Within the USA, 5-20% of the population and nearly 75% of those with type 2 diabetes have fatty liver disease.
Fatty liver is strongly associated with insulin resistance and is considered a manifestation of metabolic syndrome in the liver. The incidence of fatty liver is not uniform across ethnic groups and nationalities, but instead disproportionately affects Hispanics, Native Americans and Asians. Obesity and metabolic syndrome are closely associated with fatty liver, especially in Hispanic and Native American populations and in people with a genetic predisposition.
Limit intake of fructose-rich foods, especially foods with high-fructose corn syrup such as soda, soft drinks and fruit juices. The precise biochemical mechanisms for how insulin resistance leads to fatty liver are still being uncovered. Overconsumption of simple carbohydrates and added sugar is strongly associated with insulin resistance. Two genetic variants within the APOC3 gene that are often co-inherited are also linked with increased risk of fatty liver. To further explore mechanisms mediating these effects of vitamin D deficiency (VDD) on insulin resistance (IR) and NAFLD among overweight children, the Roth lab has developed a rat model of NAFLD induced by vitamin D deficiency and a westernized diet (high fat and high sugar intake).
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Non-alcoholic fatty liver disease (NAFLD) is one of most common chronic liver disease worldwide. Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers).
Abstract: Non-alcoholic steatohepatitis (NASH) is characterised by hepatic steatosis and inflammation and, in some patients, progressive fibrosis leading to cirrhosis.
Abstract: Accumulating evidence indicates that obesity is closely associated with an increased risk of metabolic diseases such as insulin resistance, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease.
Abstract: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide as a result of the increasing prevalence of obesity, starting from early life stages. Abstract: Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent, chronic liver diseases, worldwide.
Abstract: Non-alcoholic steatohepatitis (NASH) is a recently identified chronic liver disease, which progresses to liver cirrhosis and hepatocellular carcinoma (HCC). Abstract: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disorder worldwide. Abstract: The liver is crucial for human life, and the health of this organ often mirrors the health of the individual. Abstract: Research in nonalcoholic fatty liver disease (NAFLD), including nonalcoholic steatohepatitis (NASH), has been limited by the availability of suitable models for this disease.
Abstract: Non-alcoholic fatty liver disease (NAFLD) is characterized by triglyceride (TG) accumulation in hepatocytes. Abstract: Nonalcoholic fatty liver disease (NAFLD) encompasses a clinicopathologic spectrum of diseases ranging from isolated hepatic steatosis to nonalcoholic steatohepatitis (NASH), the more aggressive form of fatty liver disease that may progress to cirrhosis and cirrhosis-related complications, including hepatocellular carcinoma. Non-alcoholic fatty liver disease (NAFLD or fatty liver) is the leading cause of liver damage in the US and other Western societies and can progress to hepatitis and cirrhosis, ultimately requiring liver transplantation. Overtime, excess fat storage in the liver can promote inflammation, oxidative damage and ultimately fibrosis or the replacement of functional liver cells with scar tissue. Obesity is a strong risk factor for metabolic syndrome and fatty liver, however, you do not necessarily have to be obese to develop these conditions. Elevated levels of liver enzymes in the blood are a generalized sign of liver damage and can be readily detected by common blood tests.
There are two likely scenarios that lead to fat accumulation in the liver: excess production of fat (lipogenesis) and inadequate breakdown of fat (lipolysis) by the liver. The most common source of added sugar in the diet is sweetened beverages such as soda, sports drinks and fruit juice cocktails.
However, because they are not regulated in the same way, fructose is converted to fat more efficiently than glucose and therefore contributes more to fatty liver.
There are genetic variations that increase your chances of developing fatty liver if you don’t eat right. APOC3 inhibits the lipoprotein lipase (LPL) enzyme that is responsible for breaking down triglycerides. Sign up for the HealthWatch 360 online tool or download the mobile app to learn more about how your genetics can inform your health so you can take action to reduce your risk for liver disease.
