Nonalcoholic Fatty Liver Disease Research Articles

Non-invasively differentiate non-alcoholic steatohepatitis by visualizing hepatic integrin αvβ3 expression with a targeted molecular imaging modality

BACKGROUND Non-invasive methods to diagnose non-alcoholic steatohepatitis (NASH), an inflammatory subtype of non-alcoholic fatty liver disease (NAFLD), are currently unavailable. AIM To develop an integrin αvβ3-targeted molecular imaging modality to differentiate NASH. METHODS Integrin αvβ3 expression was assessed in Human LO2 hepatocytes Scultured with palmitic and oleic acids (FFA). Hepatic integrin αvβ3 expression was analyzed in rabbits fed a high-fat diet (HFD) and in rats fed a high-fat, high-carbohydrate diet (HFCD). After synthesis, cyclic arginine-glycine-aspartic acid peptide (cRGD) was labeled with gadolinium (Gd) and used as a contrast agent in magnetic resonance imaging (MRI) performed on mice fed with HFCD. RESULTS Integrin αvβ3 was markedly expressed on FFA-cultured hepatocytes, unlike the control hepatocytes. Hepatic integrin αvβ3 expression significantly increased in both HFD-fed rabbits and HFCD-fed rats as simple fatty liver (FL) progressed to steatohepatitis. The distribution of integrin αvβ3 in the liver of NASH cases largely overlapped with albumin-positive staining areas. In comparison to mice with simple FL, the relative liver MRI-T1 signal value at 60 minutes post-injection of Gd-labeled cRGD was significantly increased in mice with steatohepatitis (P < 0.05), showing a positive correlation with the NAFLD activity score (r = 0.945; P < 0.01). Hepatic integrin αvβ3 expression was significantly upregulated during NASH development, with hepatocytes being the primary cells expressing integrin αvβ3. CONCLUSION After using Gd-labeled cRGD as a tracer, NASH was successfully distinguished by visualizing hepatic integrin αvβ3 expression with MRI.

Cardiovascular and nonalcoholic fatty liver disease: Sharing common ground through SIRT1 pathways

As a non-communicable disease, cardiovascular disorders have become the leading cause of death for men and women. Of additional concern is that cardiovascular disease is linked to chronic comorbidity disorders that include nonalcoholic fatty liver disease (NAFLD). NAFLD, also termed metabolic-dysfunction-associated steatotic liver disease, is the greatest cause of liver disease throughout the world, increasing in prevalence concurrently with diabetes mellitus (DM), and can progress to nonalcoholic steatohepatitis that leads to cirrhosis and liver fibrosis. Individuals with metabolic disorders, such as DM, are more than two times likely to experience cardiac disease, stroke, and liver disease that includes NAFLD when compared individuals without metabolic disorders. Interestingly, cardiovascular disorders and NAFLD share a common underlying cellular mechanism for disease pathology, namely the silent mating type information regulation 2 homolog 1 (SIRT1; Saccharomyces cerevisiae ). SIRT1, a histone deacetylase, is linked to metabolic pathways through nicotinamide adenine dinucleotide and can offer cellular protection though multiple avenues, including trophic factors such as erythropoietin, stem cells, and AMP-activated protein kinase. Translating SIRT1 pathways into clinical care for cardiovascular and hepatic disease can offer significant hope for patients, but further insights into the complexity of SIRT1 pathways are necessary for effective treatment regimens.

Systemic treatment of hepatocellular carcinoma secondary to non-alcoholic fatty liver disease

Hepatocellular carcinoma (HCC) is the third leading cause of cancer death globally, with 15% of cases arising on a background of non-alcoholic fatty liver disease (NAFLD). NAFLD is a heterogenous condition ranging from fatty liver to cirrhosis and is itself a growing global problem, with estimated worldwide prevalence of 50% in 2040. Pathophysiology of NAFLD-HCC is not well understood, there are no dedicated screening programs, and there have been no clinical studies of anti-cancer treatments in this population specifically. However, the NAFLD-HCC population appears different than other aetiologies - patients tend to be older, diagnosed at more advanced stages, have more comorbidities, and overall worse prognosis. Understanding of best treatment options for this group of patients is an urgent unmet clinical need. This narrative review discusses NAFLD-HCC pathophysiology and systemic treatment, and offers suggestions for future directions in this therapy area.

