scholarly journals Mediterranean Diet and Fatty Liver Risk in a Population of Overweight Older Italians: A Propensity Score-Matched Case-Cohort Study

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 258
Author(s):  
Luisa Lampignano ◽  
Rossella Donghia ◽  
Annamaria Sila ◽  
Ilaria Bortone ◽  
Rossella Tatoli ◽  
...  
Keyword(s):  
Propensity Score ◽  
Fatty Liver ◽  
Propensity Score Matching ◽  
Hepatic Steatosis ◽  
Mediterranean Diet ◽  
Alcoholic Beverages ◽  
Liver Fat ◽  
Processed Meat ◽  
Inverse Association ◽  
Nonalcoholic Fatty Liver

Hepatic steatosis, often known as fatty liver, is the most common hepatic disease in Western countries. The latest guidelines for the treatment of nonalcoholic fatty liver disease emphasize lifestyle measures, such as changing unhealthy eating patterns. Using a propensity score-matching approach, this study investigated the effect of adhering to a Mediterranean diet (MedDiet) on fatty liver risk in an older population (≥65 years) from Southern Italy. We recruited 1.403 subjects (53.6% men, ≥65 years) who completed a food frequency questionnaire (FFQ) and underwent clinical assessment between 2015 and 2018. For the assessment of the liver fat content, we applied the Fatty Liver Index (FLI). To evaluate the treatment effect of the MedDiet, propensity score matching was performed on patients with and without FLI > 60. After propensity score-matching with the MedDiet pattern as treatment, we found a higher consumption of red meat (p = 0.04) and wine (p = 0.04) in subjects with FLI > 60. Based on the FLI, the inverse association shown between adherence to the MedDiet and the risk of hepatic steatosis shows that the MedDiet can help to prevent hepatic steatosis. Consuming less red and processed meat, as well as alcoholic beverages, may be part of these healthy lifestyle recommendations.

scholarly journals Prospective association between adherence to the Mediterranean diet and hepatic steatosis: the Swiss CoLaus cohort study

BMJ Open ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. e040959
Author(s):  
Saman Khalatbari-Soltani ◽  
Pedro Marques-Vidal ◽  
Fumiaki Imamura ◽  
Nita G. Forouhi
Keyword(s):  
Cohort Study ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Mediterranean Diet ◽  
Population Level ◽  
Inverse Association ◽  
Alcoholic Fatty Liver ◽  
The Mediterranean ◽  
Prospective Association

ObjectiveThe Mediterranean diet has been promoted as a healthy dietary pattern, but whether the Mediterranean diet may help to prevent hepatic steatosis is not clear. This study aimed to evaluate the prospective association between adherence to the Mediterranean diet and risk of hepatic steatosis.DesignPopulation-based prospective cohort study.SettingThe Swiss CoLaus Study.ParticipantsWe evaluated 2288 adults (65.4% women, aged 55.8±10.0 years) without hepatic steatosis at first follow-up in 2009–2012. Adherence to the Mediterranean diet was scaled as the Mediterranean diet score (MDS) based on the Mediterranean diet pyramid ascertained with responses to Food Frequency Questionnaires.Outcome measuresNew onset of hepatic steatosis was ascertained by two indices separately: the Fatty Liver Index (FLI, ≥60 points) and the non-alcoholic fatty liver disease (NAFLD) score (≥−0.640 points). Prospective associations between adherence to the Mediterranean diet and risk of hepatic steatosis were quantified using Poisson regression.ResultsDuring a mean 5.3 years of follow-up, hepatic steatosis was ascertained in 153 (6.7%) participants by FLI criteria and in 208 (9.1%) by NAFLD score. After multivariable adjustment, higher adherence to MDS was associated with lower risk of hepatic steatosis based on FLI: risk ratio 0.84 (95% CI 0.73 to 0.96) per 1 SD of MDS; 0.85 (0.73 to 0.99) adjusted for BMI; and 0.85 (0.71 to 1.02) adjusted for both BMI and waist circumference. When using NAFLD score, no significant association was found between MDS and risk of hepatic steatosis (0.95 (0.83 to 1.09)).ConclusionA potential role of the Mediterranean diet in the prevention of hepatic steatosis is suggested by the inverse association observed between adherence to the Mediterranean diet and incidence of hepatic steatosis based on the FLI. The inconsistency of this association when hepatic steatosis was assessed by NAFLD score points to the need for accurate population-level assessment of fatty liver and its physiological markers.