The close relationship with epidemic obesity and metabolic syndrome, and the potential progression towards end-stage liver diseases, such as cirrhosis and HCC, makes of NAFLD an emerging global health problem.
The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF. An understanding of the pathogenesis of NASH is still evolving but current evidence suggests multiple metabolic factors critically disrupt homeostasis and induce an inflammatory cascade and ensuing fibrosis.

Obesity results from an imbalance between food intake and energy expenditure, which leads to an excessive accumulation of adipose tissue. It is characterized by a spectrum of liver diseases ranging from simple fatty liver (NAFL) to steatohepatitis (NASH), with a possible progression to fibrosis, thus increasing liver-related morbidity and mortality. It is a multifactorial disease caused by complex interactions between genetic, epigenetic and environmental factors.
As the number of patients studied to date has been limited, clinically useful prognostic biomarkers of NASH-related HCC have not been available.
Several lines of evidence have indicated a pathogenic role of insulin resistance, and a strong association with type 2 diabetes (T2MD) and metabolic syndrome. The liver can be the target of several diseases, the most prevalent of which, as a consequence of development and changes in human lifestyles, is the nonalcoholic fatty liver disease (NAFLD). A number of rodent models have been described in which the relevant liver pathology develops in an appropriate metabolic context. Very low density lipoprotein (VLDL) is a major secretory product of the liver that transports endogenously synthesized TG. The prevalence of NAFLD, including NASH, is also increasing in parallel with the growing epidemics of obesity and diabetes. Since the expression of PNPLA3 is induced by sterol regulatory element binding protein 1c (SREBP1c), we investigate two common SREBP1c variants (rs2297508 and rs11868035) for their association with liver stiffness. Insulin resistance promotes the mobilization of free fatty acids from lipid stores in our fat (adipose) tissue which then get taken up by the liver. Additionally, whereas adequate glucose in our blood signals our brains that we are satiated, fructose does not. The most important genetic variant associated with fatty liver is the rs738409 single nucleotide polymorphism (SNP) within the PNPLA3 gene. The protective allele is found exclusively in those of African heritage (approximately 13%). Keep track of your food and symptoms to see if you are getting enough vitamin E or are consuming too much fructose.
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The mechanisms underlying these changes and the complex inter-cellular interactions that mediate fibrogenesis are yet to be fully elucidated. Adipose tissue is now recognized not only as a main site of storage of excess energy derived from food intake but also as an endocrine organ. NAFLD development is driven by the co-action of several risk factors, including obesity and metabolic syndrome, which may be both genetically induced and diet-related. In this study, we investigated the status of a cell-cycle regulator, p27, in NASH-related HCC. Importantly, NAFLD appears to enhance the risk for T2MD, as well as worsen glycemic control and cardiovascular disease in diabetic patients. NAFLD is a multifactorial disease that embraces many histo-pathologic conditions and is highly linked to metabolic derangements. 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. In 899 individuals (aged 17–83 years, 547 males) with chronic liver diseases, hepatic fibrosis was non-invasively phenotyped by transient elastography (TE). Therefore, knowing your genetics can help you make more informed decisions to prevent fatty liver.
This means that while consumption of fructose contributes to our calorie intake, it does not satisfy us.
Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. International Journal of Molecular Sciences is an international peer-reviewed Open Access monthly journal published by MDPI.
Lipotoxicity, in the setting of excess free fatty acids, obesity, and insulin resistance, appears to be the central driver of cellular injury via oxidative stress.
The expansion of adipose tissue produces a number of bioactive substances, known as adipocytokines or adipokines, which trigger chronic low-grade inflammation and interact with a range of processes in many different organs.
Recently, particular attention has been paid to the gut-liver axis, which may play a physio-pathological role in the onset and progression of the disease. Technological progress and industrialization have also had the consequence of releasing pollutants in the environment, for instance pesticides or solvents, as well as by-products of discharge, such as the particulate matter.
ApoB100 (apolipoprotein B100) is a glycoprotein and an essential protein component of VLDL.
