scholarly journals Protection of Fatty Liver by the Intake of Fermented Soybean Paste, Miso, and Its Pre-Fermented Mixture

Foods ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 291
Author(s):  
Ryoko Kanno ◽  
Tetsuo Koshizuka ◽  
Nozomu Miyazaki ◽  
Takahiro Kobayashi ◽  
Ken Ishioka ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Liver Weight ◽  
Normal Diet ◽  
Nonalcoholic Fatty Liver ◽  
Beneficial Effects ◽  
Soybean Paste ◽  
Fermented Product ◽  
Lifestyle Related Diseases ◽  
Functional Components ◽  
Japanese Diet

Soybeans and fermented soy-derived foodstuffs contain many functional components and demonstrate various beneficial effects. In this report, we demonstrate the anti-fatty liver effect of miso, a traditional fermented product made from soybeans and rice molded in Aspergillus oryzae and forming a common part of the Japanese diet. After acclimation for 2 weeks, male and female C57BL/6J mice were fed with a normal diet (ND), a high-fat diet (HFD), a HFD containing 5% miso (HFD+M), or a HFD containing 5% pre-fermented miso (HFD+PFM) for 20 weeks. Although mice in the HFD group developed typical fatty liver, the consumption of miso or PFM significantly ameliorated the progression of fatty liver in female mice. The liver weight and the average nonalcoholic fatty liver disease activity score (NAS) were significantly reduced in the HFD+M and HFD+PFM groups. In addition, leptin and resistin levels in the serum were decreased in the HFD+M and HFD+PFM groups. The progression of fatty liver was also prevented by the consumption of miso or PFM in male mice, although there were no decreases in NAS. Therefore, miso appears to be a potential food to prevent lifestyle-related diseases such as metabolic syndrome.

scholarly journals The Current View of Nonalcoholic Fatty Liver Disease-Related Hepatocellular Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 516
Author(s):  
Tomomi Kogiso ◽  
Katsutoshi Tokushige
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Current View ◽  
Nonalcoholic Fatty Liver ◽  
Obesity And Diabetes ◽  
Life Threatening ◽  
Lifestyle Related Diseases

Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and can develop into hepatocellular carcinoma (HCC). The incidence of NAFLD-related HCC, which is accompanied by life-threatening complications, is increasing. Advanced fibrosis and lifestyle-related and metabolic comorbidities, especially obesity and diabetes mellitus, are associated with HCC development. However, HCC is also observed in the non-cirrhotic liver. Often, diagnosis is delayed until the tumor is relatively large and the disease is advanced; an effective screening or surveillance method is urgently required. Recently, the NAFLD/nonalcoholic steatohepatitis (NASH) guidelines of Japan were revised to incorporate new strategies and evidence for the management and surveillance of NAFLD/NASH. Fibrosis must be tested for noninvasively, and the risk of carcinogenesis must be stratified. The treatment of lifestyle-related diseases is expected to reduce the incidence of NAFLD and prevent liver carcinogenesis.

Aromatic aldehyde compound cuminaldehyde protects nonalcoholic fatty liver disease in rats feeding high fat diet

2019 ◽  
Vol 38 (7) ◽  
pp. 823-832 ◽  
Author(s):  
MR Haque ◽  
SH Ansari
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Liver Enzymes ◽  
Liver Weight ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
And Oxidative Stress

Nonalcoholic fatty liver disease (NAFLD) is caused by fat accumulation and is related with obesity and oxidative stress. In this study, we investigated the effect of cuminaldehyde on NAFLD in rats fed a high fat diet (HFD). Male Wistar rats were fed a HFD for 42 days to induce NAFLD. The progression of NAFLD was evaluated by histology and measuring liver enzymes (alanine transaminase and aspartate transaminase), serum and hepatic lipids (total triglycerides and total cholesterol), and oxidative stress markers (thiobarbituric acid reactive substances, glutathione, superoxide dismutase, and catalase). The HFD feeding increased the liver weight and caused NAFLD, liver steatosis, hyperlipidemia, oxidative stress, and elevated liver enzymes. Administration of cuminaldehyde ameliorated the changes in hepatic morphology and liver weight, decreased levels of liver enzymes, and inhibited lipogenesis. Our findings suggest that cuminaldehyde could improve HFD-induced NAFLD via abolishment of hepatic oxidative damage and hyperlipidemia. Cuminaldehyde might be considered as a potential aromatic compound in the treatment of NAFLD and obesity through the modulation of lipid metabolism.

scholarly journals Hepatoprotective Effects of a Novel Trihoney against Nonalcoholic Fatty Liver Disease: A Comparative Study with Atorvastatin

