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Non-alcoholic fatty liver disease (NAFLD), the most common liver disease, is characterized by accumulation of fat (>5% of the liver tissue), in the absence of alcohol abuse or other chronic liver diseases. It is closely related to the epidemic of obesity, metabolic syndrome or type 2 diabetes mellitus (T2DM). NAFLD can cause liver inflammation and progress to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis or hepatocellular cancer (HCC). Nevertheless, cardiovascular disease (CVD) is the most common cause of death in NAFLD/NASH patients. Current guidelines suggest the use of pioglitazone both in patients with T2DM and in those without. The use of statins, though considered safe by the guidelines, have very limited use; only 10% in high CVD risk patients are on statins by tertiary centers in the US. There are data from several animal studies, 5 post hoc analyses of prospective long-term survival studies, and 5 rather small biopsy proven NASH studies, one at baseline and on at the end of the study. All these studies provide data for biochemical and histological improvement of NAFLD/NASH with statins and in the clinical studies large reductions in CVD events in comparison with those also on statins and normal liver. Ezetimibe was also reported to improve NAFLD. Drugs currently in clinical trials seem to have potential for slowing down the evolution of NAFLD and for reducing liver- and CVD-related morbidity and mortality, but it will take time before they are ready to be used in everyday clinical practice. The suggestion of this Expert Panel is that, pending forthcoming randomized clinical trials, physicians should consider using a PPARgamma agonist, such as pioglitazone, or, statin use in those with NAFLD/NASH at high CVD or HCC risk, alone and/or preferably in combination with each other or with ezetimibe, for the primary or secondary prevention of CVD, and the avoidance of cirrhosis, liver transplantation or HCC, bearing in mind that CVD is the main cause of death in NAFLD/NASH patients., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Objectives: We investigated whether plasma visfatin and binding protein-4 (RBP-4) levels correlate with obesity and type 2 diabetes mellitus (T2DM)., Design and Methods: Two groups were enrolled: Group 1: 40 patients with T2DM and Group 2: 40 age- and gender-matched healthy controls. Both groups were subdivided according to body mass index (BMI) into non-obese (BMI < 25 kg/m(2)) and obese subjects (BMI ≥ 30 kg/m(2)) (20 each)., Results: Plasma visfatin and RBP-4 levels were significantly increased in T2DM patients compared with controls with similar BMI values (for both p<0.001). Plasma visfatin and RBP-4 concentrations correlated with BMI, waist/hip ratio, insulin and homeostatic model assessment insulin resistance (HOMA(IR)). Visfatin and RBP-4 correlated with visceral fat and liver fat in diabetic patients (for both p<0.001)., Conclusion: Visfatin level was increased in T2DM, possibly related to hyperglycemia. Plasma RBP-4 correlated positively with liver fat and HOMA(IR) which may reflect its effects on hepatic insulin sensitivity., (Copyright © 2011 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.)

Both elevated levels of uric acid and non-alcoholic fatty liver disease (NAFLD) have been associated with increased vascular risk. Furthermore, certain drugs (e.g. lipid and blood pressure lowering) that decrease)cardiovascular risk and improve/preserve renal function were shown to influence serum uric acid (SUA) levels and/or NAFLD. A link between hyperuricaemia and NAFLD has also been suggested. This review considers the associations between hyperuricaemia, NAFLD and vascular risk. We also discuss the effects of different drug treatments on SUA and NAFLD. As NAFLD is a very common condition, future work in this field is needed with regard to a more practical definitive diagnosis, evidence- based treatments and a better understanding of the possible links between NAFLD, elevated SUA levels, cardiovascular disease and chronic kidney disease. Whether treating hyperuricaemia and NAFLD will translate into a reduced risk of vascular events requires further investigation.