Therapeutic role of niacin in the prevention and regression of hepatic steatosis in rat model of nonalcoholic fatty liver disease

2014 ◽  
Vol 306 (4) ◽  
pp. G320-G327 ◽  
Author(s):  
Shobha H. Ganji ◽  
Gary D. Kukes ◽  
Nils Lambrecht ◽  
Moti L. Kashyap ◽  
Vaijinath S. Kamanna
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Fatty Acid Synthase ◽  
Liver Fat ◽  
Mrna Levels ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD), a leading cause of liver damage, comprises a spectrum of liver abnormalities including the early fat deposition in the liver (hepatic steatosis) and advanced nonalcoholic steatohepatitis. Niacin decreases plasma triglycerides, but its effect on hepatic steatosis is elusive. To examine the effect of niacin on steatosis, rats were fed either a rodent normal chow, chow containing high fat (HF), or HF containing 0.5% or 1.0% niacin in the diet for 4 wk. For regression studies, rats were first fed the HF diet for 6 wk to induce hepatic steatosis and were then treated with niacin (0.5% in the diet) while on the HF diet for 6 wk. The findings indicated that inclusion of niacin at 0.5% and 1.0% doses in the HF diet significantly decreased liver fat content, liver weight, hepatic oxidative products, and prevented hepatic steatosis. Niacin treatment to rats with preexisting hepatic steatosis induced by the HF diet significantly regressed steatosis. Niacin had no effect on the mRNA expression of fatty acid synthesis or oxidation genes (including sterol-regulatory element-binding protein 1, acetyl-CoA carboxylase 1, fatty acid synthase, and carnitine palmitoyltransferase 1) but significantly inhibited mRNA levels, protein expression, and activity of diacylglycerol acyltrasferase 2, a key enzyme in triglyceride synthesis. These novel findings suggest that niacin effectively prevents and causes the regression of experimental hepatic steatosis. Approved niacin formulation(s) for other indications or niacin analogs may offer a very cost-effective opportunity for the clinical development of niacin for treating NAFLD and fatty liver disease.

scholarly journals Sodium-Glucose Cotransporter-2 Inhibitors for Treatment of Nonalcoholic Fatty Liver Disease: A Meta-Analysis of Randomized Controlled Trials

Metabolites ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 22
Author(s):  
Alessandro Mantovani ◽  
Graziana Petracca ◽  
Alessandro Csermely ◽  
Giorgia Beatrice ◽  
Giovanni Targher
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Meta Analysis ◽  
Liver Fat ◽  
Controlled Trials ◽  
Liver Fat Content ◽  
Nonalcoholic Fatty Liver ◽  
Randomized Controlled ◽  
Sodium Glucose Cotransporter

Recent randomized controlled trials (RCTs) tested the efficacy of sodium-glucose cotransporter-2 (SGLT-2) inhibitors to specifically treat nonalcoholic fatty liver disease (NAFLD). We systematically searched three electronic databases (up to 31 October 2020) for identifying placebo-controlled or head-to-head RCTs that used SGLT-2 inhibitors for treatment of NAFLD. No published RCTs with paired liver biopsy data were available for the meta-analysis. Primary outcome measures were changes in serum liver enzyme levels and liver fat content on imaging techniques. Overall, we included a total of twelve RCTs testing the efficacy of dapagliflozin (n = six RCTs), empagliflozin (n = three RCTs), ipragliflozin (n = two RCTs) or canagliflozin (n = one RCT) to specifically treat NAFLD for a median period of 24 weeks with aggregate data on 850 middle-aged overweight or obese individuals with NAFLD (90% with type 2 diabetes). Compared to placebo/reference therapy, treatment with SGLT-2 inhibitors significantly decreased serum alanine aminotransferase (weighted mean differences (WMD): −10.0 IU/L, 95%CI −12.2 to −7.79 IU/L; I2 = 10.5%) and gamma-glutamyltransferase levels (WMD: −14.49 IU/L, 95%CI −19.35 to −9.63 IU/L, I2 = 38.7%), as well as the absolute percentage of liver fat content on magnetic resonance-based techniques (WMD: −2.05%, 95%CI −2.61 to −1.48%; I2 = 0%). In conclusion, SGLT-2 inhibitors seem to be a promising treatment option for NAFLD.

scholarly journals Prevalence of NAFLD in Healthy and Young Male Individuals

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Asif Niaz ◽  
Zafar Ali ◽  
Shaista Nayyar ◽  
Naureen Fatima
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Alcohol Intake ◽  
Young Male ◽  
Difficult Problem ◽  
Liver Fat ◽  
Renal Diseases ◽  
Nonalcoholic Fatty Liver ◽  
History Of ◽  
Ultrasound Evidence

Introduction. Nonalcoholic fatty liver disease (NAFLD) is an important cause of liver disease in adults and the most common cause of liver disease in children (Lavine and Schwimmer 2004). The abnormalities include increased liver fat without inflammation (steatosis) and nonalcoholic steatohepatitis (NASH). NASH may lead to fibrosis, cirrhosis, and ultimately liver failure if it is not treated (Matteoni et al. 1999). The objective of the study is to estimate the magnitude of the problem which will help us to formulate strategies in managing the potentially difficult problem. Materials and Methods. We included 1000 individuals between the ages of 30 and 50 years who came for annual checkup. The patients with other comorbidities like diabetes, ischemic heart disease, chronic liver disease, or renal diseases were excluded from the study. History of alcohol ingestion was also taken; any individual with history of alcohol intake was also excluded. All of them underwent investigations including CBC, LFTs, height and weight. The individuals who were found to have increased ALT (50 to 150 u/L) further underwent investigations including ultrasound of abdomen hepatitis b and c serology RA and ANA antibodies. All the individuals who were found to have viral or autoimmune illness were excluded from the study. The individuals having raised ALT levels and ultrasound evidence of fatty liver were taken. Results. 13.5% of the individuals were found to have NAFLD among those selected for the study. Conclusion. Mass campaign regarding physical and dietary measures needs to be undertaken in general masses regarding the gravity and potential prevention of the disease.