Potential of traditional Chinese medicine in the treatment of nonalcoholic fatty liver disease: A promising future

In this editorial, we provide insights into the publication by Niu et al featured in the latest edition of the World Journal of Gastroenterology . Specifically, our focus was on exploring the potential of traditional Chinese medicine (TCM) in treating nonalcoholic fatty liver disease (NAFLD) induced by a high-fat diet through various mechanisms. NAFLD is a common liver condition, affecting approximately 25% of the world's population. It is closely linked to metabolic syndrome, insulin resistance, excessive body weight, and irregular lipid processing, leading to fat accumulation in the liver, as well as oxidative stress and inflammation. While maintaining a healthy diet and active lifestyle are essential for managing NAFLD, treatment options are limited due to undefined pathogenesis and a lack of specific medications. TCM, rooted in traditional Chinese practices, presents a promising alternative through its "syndrome differentiation and treatment" principles, enhancing liver lipid metabolism, reducing inflammation, and addressing fibrosis. Certain herbs, such as Poria cocos , Puaria lobata , and Salvia miltiorrhiza , have shown significant efficacy in reducing fat deposition and improving liver function. Due to systematic research and analysis of mechanisms, TCM is anticipated to yield new approaches to prevent and treat NAFLD, increasing its clinical application.

Study the role of xanthine oxidase inhibitor, allopurinol in experimentally induced steatohepatitis

Nonalcoholic steatohepatitis (NASH) is a chronic liver disease which can lead to cirrhosis and hepatic failure. It is observed in patients with both type 1 and type 2 diabetes mellitus (T1DM, T2DM). Allopurinol, a xanthine oxidase inhibitor that is widely used in clinical practice, has been demonstrated to reduce hepatic oxidative stress and attenuate acute liver injury which may be through activation of antioxidant pathways. This work aimed at investigating the role of Allopurinol (ALP) in attenuation of type 1 diabetes associated with Nonalcoholic fatty liver disease (NAFLD) and exploring the possible molecular mechanism by which ALP attenuates NASH in type 1 diabetes. Forty-five adult male albino rats were included in the study. They were randomly allocated to 3 equal groups: group I (control), Group II (diabetic animals), Group III (diabetic animals with allopurinol treatment). At the end of this experimental study measurements of serum glucose, ALT, AST, cholesterol, triglyceride, serum levels of uric acid, malondialdehyde (MDA), serum superoxide dismutase (SOD) were done. Histological analysis of liver tissue to diagnose steatohepatitis and gene expression of nuclear factor-erythroid-2- related factor-2 (Nrf2) & TNFα were done. Diabetic rates treated with allopurinol (group III) showed decrease in serum levels of ALT, AST, cholesterol, uric acid and MDA compared to diabetic rat group. As regards TNF, gene expression was significantly decreased in group III compared to group II. This study also demonstrated that Nrf2α was significantly increased in group III compared to group II. Allopurinol also, ameliorated the histopathological changes observed in group II. In conclusion, allopurinol treatment increases the Nrf2 gene expression in the liver of STZ-induced diabetic rats and ameliorates steatohepatitis through modulation of TNF-α gene expression. Allopurinol could be a candidate for prevention or treatment of NAFLD.

Effects of multidisciplinary therapy on energy balance, inflammation, and metabolic diseases in adolescents with obesity: A narrative review.

