scholarly journals TO STUDY THE EFFICACY OF POLY HERBO-MINERAL COMPOUND IN THE MANAGEMENT OF GRADE I & GRADE II FATTY LIVER (HEPATIC STEATOSIS)

2021 ◽  
Vol 9 (7) ◽  
pp. 1349-1357
Author(s):  
Nabaruna Bose ◽  
Gupta O.P. ◽  
Bishnu Prasad Sarma
Keyword(s):  
Clinical Trial ◽  
Cell Death ◽  
Lipid Metabolism ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Cell Injury ◽  
Fatty Change ◽  
Food Practices ◽  
Grade Ii ◽  
Immense Potential

Hepatic Steatosis is a common predicament in society due to changes in lifestyle and food practices. Depending upon the cause and amount of accumulation, fatty change may be mild and reversible, or severe producing irreversible cell injury and cell death. Disturbances of lipid metabolism in the liver due to various etiological factors lead to Fatty Liver. Ayurveda has immense potential in the management of Non-Communicable Diseases, and Fatty liver is one among them. In Ayurveda, a direct correlation of Fatty liver is not found but it can be considered under Yakrit roga and Medo roga, as a Santarpanjanya Vyadhi. Hepatic steatosis patients are treated with Triphaladi yoga and Yashtimadhu churna for 3 months, in the Department of Kayachikitsa, Govt. Ayurvedic College and Hospital, Guwahati. This trial aims to formulate a practical Ayurvedic protocol for the management of Grade I and Grade II Fatty liver. However, further research studies are needed to fulfil the aims and objectives. Keywords: Yakrit roga, Hepatic steatosis, Santarpanjanya Vyadhi, poly-herbo mineral compound, clinical trial.

scholarly journals TO STUDY THE EFFICACY OF POLY HERBO-MINERAL COMPOUND IN THE MANAGEMENT OF GRADE I & GRADE II FATTY LIVER (HEPATIC STEATOSIS)

2021 ◽  
Vol p5 (5) ◽  
pp. 2959-2967
Author(s):  
Nabaruna Bose ◽  
Gupta O.P. ◽  
Bishnu Prasad Sarma
Keyword(s):  
Clinical Trial ◽  
Cell Death ◽  
Lipid Metabolism ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Cell Injury ◽  
Fatty Change ◽  
Food Practices ◽  
Grade Ii ◽  
Immense Potential

Hepatic Steatosis is a common predicament in society due to changes in lifestyle and food practices. Depending upon the cause and amount of accumulation, fatty change may be mild and reversible, or severe producing irreversible cell injury and cell death. Disturbances of lipid metabolism in the liver due to various etiological factors lead to Fatty Liver. Ayurveda has immense potential in the management of Non-Communicable Diseases, and Fatty liver is one among them. In Ayurveda, a direct correlation of Fatty liver is not found but it can be considered under Yakrit roga and Medo roga, as a Santarpanjanya Vyadhi. Hepatic steatosis patients are treated with Triphaladi yoga and Yashtimadhu churna for 3 months, in the Department of Kayachikitsa, Govt. Ayurvedic College and Hospital, Guwahati. This trial aims to formulate a practical Ayurvedic protocol for the management of Grade I and Grade II Fatty liver. However, further research studies are needed to fulfil the aims and objectives. Keywords: Yakrit Roga, Hepatic steatosis, Santarpanjanya Vyadhi, poly-herbo mineral compound, clinical trial.

Molecular mechanism of hepatic steatosis: pathophysiological role of autophagy

2016 ◽  
Vol 18 ◽  
Author(s):  
Kewei Wang
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Pathological Condition ◽  
List Type ◽  
Abnormal Metabolism ◽  
Apoptotic Pathways ◽  
Novel Therapeutic

Steatosis is an early characteristic in the pathogenesis of fatty liver disease (FLD). Mechanisms of hepatic steatosis are aetiology-dependent. Activation of autophagy in liver ameliorates hepatic steatosis. A modulation of hepatic autophagy affects the degree of hepatocyte steatosis and the progression of FLD as demonstrated by pre-clinical models and clinical trials. This review summarises recent advances on pathophysiological roles of autophagy in hepatic lipid metabolism. A comprehensive regulation of autophagic networks holds promise for the improvement of hepatic steatosis. Autophagic signalling pathway may be a novel therapeutic target against FLD.Highlights: •Hepatic steatosis is a pathological condition wherein vacuoles of triglyceride (TG) fat are overaccumulated in liver because of abnormal metabolism of lipids.•Hepatic autophagy regulates lipid metabolism as demonstrated by macrolipophagy in response to starvation and hepatic overabundance of TG in obesity.•Autophagic signals are closely associated with apoptotic pathways. There is distinctive relationship between hepatic autophagy and apoptosis, which affects the progression of fatty liver.•Regulation of autophagic process can be a novel therapeutic strategy for fatty liver disease.

scholarly journals Chronic alcohol exposure alters circulating insulin and ghrelin levels: role of ghrelin in hepatic steatosis

