Non-alcoholic Fatty Liver Disease and Longitudinal Cognitive Changes in Middle-Aged and Elderly Adults

Background and PurposeNon-alcoholic fatty liver disease (NAFLD) and cognitive impairment are common aging-related disorders. This study aims to explore the changes of cognitive function in middle-aged and elderly population with NAFLD from a Jidong impairment cohort.MethodsA total of 1,651 middle-aged and elderly participants (>40 years) without cognitive impairment were recruited into the current study in 2015 and were followed up until to 2019. Abdominal ultrasonography was used for diagnosis of NAFLD. Global cognitive function was assessed with the Mini-Mental State Examination (MMSE). Cognitive impairment was defined as a score <18 for illiterates, a score <21 for primary school graduates, and a score <25 for junior school graduates or above. Multivariable regression analysis was performed to evaluate the association between NAFLD and the four-year cognitive changes.ResultsOut of 1,651 participants, 795 (48.2%) of them had NAFLD in 2015. Cognitive impairment occurred in 241 (14.6%) participants in 2019. Patients with NAFLD had higher 4-year incidence of cognitive impairment than non-NAFLD patients did (17.7 vs. 11.7%, p < 0.001). Multivariable linear regression analysis showed significant association of baseline NAFLD with lower MMSE score in 2019 (β = −0.36, p < 0.05). Multivariable logistic analysis found that the adjusted odds ratio (OR) with 95% confidence interval (CI) of baseline NAFLD was 1.45 (1.00–2.11) for cognitive impairment in 2019 (p = 0.05). We also identified effects of baseline NAFLD on subsequent cognitive impairment as modified by age (interaction p < 0.01) and carotid stenosis (interaction p = 0.05) but not by gender.ConclusionsNAFLD is associated with cognitive decline, especially in middle-aged and with carotid stenosis population.

Impact of Sarcopenia and Myosteatosis in Non-Cirrhotic Stages of Liver Diseases: Similarities and Differences across Aetiologies and Possible Therapeutic Strategies

Sarcopenia is defined as a loss of muscle strength, mass and function and it is a predictor of mortality. Sarcopenia is not only a geriatric disease, but it is related to several chronic conditions, including liver diseases in both its early and advanced stages. Despite the increasing number of studies exploring the role of sarcopenia in the early stages of chronic liver disease (CLD), its prevalence and the relationship between these two clinical entities are still controversial. Myosteatosis is characterized by fat accumulation in the muscles and it is related to advanced liver disease, although its role in the early stages is still under researched. Therefore, in this narrative review, we firstly aimed to evaluate the prevalence and the pathogenetic mechanisms underlying sarcopenia and myosteatosis in the early stage of CLD across different aetiologies (mainly non-alcoholic fatty liver disease, alcohol-related liver disease and viral hepatitis). Secondly, due to the increasing prevalence of sarcopenia worldwide, we aimed to revise the current and the future therapeutic approaches for the management of sarcopenia in CLD.

Association of Dietary Patterns with MRI Markers of Hepatic Inflammation and Fibrosis in the MAST4HEALTH Study

Whereas the etiology of non-alcoholic fatty liver disease (NAFLD) is complex, the role of nutrition as a causing and preventive factor is not fully explored. The aim of this study is to associate dietary patterns with magnetic resonance imaging (MRI) parameters in a European population (Greece, Italy, and Serbia) affected by NAFLD. For the first time, iron-corrected T1 (cT1), proton density fat fraction (PDFF), and the liver inflammation fibrosis score (LIF) were examined in relation to diet. A total of 97 obese patients with NAFLD from the MAST4HEALTH study were included in the analysis. A validated semi-quantitative food frequency questionnaire (FFQ) was used to assess the quality of diet and food combinations. Other variables investigated include anthropometric measurements, total type 2 diabetes risk, physical activity level (PAL), and smoking status. Principal component analysis (PCA) was performed to identify dietary patterns. Six dietary patterns were identified, namely “High-Sugar”, “Prudent”, “Western”, “High-Fat and Salt”, “Plant-Based”, and “Low-Fat Dairy and Poultry”. The “Western” pattern was positively associated with cT1 in the unadjusted model (beta: 0.020, p-value: 0.025) and even after adjusting for age, sex, body mass index (BMI), PAL, smoking, the center of the study, and the other five dietary patterns (beta: 0.024, p-value: 0.020). On the contrary, compared with low-intake patients, those with medium intake of the “Low-Fat Dairy and Poultry” pattern were associated with lower values of cT1, PDFF, and LIF. However, patients with a “Low-Fat Dairy and Poultry” dietary pattern were negatively associated with MRI parameters (cT1: beta: −0.052, p-value: 0.046, PDFF: beta: −0.448, p-value: 0.030, LIF: beta: −0.408, p-value: 0.025). Our findings indicate several associations between MRI parameters and dietary patterns in NAFLD patients, highlighting the importance of diet in NAFLD.