Obesity is a consequence of multiple factors, including genetics, lifestyle and nutritional choices, physical activity, sleep duration, screen time, and mood disorders. These behavioral elements can impair the regulation of energy balance and obesity management that link obesity to a constellation of chronic conditions that lead to a high prevalence of cardiometabolic risk factors, metabolic syndrome, and nonalcoholic fatty liver disease. Multidisciplinary therapy is defined as an approach delivered by a multidisciplinary-trained health team covering at least two components of behavior, physical activity/exercise, dietary habits, and/or psychological counseling associated with clinical interventions. This narrative review summarizes the effects of multidisciplinary therapy on neuroendocrine regulation of energy balance, inflammatory biomarkers, cardiometabolic risk factors, metabolic syndrome, nonalcoholic fatty liver diseases, behavior, and quality of life. We found that multidisciplinary therapy, including medical, nutritional, exercise, and behavioral counseling, and/or education, was useful for addressing outcomes such as visceral adiposity, neuroendocrine regulation of energy balance, inflammatory biomarkers, cardiometabolic risk factors, nonalcoholic fatty liver disease, and metabolic syndrome. The effects were mediated by improvements in neuroendocrine regulation of energy balance, downregulation of the pro-inflammatory states, and a reduction in comorbidities. Multidisciplinary therapy also improved mood disorders and quality of life.

Seasonal variation in dietary intake and its association with obesity-related chronic diseases in northeast China

Abstract Objective The objective of this study was to assess seasonal changes in dietary and nutrient intake of residents (18-75 years old) in Northeast China during summer and winter, and to explore the associations between fatty acids, phytosterols, and the prevalence of obesity-related chronic diseases, particularly obesity, hyperlipidemia, and NAFLD. Methods A total of 4773 participants from the Internet-based Dietary Questionnaire for Chinese (IDQC) were included in this study. Dietary intake information was collected using a validated food frequency questionnaire. Student’s t-test or Mann-Whitney U-test was used to analyze continuous variables, while Chi-squared tests were used to compare categorical variables. Multivariable logistic regression was employed to assess the relationship between fatty acids, phytosterols, and obesity-related chronic diseases. Results The mean consumption of legumes, vegetables, fruits, nuts, dairy products, fish, condiments, energy, protein, fat, and carbohydrate differed significantly between summer and winter (P < 0.05). Significant inverse associations were found between both fatty acids and phytosterols and obesity-related chronic diseases in multivariate adjusted models. Summer polyunsaturated fatty acid (PUFA) intake was negatively associated with the prevalence of hyperlipidemia (Q4, OR, 0.515; 95%CI, 0.283-0.921; P < 0.05) and non-alcoholic fatty liver disease (NAFLD) (Q4, OR, 0.331; 95%CI, 0.176-0.599; P < 0.001). Phytosterols intake was negatively associated with the prevalence of obesity (Q4, OR, 0.603; 95%CI, 0.414-0.873; P < 0.05), hyperlipidemia (Q4, OR, 0.420; 95%CI, 0.233-0.731; P < 0.001), and NAFLD (Q4, OR, 0.206; 95%CI, 0.111-0.360; P < 0.001) during the summer. Conclusions Higher PUFA intake was associated with a lower prevalence of obesity, hyperlipidemia, and NAFLD. Phytosterol intake was inversely associated with the prevalence of hyperlipidemia and NAFLD. These findings suggest that the associations between PUFA and phytosterols and the prevalence of obesity-related chronic diseases may be influenced by seasonal differences in food intake.

Associations of Metabolic Dysfunction-Associated Fatty Liver Disease With Peripheral Artery Disease: Prospective Analysis in the UK Biobank and ARIC Study.