Background: In animal models, histological and biochemical changes are observed in response to choline deficiency. It is unclear whether dietary choline is linked to non-alcoholic fatty liver disease (NAFLD). Objective: We examined the link among liver tests, fatty liver index (FLI), and choline consumption. Furthermore, we evaluated the impact of adiposity on this association. Method: The National Health and Nutrition Examination Survey (NHANES) was used to obtain data on choline intake and liver function biomarkers. Masked variance and weighting methodology were performed to account for the complex NHANES data. Results: Of the 20,643 participants, 46.8% were men and 45.6% had NAFLD (defined as United States FLI ≥30). In a fully adjusted model (for demographic, dietary, and clinical factors), a significant negative association was found between FLI and choline consumption (β = -0.206, p < 0.001). Participants in the highest quartile (Q4) of choline intake had a 14% lower risk of NAFLD compared with those in the first quartile (Q1). This link was stronger for postmenopausal women; women in Q4 had a 26% lower risk of NAFLD compared with those in Q1. Body mass index (BMI) strongly moderated the link between FLI and choline intake. For example, when choline consumption increased from low (272 mg/d) to high (356 mg/d), FLI decreased from 79.3 to 74.1 in the low BMI category (mean BMI = 22.1 kg/m2) and from 32.1 to 20.6 in the high BMI category (mean BMI =35.9 kg/m2). Conclusions: Our results suggest the presence of a reverse significant association between choline intake and risk of NAFLD. Furthermore, BMI was shown to mediate this relationship since changes in FLI, in relation to choline consumption, were more pronounced in participants with a higher BMI. [ABSTRACT FROM AUTHOR]

Little is known about the role of liver enzymes as predictors of non-liver-related morbidity and mortality. The ideal cardiovascular health (CVH) score proposed by the American Heart Association (AHA) can be used to predict mortality and morbidity. We investigated the association of the CVH score with liver enzymes and the risk of non-alcoholic fatty liver disease (NAFLD) among US adults. By using the National Health and Nutrition Examination Survey database (cross-sectional), the CVH score was calculated as meeting ideal levels of the following components: 4 behaviors (smoking, body mass index, physical activity and diet adherence) and 3 factors (total cholesterol, blood pressure and fasting glucose). Individuals with a higher CVH score ("better CVH") had a more favorable profile of liver biomarkers. Adjusted (for age, gender, race, poverty to income ratio, education, marital status and alcohol intake) linear regression indicated significant and negative associations between liver biomarkers and CVH score: (β = −0.069, p < 0.001) for alanine aminotransferase, (β = −0.095, p < 0.001), aspartate aminotransferase, (β = −0.067, p < 0.001), alkaline phosphatase and (β = −0.125, p < 0.001) and fatty liver index. In the logistic regression, with the same confounders, individuals with a higher CVH score had 12% less likelihood of NAFLD compared with those with a lower score. Furthermore, each CVH metric separately was inversely linked to the risk of NAFLD. For the first time among US adults, our findings shed light on the role CVH on liver biomarkers. • To investigate the association between the cardiovascular health score (CVH) score, liver enzyme biomarkers and the risk of non-alcoholic fatty liver disease (NAFLD). • Individuals with a higher CVH score had a more favorable profile of liver biomarkers. • Individuals with a higher CVH score had 12% less likelihood of NAFLD compared with those with a lower score. • Each CVH component separately was associated with the risk of NAFLD. [ABSTRACT FROM AUTHOR]

Limited information exists on the impact of flavonoid intake on nonalcoholic fatty liver disease (NAFLD). We evaluated the link between flavonoid intake, liver tests and risk of NAFLD in a randomly selected sample of US adults (from the National Health and Nutrition Examination Survey, NHANES, 2005-2010). Of the 17,685 participants, 46.9% were men and 45.4% had NAFLD. NAFLD patients had a significantly lower mean flavonoid intake than healthy individuals (111.3±3.6 vs. 201.3±2.3 mg/d, respectively; P<.001). Fatty liver index (FLI) and serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were significantly higher in the first tertile (T1) of flavonoid intake compared with the highest tertile (T3: with the highest flavonoid intake) (FLI: 67.1 vs. 36.2, AST: 31.2 VS 26.8 U/L and, ALT: 34.2 vs. 24.2 U/L, respectively; P<.001 for all comparisons). Adjusted linear regression displayed significant and negative associations between FLI, AST, ALT and flavonoid intake (P<.001 for all comparisons). Multivariable logistic regression showed that the risk for NAFLD significantly decreased as flavonoid intake tertiles increased in a stepwise manner (odds ratio: 0.81, 95% confidence interval: 0.78-0.86). Moderation analysis revealed that C-reactive protein (CRP) strongly modulated the impact of flavonoid intake on FLI; participants with higher CRP levels benefited less from flavonoid intake compared with those with lower CRP concentrations. In conclusions, our results suggest a reverse significant association between flavonoid consumption, liver tests and the risk for NAFLD. Furthermore, CRP was shown to essentially moderate this relationship. These findings support recommendations for consumption of flavonoid-rich foods to prevent cardiometabolic diseases. [ABSTRACT FROM AUTHOR]

