1) is a delta-9 fatty acid desaturase that converts saturated fatty acids into monounsaturated fatty acids (MUFA) and this activity is elevated by dietary carbohydrate. Mice lacking Scd1 are protected from obesity and insulin resistance and are characterized by decreased fatty acid synthesis and increased fatty acid oxidation. In this review, we address the association of high-carbohydrate diets with increased SCD activity and summarize the current literature on the subject of SCD1 and body weight regulation.
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PMID:Stearoyl-CoA desaturase and its relation to high-carbohydrate diets and obesity. 1916 67

Non-alcoholic fatty liver disease (NAFLD) includes a broad spectrum of fat-induced liver injury, ranging from mild steatosis to cirrhosis and liver failure. The presence of obesity and insulin resistance is strongly associated with non-alcoholic fatty liver and a greater risk of advanced disease. We present here a review of the mechanisms involved in the pathogenesis of NAFLD, advances in the diagnosis, and options for treatment.
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PMID:Non-alcoholic steatohepatitis: an overview. 2224 38

Prevalence of non-alcoholic steatohepatitis (NASH) rises steadily in Western countries with the obesity epidemic. NASH is associated with activation of liver fibrogenesis and predisposes to cirrhosis and associated morbi-mortality. The cannabinoid system is increasingly emerging as a crucial mediator of acute and chronic liver injury. Recent experimental and clinical data indicate that peripheral activation of cannabinoid CB1 receptors promotes insulin resistance and liver steatogenesis, two key steps in the pathogenesis of non-alcoholic fatty liver disease. Moreover, CB1 receptors enhance progression of liver fibrogenesis. These findings provide a strong rationale for the use of CB1 antagonists in the management of NASH.
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PMID:Cannabinoid receptors as novel therapeutic targets for the management of non-alcoholic steatohepatitis. 1919 30

Obesity is an increasingly serious socioeconomic and clinical problem. Between (1/4)-(1/3) of population in the developed countries can be classified as obese. Four major etiological factors for development of obesity are genetic determinants, environmental factors, food intake and exercise. Obesity increases the risk of the development of various pathologic conditions including: insulin-resistant diabetes mellitus, cardiovascular disease, non-alcoholic fatty liver disease, endocrine problems, and certain forms of cancer. Thus, obesity is a negative determinant for longevity. In this review we provide broad overview of pathophysiology of obesity. We also discuss various available, and experimental therapeutic methods. We highlight functions of adipocytes including fat storing capacity and secretory activity resulting in numerous endocrine effects like leptin, IL-6, adiponectin, and resistin. The anti-obesity drugs are classified according to their primary action on energy balance. Major classes of these drugs are: appetite suppressants, inhibitors of fat absorption (i.e. orlistat), stimulators of thermogenesis and stimulators of fat mobilization. The appetite suppressants are further divided into noradrenergic agents, (i.e. phentermine, phendimetrazine, benzphetamine, diethylpropion), serotoninergic agents (i.e. dexfenfluramine), and mixed noradrenergic-serotoninergic agents (i.e. sibutramine). Thus, we highlight recent advances in the understanding of the central neural control of energy balance, current treatment strategies for obesity and the most promising targets for the development of novel anti-obesity drugs.
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PMID:Obesity: pathophysiology and clinical management. 1919 18

The authors summarize and update the most recent knowledge in the field of prevalence, natural history and incidence of Non Alcoholic Fatty Liver Disease (NAFLD) and Non Alcoholic Steatohepatitis (NASH). These novel diseases, firstly recognized at the beginning of the second millennium, arose suddenly to the attention of the clinicians, because they are the hepatic expression of the "so-called" metabolic syndrome. Due to the epidemic burden of obesity, diabetes, and metabolic diseases, NAFLD and NASH will become soon probably the most common hepatic disease worldwide, and they surely will keep busy our future young hepatologists.
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PMID:Epidemiology and natural history of non-alcoholic fatty liver disease (NAFLD). 1938 Nov 18

In the last three decades prevalence of insulin related diseases has been growing worldwide with epidemic obesity, type 2 diabetes mellitus and non alcoholic fatty liver disease. In children such epidemics are particularly worrisome, since metabolic abnormalities track to the adulthood with significant implications for the health care system. Epidemiological studies support a close association between type 2 diabetes and fatty liver disease. We review the most recent epidemiological data on prevalence of both diseases in youth and their association.
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PMID:Association between type two diabetes and non-alcoholic fatty liver disease in youth. 1938 Nov 24

With the growing epidemic of obesity and diabetes, more attention has been placed on metabolic syndrome and its associated hepatic manifestation, non-alcoholic fatty liver disease (NAFLD). Within the spectrum of clinico-pathologic conditions known as NAFLD, only a minority of patients has the histological features characteristic of non-alcoholic steatohepatitis (NASH), which has the potential to progress to cirrhosis and hepatocellular carcinoma. Therefore, diagnosis and therapy should target patients with NASH. Current treatment recommendations include weight loss and the reversal of other components of metabolic syndrome, but several other treatment modalities are under investigation. To date, no pharmacologic treatment has been reliably shown to be effective for NASH. This article reviews all available treatment modalities, including lifestyle changes, bariatric surgery, weight loss medications, insulin sensitizers, lipid lowering agents, antioxidants, cytoprotective agents, and other novel treatments.
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PMID:Treatment regimens for non-alcoholic fatty liver disease. 1938 Nov 25


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