There is currently limited evidence comparing the association between metabolic dysfunction-associated fatty liver disease (MAFLD), nonalcoholic fatty liver disease (NAFLD), and the risk of peripheral artery disease (PAD). This study aims to analyze the associations of MAFLD and NAFLD with incident PAD. Two longitudinal studies, the UKB (UK Biobank) study (n=372 216) and the ARIC (Atherosclerosis Risk in Communities) study (n=4681), categorized participants into MAFLD/non-MAFLD groups and NAFLD/non-NAFLD groups. Subsequently, participants were classified into 4 groups: non-fatty liver disease, MAFLD-only, NAFLD-only, and both MAFLD and NAFLD groups. Cox proportional hazard model estimated associations of MAFLD/NAFLD status, subtypes, and liver fibrosis severity with PAD risk. The MAFLD group had a higher risk of incident PAD compared with the non-MAFLD group, and similarly, the NAFLD group had a higher risk compared with the non-NAFLD group. Among these 4 groups, the MAFLD-only group had the strongest association with the risk of incident PAD, while the NAFLD-only group was not independently associated. Diabetic MAFLD subtype was significantly associated with increased PAD risk, and higher level of liver fibrosis scores correlated with elevated PAD risk. Both MAFLD and NAFLD are significantly associated with an increased incidence of PAD, with stronger associations in MAFLD and diabetic MAFLD population. These findings emphasize that the need for screening and prevention strategies for PAD in this high-risk population is warranted. The assessment of MAFLD and its subtypes should be considered as an integral component of cardiovascular risk assessment.

Mesenchymal Stem Cell-Derived Extracellular Vesicles Carrying Circ-Tulp4 Attenuate Diabetes Mellitus with Nonalcoholic Fatty Liver Disease by Inhibiting Cell Pyroptosis through the HNRNPC/ABHD6 Axis.

Diabetes mellitus with nonalcoholic fatty liver disease (DM-NAFLD) represents a complex metabolic syndrome with significant clinical challenges. This study explores the therapeutic potential and underlying mechanisms of umbilical cord-derived mesenchymal stem cells (UCMSCs)-derived extracellular vesicles (EVs) in DM-NAFLD. UCMSCs-EVs were isolated and characterized. DM-NAFLD mouse model was developed through high-energy diet and streptozotocin injection. Additionally, primary mouse hepatocytes were exposed to high glucose to simulate cellular conditions. Hepatic tissue damage, body weight changes, lipid levels, glucose and insulin homeostasis, and hepatic lipid accumulation were evaluated. The interaction between UCMSCs-EVs and hepatocytes was assessed, focusing on the localization and function of circ-Tulp4. The study also investigated the expression of circularRNA TUB-like protein 4 (circ-Tulp4), heterogeneous nuclear ribonucleoprotein C (HNRNPC), abhydrolase domain containing 6 (ABHD6), cleaved Caspase-1, NLR family pyrin domain containing 3 (NLRP3) and cleaved N-terminal gasdermin D (GSDMD-N). The binding of circ-Tulp4 to lysine demethylase 6B (KDM6B) and the subsequent epigenetic regulation of ABHD6 by H3K27me3 were analyzed. Circ-Tulp4 was reduced, while HNRNPC and ABHD6 were elevated in DM-NAFLD models. UCMSCs-EVs attenuated hepatic steatosis and inhibited the NLRP3/cleaved Caspase-1/GSDMD-N pathway. EVs delivered circ-Tulp4 into hepatocytes, thereby restoring circ-Tulp4 expression. Elevated circ-Tulp4 enhanced the recruitment of H3K27me3 to the HNRNPC promoter through interaction with KDM6B, thus suppressing HNRNPC and ABHD6. Overexpression of HNRNPC or ABHD6 counteracted the protective effects of UCMSCs-EVs, exacerbating pyroptosis and hepatic steatosis in DM-NAFLD. UCMSCs-EVs deliver circ-Tulp4 into hepatocytes, where circ-Tulp4 inhibits the HNRNPC/ABHD6 axis, thereby reducing pyroptosis and alleviating DM-NAFLD. These findings provide a novel therapeutic avenue for targeting DM-NAFLD through modulation of cell pyroptosis.