Abstract Background The prevalence of non-alcoholic fatty liver disease (NAFLD) is rising. This increase may be associated with obesity. It has been suggested that trans -fatty acids (TFAs) play an important role in non-communicable diseases. Aim We examined the link between liver tests, fatty liver index (FLI) and plasma TFAs. Furthermore, we evaluated the impact of adiposity on this link. Methods The National Health and Nutrition Examination Survey (NHANES) was used to obtain the data on TFAs and liver function biomarkers. We took account of complex NHANES data, masked variance and weighting methodology. Results Of the 4252 participants, 46.4% were men. The mean age was 50.6 years overall; 51.3 years for men and 49.8 years for women (p = 0.206). In a fully adjusted model (demographic and clinical factors), FLI increased as trans -9-hexadecenoic acid and trans -11-octadecenoic acid levels increased; FLI was 38.1 and 42.3 for the first quarter (Q1) of trans -9-hexadecenoic acid and trans -11-octadecenoic acid, respectively, reaching 65.1 and 69.3 for the highest quarters (Q4) (p < 0.001 for all comparisons). Multivariable logistic regression showed for all four studied TFAs, the likelihood of NAFLD (determined by FLI) increased with increasing TFAs levels (quartiles) in a stepwise manner (p < 0.001 for all comparisons). Based on moderation analysis, a strong impact of body mass index (BMI) on the link between FLI and TFAs was observed. Conclusions Our results suggest a direct significant association between plasma TFAs, liver tests and NAFLD (assessed by FLI). Furthermore, BMI was shown to mediate this relationship. These findings highlight the importance of avoiding TFAs consumption in order to minimize cardiometabolic risk. Highlights • The link between liver tests, fatty liver index (FLI) and plasma trans-fatty acids (TFAs) was evaluated. • In the fully adjusted model, FLI increased as trans -9-hexadecenoic acid and trans -11-octadecenoic acid levels increased. • Moderation analysis showed a strong impact of body mass index on the link between FLI and TFAs. [ABSTRACT FROM AUTHOR]

The importance of metabolic syndrome (MetS) lies in its associated risk of cardiovascular disease and type 2 diabetes, as well as other harmful conditions such as nonalcoholic fatty liver disease. In this report, the available scientific evidence on the associations between lifestyle changes and MetS and its components is reviewed to derive recommendations for MetS prevention and management. Weight loss through an energy-restricted diet together with increased energy expenditure through physical activity contribute to the prevention and treatment of MetS. A Mediterranean-type diet, with or without energy restriction, is an effective treatment component. This dietary pattern should be built upon an increased intake of unsaturated fat, primarily from olive oil, and emphasize the consumption of legumes, cereals (whole grains), fruits, vegetables, nuts, fish, and low-fat dairy products, as well as moderate consumption of alcohol. Other dietary patterns (Dietary Approaches to Stop Hypertension, new Nordic, and vegetarian diets) have also been proposed as alternatives for preventing MetS. Quitting smoking and reducing intake of sugar-sweetened beverages and meat and meat products are mandatory. Nevertheless, there are inconsistencies and gaps in the evidence, and additional research is needed to define the most appropriate therapies for MetS. In conclusion, a healthy lifestyle is critical to prevent or delay the onset of MetS in susceptible individuals and to prevent cardiovascular disease and type 2 diabetes in those with existing MetS. The recommendations provided in this article should help patients and clinicians understand and implement the most effective approaches for lifestyle change to prevent MetS and improve cardiometabolic health. [ABSTRACT FROM AUTHOR]

An introduction is presented in which the author discuss issue on topics including role of perirenal fat as an emerging cardiovascular risk factor, the risk of coronary heart disease, and absence of alcohol abuse or other chronic liver diseases.