The SREBP1c single nucleotide polymorphisms (SNPs) were genotyped using PCR-based assays with 5'-nuclease and fluorescence detection. Thus we likely continue eating, further contributing to obesity, insulin resistance, metabolic syndrome and fatty liver.

The G variant is found in approximately 26% of the general population and nearly 50% of those with Hispanic or Native American heritage and about 35% of those of East Asian heritage. Although the precise mechanisms are still unclear, dysregulated production or secretion of these adipokines caused by excess adipose tissue and adipose tissue dysfunction can contribute to the development of obesity-related metabolic diseases. The gut microbiota is intended to act as a bioreactor that can guarantee autonomous metabolic and immunological functions and that can drive functional strategies within the environment of the body in response to external stimuli. A total of 22 cases with NASH-related HCC were analyzed for p27 protein expression, and phosphorylation at threonine 157 (T157) and serine 10 (S10) by immunohistochemical analysis. The opportunity to take into account NAFLD in T2MD prevention and care has stimulated several clinical studies in which antidiabetic drugs, such as metformin, thiazolidinediones, GLP-1 analogues and DPP-4 inhibitors have been evaluated in NAFLD patients. In the last decade, a growing body of evidence has emerged, shedding light on the potential impact of environmental pollutants on liver health and, in particular, on NAFLD occurrence. 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. A high-fat diet is widely used to produce hepatic steatosis and NASH in experimental animals.
For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website. Current evidence suggests that periportal components, including the ductular reaction and expansion of the hepatic progenitor cell compartment, may be involved and that the Th17 response may mediate disease progression. In this review, we focus on the role of several adipokines associated with obesity and the potential impact on obesity-related metabolic diseases. The correlation of p27 with tumor characteristics, disease-free survival (DFS), and overall survival was analyzed. In this review, we provide an overview of preclinical and clinical evidences on the possible efficacy of antidiabetic drugs in NAFLD treatment. These contaminants have a great steatogenic potential and need to be considered as tangible NAFLD risk factors. 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. This review aims to provide an overview of the pathogenesis of NASH and summarises the evidence pertaining to key mechanisms implicated in the transition from steatosis and inflammation to fibrosis. Multiple lines evidence provides valuable insights into the roles of adipokines in the development of obesity and its metabolic complications.
In group 3, hepatic TBFs were not significantly different when comparing patients with NASH and those with CH-C. Therefore, the concept of the gut-liver axis must be complemented with the gut-microbiota-liver network due to the high intricacy of the microbiota components and metabolic activities; these activities form the active diet-driven power plant of the host. Overall, available data suggest that metformin has beneficial effects on body weight reduction and metabolic parameters, with uncertain effects on liver histology, while pioglitazone may improve liver histology. There is an urgent need for a deeper comprehension of their molecular mechanisms of action, as well as for new lines of intervention to reduce their worldwide diffusion. In this study, we cloned the GLT8D2 (glycosyltransferase 8 domain containing 2) gene from HepG2 cells and generated a series of plasmids for in vitro studies of its molecular functions. Carriers of both PNPLA3 and SREBP1c risk genotypes displayed significantly (p = 0.005) higher median liver stiffness, as compared to patients carrying none of these variants. Studies show that those with the risk variant make a PNPLA3 enzyme with reduced capacity to breakdown triglycerides.
Currently there are limited treatments for NASH although an increasing understanding of its pathogenesis will likely improve the development and use of interventions in the future.
Further research is still required to fully understand the mechanisms underlying the metabolic actions of a few newly identified adipokines. Such complexity can only be revealed using systems biology, which can integrate clinical phenomics and gut microbiota data. This review wishes to sensitize the community to the effects of several environmental pollutants on liver health. 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. The heterogeneity of these studies and the small number of patients do not allow for firm conclusions about treatment guidelines, and further randomized, controlled studies are needed. Our study supports a role of the SREBP1c-PNPLA3 pathway as a “disease module” that promotes hepatic fibrogenesis.
Patients with NASH should be monitored carefully for portal hypertensive complications in the early fibrosis stage.

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