Liver knockout of MCU leads to greater dysregulation of lipid metabolism in MAFLD.

Metabolic-associated fatty liver disease (MAFLD) is a common chronic condition that poses a significant threat to human health. Mitochondrial dysfunction, particularly involving the mitochondrial Ca2+ uniporter (MCU), plays a key role in its pathogenesis. This study aimed to investigate the impact of the MCU gene on hepatic lipid metabolism in mice fed a high-fat diet. Using MCU knockout and wild-type mice, subjected to either a high-fat or normal diet for 14weeks, we observed notable Steatosis and liver weight gain in MCU-deficient mice. Liver function markers, serum triglycerides, very low-density lipoprotein (VLDL) levels, and ApoB protein expression were all significantly elevated. Mechanistic studies revealed that MCU deletion led to mitochondrial dysfunction, increased oxidative stress. These findings highlight the critical role of the MCU gene in maintaining hepatic lipid balance and suggest its potential as a therapeutic target for managing nonalcoholic fatty liver disease.

Evaluating the roles of microRNAs associated with nonalcoholic fatty liver disease in hepatocellular carcinoma tumorigenesis: a systematic review and network analysis

IntroductionNon-alcoholic fatty liver disease (NAFLD) has become the leading cause of chronic liver disease worldwide. Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide, with high morbidity and mortality. The rapidly increasing incidence of NAFLD is becoming an essential precursor of HCC globally. MicroRNAs (miRNAs) are involved in the progression of NAFLD and HCC.MethodPotential miRNAs associated with NAFLD in HCC tumorigenesis were identified through a systematic review, and their roles were evaluated by data mining analysis. The biological function of the potential miRNA and its target genes in NAFLD and HCC were evaluated by bioinformatic analysis.ResultMIR122 was identified as the potential miRNA associated with NAFLD and HCC. Then, MIR122 expression was significantly lower in HCC patients, and higher MIR122 levels were associated with significantly better overall survival. Next, the biological functions of MIR122 and target genes were predicted to be involved in inflammation, fibrosis, cell proliferation, invasion, metastasis, and apoptosis. In particular, the FOXO signaling pathway may regulate the above biological functions.ConclusionMIR122 was suggested to be involved in progressing from NAFLD to HCC through the PI3K/AKT/FOXO pathway.Systematic review registrationPROSPERO, identifier: CRD 42024517940.

Short-term exposure to low doses of aflatoxin B1 aggravates nonalcoholic steatohepatitis by TLR4-mediated necroptosis.

Aflatoxin B1 (AFB1), a worldwide mycotoxin found in food and foodstuffs, is a potent hepatotoxin in humans and animals. Non-alcoholic fatty liver disease (NAFLD), a widespread disease, could progress from simple steatosis to non-alcoholic steatohepatitis (NASH), hepatic cirrhosis, and even hepatocellular carcinoma (HCC). To date, little is known concerning the relationship between AFB1 and the progression of NAFLD. The effects of low doses of AFB1 on the development of NASH and their mechanism were investigated in vivo and in vitro. The results in vivo showed that AFB1 at 20 and 40 μg/kg.bw aggravated CDAHFD-induced NASH in mice as demonstrated by increasing the serum and liver lipid accumulation, liver inflammation and injury. The results in vitro showed that AFB1 at 1.0 μM aggravated FFA-induced lipid accumulation, inflammation and cell damage in HepG2 cells. In addition, RNA-seq indicated that necroptosis, Toll like receptor signaling and TNF-α signaling showed a significant change in KEGG pathway enrichment in AFB1 at 40 μg/kg.bw. AFB1 significantly upregulated the mRNA and protein levels of TLR4, RIPK3, p-RIPK3, MLKL and p-MLKL, and increased TUNEL positive cells. Also, immunofluorescence results showed that TUNEL, TLR4, TNF-α had co-localized with RIPK3, respectively. Necroptosis inhibitor (GSK-872) attenuated the aggravating effects of AFB1 on NASH. Knockout of TLR4 inhibited necroptosis and rescued the aggravating effects of AFB1 on NASH. These data indicate that low dose of AFB1 aggravated NASH via TLR4-mediated necroptosis. This suggests that low dose of AFB1 is potentially harmful to animals and humans, as they exacerbate NASH.