Non-alcoholic fatty liver (NAFLD) is the most common liver disease worldwide, progressing from simple steatosis to necroinflammation and fibrosis (leading to non-alcoholic steatohepatitis, NASH), and in some cases to cirrhosis and hepatocellular carcinoma. Inflammation, oxidative stress and insulin resistance are involved in NAFLD development and progression. NAFLD has been associated with several cardiovascular (CV) risk factors including obesity, dyslipidemia, hyperglycemia, hypertension and smoking. NAFLD is also characterized by atherogenic dyslipidemia, postprandial lipemia and high-density lipoprotein (HDL) dysfunction. Most importantly, NAFLD patients have an increased risk for both liver and CV disease (CVD) morbidity and mortality. In this narrative review, the associations between NAFLD, dyslipidemia and vascular disease in NAFLD patients are discussed. NAFLD treatment is also reviewed with a focus on lipid-lowering drugs. Finally, future perspectives in terms of both NAFLD diagnostic biomarkers and therapeutic targets are considered. [ABSTRACT FROM AUTHOR]

The article presents author's views on characterization of non-alcoholic fatty liver disease (NAFLD) by hepatic fat. Topics discussed include chronic liver diseases (CLD) and median prevalence, normal glucose tolerance and public health concerns, alterations in free fatty acids (FFA), and liver manifestation.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and cause of elevated serum liver enzyme activities in the developed world1. Obesity, diabetes mellitus (DM), and dyslipidaemia, common components of the metabolic syndrome (MetS), are frequently associated with NAFLD; 75-100% of patients with MetS or DM have NAFLD2. NAFLD is characterized by hepatic triglyceride (TG) infiltration in the absence of alcohol abuse or chronic liver disease1. NAFLD includes a spectrum of conditions varying from steatosis to steatosis with inflammation [steatohepatitis (NASH)], necrosis, fibrosis or cirrhosis that rarely progresses to hepatocellular carcinoma3. NAFLD and NASH are the hepatic manifestations of MetS and are associated with increased cardiovascular disease (CVD) risk4. Most NAFLD/NASH patients die from CVD rather than from liver disease4,5. There is no universally accepted treatment for NAFLD1-5. [ABSTRACT FROM AUTHOR]

The article argues for the study of the effects of lifestyle measures on features of non-alcoholic steatohepatitis (NASH) and trial on patients with severe NASH and diabetes mellitus and also argues for the conclusion of the study.

The authors talk about an article published in the issue, focusing on abnormal peri-organ and intra-organ fat (APIFat) deposition and its association with vascular risk. Topics discussed include the nonalcoholic fatty liver disease (NAFLD), the adverse effect of epicardial fat on cardiac function, and the need to provide treatment to these patients to prevent hepatic and vascular diseases.

Chronic obstructive pulmonary disease (COPD) is a common disorder with an increasing prevalence, characterised by persistent respiratory symptoms and airflow limitation. Systemic inflammation is involved in the pathogenesis of COPD and can also predispose to metabolic disorders (e.g., metabolic syndrome (MetS) and non-alcoholic fatty liver disease (NAFLD)). Such comorbidities can negatively affect COPD outcomes, cardiovascular risk, and quality of life. Apart from NAFLD, abnormal peri-organ or intra-organ fat (APIFat) could be considered as markers for cardiometabolic diseases and even for COPD. The present narrative review considers the associations of COPD with MetS, NAFLD, and other APIFat, including epicardial, perirenal, peripancreatic, and intramuscular adipose tissue. Further research is needed to define these relationships and identify any potential clinical implications. [ABSTRACT FROM AUTHOR]

Non-Alcoholic Fatty Liver Disease (NAFLD) is a common condition affecting around 10–25% of the general adult population, 15% of children, and even > 50% of individuals who have type 2 diabetes mellitus. It is a major cause of liver-related morbidity, and cardiovascular (CV) mortality is a common cause of death. In addition to being the initial step of irreversible alterations of the liver parenchyma causing cirrhosis, about 1/6 of those who develop NASH are at risk also developing CV disease (CVD). More recently the acronym MAFLD (Metabolic Associated Fatty Liver Disease) has been preferred by many European and US specialists, providing a clearer message on the metabolic etiology of the disease. The suggestions for the management of NAFLD are like those recommended by guidelines for CVD prevention. In this context, the general approach is to prescribe physical activity and dietary changes the effect weight loss. Lifestyle change in the NAFLD patient has been supplemented in some by the use of nutraceuticals, but the evidence based for these remains uncertain. The aim of this Position Paper was to summarize the clinical evidence relating to the effect of nutraceuticals on NAFLD-related parameters. Our reading of the data is that whilst many nutraceuticals have been studied in relation to NAFLD, none have sufficient evidence to recommend their routine use; robust trials are required to appropriately address efficacy and safety. [Display omitted] [ABSTRACT FROM AUTHOR]