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Hamad Abdulsalam Hamad Alfarisi ◽  
Muhammad Bin Ibrahim ◽  
Zenab B. Hamad Mohamed ◽  
Nuraniza Azahari ◽  
Asmah Hanim Bt. Hamdan ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Function ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Normal Diet ◽  
Cholesterol Diet ◽  
Nonalcoholic Fatty Liver ◽  
Hepatoprotective Effects ◽  
Glutamyl Transferase

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disorder worldwide with no curative therapy. The aim of this study was to investigate the hepatoprotective effects of a novel Trihoney against biochemical and histological manifestations of NAFLD in hypercholesterolemic rabbits. Methodology. Forty-eight male New Zealand white (NZW) rabbits were grouped into normal diet (C), normal diet with 0.6 g/kg/day of Trihoney (C + H), 1% cholesterol diet (HCD), 1% cholesterol diet with 0.3 g/kg/day of Trihoney (HCD + H1), 1% cholesterol diet with 0.6 g/kg/day of Trihoney (HCD + H2), and 1% cholesterol diet with 2 mg/kg/day of atorvastatin (HCD + At.). Animals were sacrificed after 12 weeks of treatment. Serum lipids and liver function test (LFT) were measured prior to and at the endpoint of the experiment for total cholesterol (TC), low-density lipoprotein (LDL-c), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and total bilirubin (T. Bil.). Liver was processed for histopathology study. Liver homogenate was analysed for oxidative stress parameters: superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA). Results. Lipid analysis approved the induction of hypercholesterolemia. A significant elevation (p<0.01) of serum AST and ALT levels showed by the HCD group was compared to C and C + H groups. Trihoney exhibited a significant reduction (p<0.001) of AST and ALT compared to the HCD group. Likewise, AST and ALT reduced significantly in the HCD + At. group (p<0.001). Trihoney supplementation induced significant (p<0.05) enhancement of SOD and GPx activities. Atorvastatin treatment was associated with significant (p<0.05) reduction of SOD and GPx activities in the liver. Trihoney and atorvastatin showed marked (p<0.001) reduction of hepatic lipid peroxidation. Trihoney showed histological protection against progression of NAFLD to nonalcoholic steatohepatitis (NASH). Atorvastatin exhibited no beneficial impact on hepatic architecture. Conclusion. Trihoney was able to maintain normal liver function and showed hepatoprotection against progression of NAFLD to NASH probably through hypocholesterolaemic and antioxidant functions.

scholarly journals New therapeutic strategies in nonalcoholic fatty liver disease: a focus on promising drugs for nonalcoholic steatohepatitis

2020 ◽  
Vol 72 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Natalia Pydyn ◽  
Katarzyna Miękus ◽  
Jolanta Jura ◽  
Jerzy Kotlinowski
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Nonalcoholic Steatohepatitis ◽  
Fatty Liver Disease ◽  
Therapeutic Agents ◽  
Global Burden ◽  
Future Perspectives ◽  
Nonalcoholic Fatty Liver ◽  
Beneficial Effects

AbstractThe prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide. Globally, it is currently the most common liver disease and is estimated to affect up to 25% of the population. In the first stage, NAFLD is characterized by simple hepatic steatosis (NAFL, nonalcoholic fatty liver) that might progress to nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis or hepatocellular carcinoma. In this review, we discuss the global burden of NAFLD, together with future perspectives on how this epidemic could be restrained. There is also an urgent need for the development of new medical strategies for NAFLD patients. We aim to present the beneficial effects of life-style modifications that should be advised to both non-obese and obese NAFLD patients. Since there are currently no medications directly used for the treatment of more advanced NAFLD stages, the central part of this review summarizes ongoing and recently completed clinical trials testing promising drugs for NASH resolution. The marketing of new therapeutic agents would greatly increase the odds of reducing the global burden of NAFLD.

scholarly journals Loss of hepatic Lgr4 and Lgr5 promotes nonalcoholic fatty liver disease

2021 ◽  
Author(s):  
Enrica Saponara ◽  
Carlos Penno ◽  
Meztli L Matadamas Guzmán ◽  
Virginie Brun ◽  
Benoit Fischer ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Lipid Analysis ◽  
Ex Vivo ◽  
Serum Lipoprotein ◽  
Normal Diet ◽  
Nonalcoholic Fatty Liver ◽  
Lipid Species