Prolonged survival in women with Hepatocellular Carcinoma: a French observational study.

Less than 25% of hepatocellular carcinoma (HCC) occurs in women, in whom prognosis could be better. Due to the lack of date in Europe, this study aims to assess survival of patients with HCC according sex in a tertiary French liver center. Every patient diagnosed with a first diagnosis of HCC presented at our weekly multidisciplinary tumor board between 2013 and 2017 were included. Baseline characteristics of patients and tumors were compared according sex using the Mann-Whitney test for Continuous variables and the Fisher or Chi-square test for dichotomous variables. Survival analyses according sex were conducted using the Kaplan-Meier method, the log-rank test, Cox models and a propensity score. 694 patients were included, of whom 130 (18.7%) were women. Among them, 587 (86%) had cirrhosis, mainly compensated (Child A 62.7%), and related to alcohol (48.7%), HCV (27.2%), and/or metabolic-associated fatty liver disease (25.8%). HCC was unifocal in 54% of cases, with a mean main nodule size of 37 mm. Curative treatment was administered in 45.4% of cases (percutaneous ablation 93%). Compared to men, women diagnosed with HCC were older (73 vs. 65 years, p < 0.001), were more frequently HCV-infected (40% vs. 24%, p = 0.0003) and presented more often with a solitary HCC (63% vs. 52%, p = 0.020). After a median follow-up of 57 months, overall survival was significantly longer in women both in multivariate analysis (aHR 1.39 (CI95%: 1.07-1.81) p=0.014) and using a propensity score (HR 1.51 (1.13-2.02, p=0.005)). Despite being diagnosed at an older age, women with HCC exhibit significant better overall survival.

Exploring the Updated Roles of Ferroptosis in Liver Diseases: Mechanisms, Regulators, and Therapeutic Implications.

Ferroptosis, a newly discovered mode of cell death, is a type of iron-dependent regulated cell death characterized by intracellular excessive lipid peroxidation and imbalanced redox. As the liver is susceptible to oxidative damage and the abnormal iron accumulation is a major feature of most liver diseases, studies on ferroptosis in the field of liver diseases are of great interest. Studies show that targeting the key regulators of ferroptosis can effectively alleviate or even reverse the deterioration process of liver diseases. System Xc- and glutathione peroxidase 4 are the main defense regulators of ferroptosis, while acyl-CoA synthetase long chain family member 4 is a key enzyme causing peroxidation in ferroptosis. Generally speaking, ferroptosis should be suppressed in alcoholic liver disease, non-alcoholic fatty liver disease, and drug-induced liver injury, while it should be induced in liver fibrosis and hepatocellular carcinoma. In this review, we summarize the main regulators involved in ferroptosis and then the mechanisms of ferroptosis in different liver diseases. Treatment options of drugs targeting ferroptosis are further concluded. Determining different triggers of ferroptosis can clarify the mechanism of ferroptosis occurs at both physiological and pathological levels.

Impact of PNPLA3 in Lean Individuals and in Cryptogenic Steatotic Liver Disease.