scholarly journals Dissociation of hepatic insulin resistance from susceptibility of nonalcoholic fatty liver disease induced by a high-fat and high-carbohydrate diet in mice

2014 ◽  
Vol 306 (6) ◽  
pp. G496-G504 ◽  
Author(s):  
Akihiro Asai ◽  
Pauline M. Chou ◽  
Heng-Fu Bu ◽  
Xiao Wang ◽  
M. Sambasiva Rao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Diet Group ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Akt Phosphorylation ◽  
High Carbohydrate

Liver steatosis in nonalcoholic fatty liver disease is affected by genetics and diet. It is associated with insulin resistance (IR) in hepatic and peripheral tissues. Here, we aimed to characterize the severity of diet-induced steatosis, obesity, and IR in two phylogenetically distant mouse strains, C57BL/6J and DBA/2J. To this end, mice (male, 8 wk old) were fed a high-fat and high-carbohydrate (HFHC) or control diet for 16 wk followed by the application of a combination of classic physiological, biochemical, and pathological studies to determine obesity and hepatic steatosis. Peripheral IR was characterized by measuring blood glucose level, serum insulin level, homeostasis model assessment of IR, glucose intolerance, insulin intolerance, and AKT phosphorylation in adipose tissues, whereas the level of hepatic IR was determined by measuring insulin-triggered hepatic AKT phosphorylation. We discovered that both C57BL/6J and DBA/2J mice developed obesity to a similar degree without the feature of liver inflammation after being fed an HFHC diet for 16 wk. C57BL/6J mice in the HFHC diet group exhibited severe pan-lobular steatosis, a marked increase in hepatic triglyceride levels, and profound peripheral IR. In contrast, DBA/2J mice in the HFHC diet group developed only a mild degree of pericentrilobular hepatic steatosis that was associated with moderate changes in peripheral IR. Interestingly, both C57BL/6J and DBA/2J developed severe hepatic IR after HFHC diet treatment. Collectively, these data suggest that the severity of diet-induced hepatic steatosis is correlated to the level of peripheral IR, not with the severity of obesity and hepatic IR. Peripheral rather than hepatic IR is a dominant factor of pathophysiology in nonalcoholic fatty liver disease.

Abstract 007: Nonalcoholic Fatty Liver Disease and Subclinical Atherosclerosis: Analyses from the Coronary Artery Risk Development in Young Adults (CARDIA) Study

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Lisa B VanWagner ◽  
Christina M Shay ◽  
Hongyan Ning ◽  
John Wilkins ◽  
Cora E Lewis ◽  
...  
Keyword(s):  
Risk Factors ◽  
Young Adults ◽  
Liver Disease ◽  
Coronary Artery ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Fat ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Nonalcoholic Fatty Liver

Background: Nonalcoholic Fatty Liver Disease (NAFLD) and excess visceral adipose tissue (VAT) are associated with cardiovascular disease (CVD). Recent studies suggest that NAFLD and coronary artery calcification (CAC) are related independent of VAT. In a population-based cross-sectional sample of black and white adults free from prevalent liver or heart disease, we tested the hypothesis that NAFLD is associated with the presence of CAC and abdominal aortoiliac calcification (AAC) independent of VAT and other CVD risk factors. Methods: Participants from the Coronary Artery Risk Development in Young Adults study (Y25 exam) with concurrent computed tomography quantification of liver fat, CAC and AAC were included (n=2,163). NAFLD was defined as liver attenuation ≤ 40 Hounsfield Units after exclusion of other causes of liver fat (medication/alcohol use). Using the Agatston method, CAC/AAC presence was defined as a score > 0. Logistic regression models were used to calculate odds ratios and 95% confidence intervals. Results: Participant age was 49.9 (3.7) years and the sample was equally distributed by sex (55.6% female) and race (50.1% black). Mean BMI was 30.6 (7.1). The CAC and AAC prevalence was 26.5% and 49.6%. NAFLD prevalence was 9.6%. NAFLD participants were 50.1 (3.7) years old and more likely to be male (59.8% vs. 51.7%, p<0.0001), white (56.5% vs. 49.3%, p<0.05) and have the metabolic syndrome (70.1% vs. 22.6%, p<0.0001) than those with no NAFLD. They were also more likely to have CAC (37.2%) and AAC (60.9%) than those with no NAFLD (25.4% and 49.4%, respectively). In multivariable analyses adjusted for demographics and health behaviors, NAFLD was associated with the presence of CAC and AAC (Table 1). This association was attenuated after adjustment for CVD risk factors and VAT. Effect modification by race and sex was not statistically significant. Conclusion: In contrast to prior studies, our results suggest that the relationship between NAFLD and subclinical CVD is mediated by the presence of other CVD risk factors.

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