Association of Non-Alcoholic Fatty Liver Disease with Metabolic Syndrome: A Single Center Study

Background: NAFLD is a condition defined by excessive fat accumulation in the form of triglycerides (steatosis) in the liver (> 5% of hepatocytes histologically). Non-alcoholic fatty liver disease is increasingly being recognized as a major cause of liver-related morbidity and mortality among 15-40% of the general population. Aim of the study: To evaluate the clinical profile of patients with non-alcoholic fatty liver disease and its association with metabolic syndrome.Methods:The present cross-sectional, retro-spective study was conducted as outdoor patient basis in the Department of Medicine, Jashore medical college hospital & a private diagnostic centre, Jashore.. A total of 74 cases were included for the study. All patients in the study underwent routine investigations including complete blood counts, blood sugar, liver function tests, HBsAg, anti-HCV, lipid profile andUSG of whole abdomen. The data was collected during OPD treatment and was recorded in predesigned and pretested proforma and analyzed.Results:Mean age of the patient was 53.70±7.22 years. On physical examination findings showed the mean BMI was 27.6±4.39 kg/m2, mean waist circumference was 74.22±7.44 cm. Mean diastolic blood pressure (mm Hg) was 92.87±6.25 and mean systolic blood pressure (mm Hg) 132.0±18.17. Maximum 52% patients had triglycerides >150 mg/dl while low serum HDL level was seen in 37% patients and increased waist circumference was found in 32% patients. Altered ALT ≥41 IU was observed in 10 (62.50%) of Grade II of patients with NAFLD with metabolic syndrome. Central obesity was observed in 12 (75.00%) of Grade II patients with NAFLD with metabolic syndrome. While 14 (87.50%) Grade II of patients with NAFLD with metabolic syndrome showed impaired fasting glucose (>110 mg/dl). Hypertriglyceridemia (>150 mg/dl) in 12 (70.58%) seen in Grade I of patients with NAFLD without metabolic syndrome.Conclusion:Higher prevalence of all the components of metabolic syndrome in cases of NAFLD was observed. It can be concluded that symptoms and signs of NAFLD are non-specific and occur later in the course of the disease hence the physician should have a high index of suspicion in order to detect NAFLD early in the course of the disease.

Therapeutic potential of policosanol in the concurrent management of dyslipidemia and non-alcoholic fatty liver disease

Background High-fat diet (HFD) possesses a major cause of cardiovascular disease, and hepatosteatosis. Unfortunately, long-term use of statins has a theoretical possibility of worsening of hepatic histology in the patients with non-alcoholic fatty liver disease (NAFLD). The objective of the study was to explore hepatoprotective potential of policosanol as an alternative to statins in experimental NAFLD. For the same, young male Wistar rats were fed with HFD for 8 weeks to induce NAFLD. 48 adult Wistar rats were distributed into six investigational groups: normal control, HFD control, and four treatment groups, receiving policosanol (50 and 100 mg/kg/day), atorvastatin (30 mg/kg/day), and silymarin (100 mg/kg/day) for 8 weeks along with HFD. Result HFD consumption caused profound hepatotoxicity evident by hepatic oxidative stress, increased Serum glutamic oxaloacetic transaminase (SGOT), Serum glutamic pyruvic transaminase (SGPT), Alkaline phosphatase (ALP), and bilirubin content. Treatment with policosanol (100 mg/kg) markedly reduced the elevated SGOT, SGPT, and ALP levels in HFD-fed rats. Moreover, policosanol significantly reduced hepatic oxidative stress manifest by reduced malondialdehyde (MDA) and increased glutathione (GSH) level. The treatment with policosanol (100 mg/kg) was found to be more active in attenuating the HFD-induced hepatotoxicity as compared to policosanol (50 mg/kg) and atorvastatin (30 mg/kg). Moreover, we observed that the hepatoprotective potential of policosanol was comparable to the silymarin. Conclusions The results of the study clearly indicated that the policosanol could be considered an intriguing approach for the treatment of NAFLD.