Although metabolic dysfunction-associated steatotic liver disease (MASLD) is strongly associated with obesity, around 20% of individuals with hepatic steatosis may nonetheless have normal body mass index, a condition often referred to as lean nonalcoholic fatty liver disease (NAFLD). Under the new nomenclature and definition of MASLD, lean NAFLD can be further divided into lean MASLD (when there is one or more cardiometabolic risk factors) and cryptogenic steatotic liver disease (when there is no cardiometabolic risk factor). Current studies suggest that the at-risk PNPLA3 rs738409 variant is more common among individuals with lean NAFLD than their overweight and obese counterparts. However, even in this group, cardiometabolic risk factors are often required for the development of hepatic steatosis and liver injury. In the general population, PNPLA3 gene polymorphism is associated with an increased risk of MASLD, more severe liver histology (i.e., the presence of steatohepatitis and fibrosis) and future development of hepatocellular carcinoma and cirrhotic complications. Emerging data also suggest that individuals carrying the PNPLA3 GG genotype might have a greater reduction in hepatic steatosis and liver enzymes with lifestyle intervention and metabolic treatments, such as glucagon-like peptide-1 receptor agonists. Studies have not specifically examined the impact of PNPLA3 in lean individuals.

A Systemic Review on Phytochemicals and Novel Approaches for the Management of Hepatic Cancer

Introduction: Hepatic cancer, an aggressive tumour that often develops along with cirrhosis and chronic liver disease like infections with the hepatitis B and hepatitis C viruses, while nonalcoholic steatohepatitis, is linked to metabolic syndrome or diabetes mellitus. It is the third most prevalent cause of cancer-related mortality globally and ranks fifth in cancer incidence. According to GLOBOCON, the prevalence is expected to rise by 55.0% and the fatalities by 56.4% in the near future. Objective: The present review offered natural plant-based substances and compounds having curative effects on liver cancer, along with novel drug delivery systems and nanocarrier-based therapies. Methods: The literature has been taken from PubMed, Google Scholar, SciFinder, Springer Nature, Bentham Science, PLOS one, or other internet sites. Result: Treatment for heterogeneous malignancy is multidimensional, and care guidelines differ depending on the specialty and location. Several nutritional herbal remedies and their active phytoconstituents may have an abundance of impacts on the management of liver cancer, including preventing the growth and spread of tumor cells, shielding the body from liver carcinogens, boosting the effects of chemotherapy and immunomodulating the body. Conclusion: The treatment of liver cancer involves multidisciplinary and multimodel therapy. The literature is a compilation of extract, compounds, and novel approaches like nanoparticles, microsphere, liposomes, niosomes, phytosomes and microparticles. These approaches not only manage cancer but also boost the immunity of the individuals.

Sequential fermentation of Ginkgo biloba seeds by Bacillus subtilis natto and Lactobacillus plantarum enhanced nutrition, flavor and lipid-lowering activity.

Ginkgo biloba seeds (GBS) are rich in flavonoids, proteins and reducing sugar, and have been consumed as food and medicinal nuts for thousands of years. However, the presence of ginkgotoxins and their poor palatability limit people's consumption of them. This study used solid-state fermentation with Bacillus subtilis natto and Lactobacillus plantarum to enhance the safety and benefits of GBS. Optimized fermentation conditions increased the content of beneficial components like total flavonoids, soluble protein and reducing sugar while eliminating unpleasant odors (isoamyl aldehyde and hexanal) and reducing the toxin 4'-O-methylpyridoxine by 91.17%. Fermentation of GBS powder can significantly enhance its anti-inflammatory and antioxidant activities in vitro (P < 0.001). Furthermore, it exhibits a dose-dependent effect within a certain concentration range. Mixed fermentation (FBnLp) was evaluated for its effects on obesity and metabolic syndrome in mice fed a high-fat diet. FBnLp significantly reduced body and liver weight gain, prevented dyslipidemia and decreased inflammatory and oxidative stress compared to unfermented GBS. Histological analysis showed that FBnLp improved liver health by reducing fat accumulation and preventing non-alcoholic fatty liver disease. Meanwhile, it was found that feeding FBnLp increased the expression of CPT-1α, which regulates energy expenditure and fat breakdown, and downregulated the expression of SREBP-1c, FAS and ACC, which regulate fat synthesis. This research provides new insights and technological support for the application and development of FBnLp as a functional product, addressing key issues in its use and industry growth. © 2024 Society of Chemical Industry.