Background & Aims: The Rspo–Lgr4/5–Znrf3/Rnf43 module is a master regulator of hepatic Wnt/β–catenin signaling and metabolic zonation, but its impact on nonalcoholic fatty liver disease (NAFLD) remains unclear. We studied whether liver–specific loss of the Wnt/β–catenin modulators Leucine–Rich Repeat–Containing G Protein–Coupled Receptor 4/5 (Lgr4/5) promotes nonalcoholic fatty liver disease (NAFLD). Methods: Mice with liver–specific deletion of both receptors Lgr4/5 (Lgr4/5dLKO) were fed with normal diet (ND) or high fat diet (HFD). Livers of these mice were analyzed for lipid and fibrotic content by tissue staining and immunohistochemistry (IHC), and lipoproteins, inflammation and liver enzyme markers were measured in blood. Mechanistic insights into hepatic lipid accumulation were obtained by using ex vivo primary hepatocyte cultures derived from the Lgr4/5dLKO mice. Lipid analysis of mouse livers was performed by mass spectrometry (MS)–based untargeted lipidomic analysis. Results: We demonstrated that liver-specific ablation of Lgr4/5–mediated Wnt signaling resulted in hepatic steatosis, impaired bile acid (BA) secretion and predisposition to liver fibrosis. Under HFD conditions, we observed progressive intrahepatic fat accumulation, developing into macro–vesicular steatosis. Serum lipoprotein levels in HFD–fed Lgr4/5dLKO mice were decreased, rather than increased, suggesting that accumulation of fat in the liver was due to impaired lipid secretion by hepatocytes. Our lipidome analysis revealed a severe alteration of several lipid species in livers of Lgr4/5dLKO mice, including triacylglycerol estolides (TG–EST), a storage form of bioactive free fatty acid (FA) esters of hydroxy FAs (FAHFAs). Conclusions: Loss of hepatic Wnt/β–catenin activity by Lgr4/5 deletion led to deregulation of lipoprotein pathways, loss of BA secretion, intrinsic alterations of lipid homeostasis and the onset of NAFLD.

scholarly journals Assessment and Evaluation of the Leaf Extract of Begonia barbata to the Reduction LDL-Cholesterol in Carbamazepine Induced Obese Rats

2021 ◽  
pp. 17-28
Keyword(s):  
Cholesterol Level ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Liver Weight ◽  
Normal Diet ◽  
The Body ◽  
Lipid Lowering ◽  
Beneficial Effects

Scientific endeavor has made it possible to discover and synthesize lipid-lowering drugs but, in most cases, their beneficial effects are overshadowed by their adverse effects. Hence, research interest in the screening of medicinal plants has intensified in recent years with a view of discovering potential antioxidants, lipid, and glucose-lowering phytochemicals. Four-month feeding of carbamazepine (both 5 mg/kg and 20 mg/kg body weight) with a normal diet increased the body mass of rats. Low-density lipoprotein (LDL) cholesterol level was increased based on the oral execution of carbamazepine. But high-density lipoprotein (HDL) cholesterol level and weight of the liver increased slightly and the level of triacylglycerol (TG) and total cholesterol (TC) level remain unchanged. Nonetheless, the Begonia barbata feeding with a normal diet reduced carbamazepine-induced obesity at both high and low doses. The level of LDL cholesterol and liver weight was significantly decreased due to the oral execution of B. barbata together with normal diet and carbamazepine, where HDL level was changed but not significantly.

scholarly journals Protective roles of adiponectin in obesity-related fatty liver diseases: mechanisms and therapeutic implications

2009 ◽  
Vol 53 (2) ◽  
pp. 201-212 ◽  
Author(s):  
Yu Wang ◽  
Mingyan Zhou ◽  
Karen S. L. Lam ◽  
Aimin Xu
Keyword(s):  
Fatty Liver ◽  
Liver Diseases ◽  
Experimental Studies ◽  
Biological Properties ◽  
Cellular Mechanisms ◽  
Nonalcoholic Fatty Liver ◽  
Therapeutic Implications ◽  
Beneficial Effects ◽  
Liver Injuries ◽  
Oligomeric Complex

Adiponectin is an insulin-sensitizing adipokine possessing multiple beneficial effects on obesity-related medical complications. This adipokine is secreted from adipocytes into the circulation as three oligomeric isoforms, including trimer, hexamer and the high molecular weight (HMW) oligomeric complex. Each oligomeric isoform of adiponectin possesses distinct biological properties and activates different signaling pathways in various target tissues. The hepato-protective activities have been demonstrated by many clinical and experimental studies. The decreased level of serum adiponectin represents an independent risk factor for nonalcoholic fatty liver disease (NAFLD) and liver dysfunctions in humans. In animals, elevation of circulating adiponectin by either pharmacological or genetic approaches leads to a significant alleviation of hepatomegaly, steatosis and necro-inflammation associated with various liver diseases. In adiponectin knockout mice, there is a pre-existing condition of hepatic steatosis and mitochondria dysfunction, which might contribute to the increased vulnerabilities of these mice to the secondary liver injuries induced by obesity and other conditions. This review aims to summarize recent advances on delination of the structural, molecular and cellular mechanisms underlying the hepato-protective properties of adiponectin.

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