Limosilactobacillus fermentum MG4295 Improves Hyperglycemia in High-Fat Diet-Induced Mice

Hyperglycemia due to uncontrolled glucose regulation is widely known as cause of diabetes, non-alcoholic fatty liver disease (NAFLD), and other complications. NAFLD refers to a condition in which fat is excessively accumulated, whether inflamed or not, and has caused serious medical problems in recent years. The aim of this study was to explore the antihyperglycemia effects of Limosilactobacillus fermentum MG4295 (L. fermentum MG4295) in high-fat diet (HFD)-induced in vivo. We demonstrated the suitability of L. fermentum MG4295 as a probiotic by observing its stability, survivability, and proliferation under simulated gastrointestinal conditions, and safety, antibiotic susceptibility, hemolysis, and enzyme activity. The potential antihyperglycemic activity of L. fermentum MG4295 was investigated in an HFD and sugar-water-induced mouse model. Administration of this strain for 12 weeks showed an improved trend in glucose tolerance, insulin, alanine amino transferase, total cholesterol, low-density lipoprotein cholesterol, and glucagon-like peptide-1. Histopathological analysis revealed that L. fermentum MG4295 significantly reduced the histopathological scores of hepatic steatosis, inflammation, and hepatocellular hypertrophy in liver tissues and lipid content in adipose tissues. Administration of L. fermentum MG4295 upregulated IRS-1, AKT, and GLUT4 and downregulated G6Pc and PEPCK expression in liver and/or muscle tissues. Our results suggest that L. fermentum MG4295 can improve hyperglycemia. Furthermore, it can be used as a dietary functional supplement to manage blood glucose.

Genetic and Life Style Risk Factors for Recurrent Non-alcoholic Fatty Liver Disease Following Liver Transplantation

Recurrent or de novo non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) following liver transplantation (LT) is a frequent event being increasingly recognized over the last decade, but the influence of recurrent NASH on graft and patient outcomes is not yet established. Taking into consideration the long term survival of liver transplanted patients and long term complications with associated morbidity and mortality, it is important to define and minimize risk factors for recurrent NAFLD/NASH. Metabolic syndrome, obesity, dyslipidemia, diabetes mellitus are life style risk factors that can be potentially modified by various interventions and thus, decrease the risk of recurrent NAFLD/NASH. On the other hand, genetic factors like recipient and/or donor PNPLA3, TM6SF2, GCKR, MBOAT7 or ADIPOQ gene polymorphisms proved to be risk factors for recurrent NASH. Personalized interventions to influence the different metabolic disorders occurring after LT in order to minimize the risks, as well as genetic screening of donors and recipients should be performed pre-LT in order to achieve diagnosis and treatment as early as possible.

Chenopodium quinoa to Modulate Innate Myeloid Cells in the Induction of Obesity

Complex interactions between innate and adaptive immune effectors are an important component in the induction of obesity. Particularly, different subsets of myeloid cells play key roles in metabolic liver diseases and, therefore, are promising targets for intervention strategies. Chenopodium quinoa seeds constitute a good source of immunonutritional compounds, which help prevent high-fat, diet-enhanced innate immune signaling via TLR4/MyD88 that boosts inflammation. Herein, two metabolic mouse models—wild type (WT) and tributyltin treated (TBT)—were used to examine the effects associated with non-alcoholic fatty liver disease (NAFLD); mice were fed with a high-fat diet (HFD) and administered with wheat or C. quinoa bread. Variations in myeloid cells were obtained from a hemogram analysis, and rt-qPCR (mRNA) served to evaluate macrophage markers (i.e., CD68/CD206 ratio) as well as liver inflammation (i.e., Lyve-1) to gain insights into their selective functional differentiation into metabolically injured livers. Only administration of C. quinoa bread prevented alterations in the liver/body weight ratio either in WT animals or those treated with TBT. These effects were associated with significantly increased variations in the peripheral myeloid cell population. Hepatic mRNA markers revealed that C. quinoa enables a selective functional differentiation and function of intrahepatic monocyte-derived macrophages preserving tissue integrity and function.