Efficacy and safety of electroacupuncture for metabolic dysfunction-associated fatty liver disease: a study protocol for a multicentre, randomised, sham acupuncture-controlled, patient-blinded clinical trial

BackgroundMetabolic dysfunction-associated fatty liver disease (MAFLD) is the most common chronic liver disease in the world and carries an increased risk of liver-related events, but no approved medicine. Electroacupuncture has...

Association Between Fatty Liver Index and Incidence of Cataract Surgery in Individuals Aged 50 Years and Older Based on the Korean National Health Insurance Service-Health Screening Cohort (NHIS-HEALS) Data: Longitudinal Retrospective Cohort Study.

Cataract is a leading cause of vision impairment. Obesity-related risk factors, including insulin resistance, increase the risk of cataract. The fatty liver index (FLI) is a biomarker for noninvasive fat layer prediction of nonalcoholic fatty liver disease. The FLI has been used to evaluate the metabolic contribution in other organs besides the eye. However, no study exists on the FLI and eye disease. This retrospective cohort study for the association between the FLI and incidence of cataract surgery in individuals older than 50 years was designed to show that a higher FLI is associated with an increased incidence of cataract surgery in individuals aged 50 years and older. This study was retrospectively designed based on the Korean National Health Insurance Service-Health Screening Cohort (NHIS-HEALS) cohort (median follow-up of 9.8 years). Participants were assigned to 1 of 3 groups based on the FLI: low (FLI<30), intermediate (FLI 30-59), or high (FLI≥60). Kaplan-Meier survival analysis was performed on the cumulative incidence of all-cataract and senile-cataract surgery. Multivariable Cox proportional hazards regression models were used to study the association between the FLI group and cataract surgery after adjusting for potential confounders. Of the 138,347 included participants, the incidence of cataract surgery was 12.49% (4779/38,274), 13.95% (6680/47,875), and 14.16% (7496/52,930) in the low, intermediate, and high FLI groups, respectively. After adjusting for all confounding factors, hazard ratios (HRs; 95% CIs) in the high FLI group for all-cataract surgery were 1.111 (1.028-1.199) and 1.184 (1.101-1.274) in men and women, respectively, when compared with the low FLI group. HRs (95% CIs) in the high FLI group for senile-cataract surgery were 1.106 (1.022-1.197) and 1.147 (1.065-1.237) in men and women, respectively, when compared with the low FLI group. The project was conducted between August 2023 and February 2024 without donations from external bodies. Individuals with a higher FLI had a higher risk of all-cataract surgery. This association was maintained even after limiting the analyses to senile-cataract surgery.

The Impact of Sira Vedha (Phlebotomy) at the Right Elbow Joint in the Treatment of Non-Alcoholic Fatty Liver Disease - A Research Report

ABSTRACT Non-alcoholic fatty liver disease (NAFLD) affects 9%–53% of the Indian population. No Indian studies have examined Sira Vedha (phlebotomy) for NAFLD, although it has been studied for other conditions. Sushruta recommended Sira Vedha at the right elbow joint for liver diseases, but clinical evidence for its efficacy in NAFLD is lacking. This clinical trial aimed to generate evidence for Sira Vedha in NAFLD patients. One hundred eleven patients with Grade I/II NAFLD were randomly assigned to either a control group (diet and exercise) or an intervention group (Sira Vedha, diet, and exercise). Blood samples were collected for lipid profile and liver function tests before and after treatment. Results showed significant improvements in SGOT, SGPT, cholesterol, HDL, and triglyceride levels in the intervention group compared to the control group, supporting the efficacy of Sira Vedha in NAFLD treatment. This study highlights the need for clinical evidence to confirm traditional Ayurvedic practices.