2019 ◽  
Vol 316 (4) ◽  
pp. G453-G461 ◽  
Author(s):  
Karuna Rasineni ◽  
Paul G. Thomes ◽  
Jacy L. Kubik ◽  
Edward N. Harris ◽  
Kusum K. Kharbanda ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Insulin Secretion ◽  
Lipid Metabolism ◽  
Fatty Liver ◽  
Pancreatic Islets ◽  
Hepatic Steatosis ◽  
Liver Tissue ◽  
Serum Ghrelin ◽  
Altered Lipid Metabolism ◽  
Altered Lipid

Fatty liver is the earliest response of the liver to excessive ethanol consumption. Central in the development of alcoholic steatosis is increased mobilization of nonesterified free fatty acids (NEFAs) to the liver from the adipose tissue. In this study, we hypothesized that ethanol-induced increase in ghrelin by impairing insulin secretion, could be responsible for the altered lipid metabolism observed in adipose and liver tissue. Male Wistar rats were fed for 5–8 wk with control or ethanol Lieber-DeCarli diet, followed by biochemical analyses in serum and liver tissues. In addition, in vitro studies were conducted on pancreatic islets isolated from experimental rats. We found that ethanol increased serum ghrelin and decreased serum insulin levels in both fed and fasting conditions. These results were corroborated by our observations of a significant accumulation of insulin in pancreatic islets of ethanol-fed rats, indicating that its secretion was impaired. Furthermore, ethanol-induced reduction in circulating insulin was associated with lower adipose weight and increased NEFA levels observed in these rats. Additionally, we found that increased concentration of serum ghrelin was due to increased synthesis and maturation in the stomach of the ethanol-fed rats. We also report that in addition to its effect on the pancreas, ghrelin can also directly act on hepatocytes via the ghrelin receptors and promote fat accumulation. In conclusion, alcohol-induced elevation of circulating ghrelin levels impairs insulin secretion. Consequently, reduced circulating insulin levels likely contribute to increased free fatty acid mobilization from adipose tissue to liver, thereby contributing to hepatic steatosis. NEW & NOTEWORTHY Our studies are the first to report that ethanol-induced increases in ghrelin contribute to impaired insulin secretion, which results in the altered lipid metabolism observed in adipose and liver tissue in the setting of alcoholic fatty liver disease.

scholarly journals The Effects of PPAR Agonists on Atherosclerosis and Nonalcoholic Fatty Liver Disease in ApoE−/−FXR−/− Mice

2021 ◽  
Vol 36 (6) ◽  
pp. 1243-1253
Author(s):  
Yenna Lee ◽  
Bo-Rahm Kim ◽  
Geun-Hyung Kang ◽  
Gwan Jae Lee ◽  
Young Joo Park ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Bile Acid ◽  
Fatty Liver ◽  
Mrna Expression ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Nonalcoholic Fatty Liver ◽  
Ppar Agonists ◽  
Pparα Agonist

Background: Farnesoid X receptor (FXR), a bile acid–activated nuclear receptor, is a potent regulator of glucose and lipid metabolism as well as of bile acid metabolism. Previous studies have demonstrated that FXR deficiency is associated with metabolic derangements, including atherosclerosis and nonalcoholic fatty liver disease (NAFLD), but its mechanism remains unclear. In this study, we investigated the role of FXR in atherosclerosis and NAFLD and the effect of peroxisome proliferator-activated receptor (PPAR) agonists in mouse models with FXR deficiency.Methods: En face lipid accumulation analysis, liver histology, serum levels of glucose and lipids, and mRNA expression of genes related to lipid metabolism were compared between apolipoprotein E (ApoE)−/− and ApoE−/−FXR−/− mice. The effects of PPARα and PPARγ agonists were also compared in both groups of mice.Results: Compared with ApoE−/− mice, ApoE−/−FXR−/− mice showed more severe atherosclerosis, hepatic steatosis, and higher levels of serum cholesterol, low-density lipoprotein cholesterol, and triglycerides, accompanied by increased mRNA expression of FAS, ApoC2, TNFα, IL-6 (liver), ATGL, TGH, HSL, and MGL (adipocytes), and decreased mRNA expressions of CPT2 (liver) and Tfam (skeletal muscle). Treatment with a PPARα agonist, but not with a PPARγ agonist, partly reversed atherosclerosis and hepatic steatosis, and decreased plasma triglyceride levels in the ApoE−/−FXR−/− mice, in association with increased mRNA expression of CD36 and FATP and decreased expression of ApoC2 and ApoC3 (liver).Conclusion: Loss of FXR is associated with aggravation of atherosclerosis and hepatic steatosis in ApoE-deficient mice, which could be reversed by a PPARα agonist through induction of fatty acid uptake, β-oxidation, and triglyceride hydrolysis.

Resveratrol protects against nonalcoholic fatty liver disease by improving lipid metabolism and redox homeostasis via the PPARα pathway

2020 ◽  
Vol 45 (3) ◽  
pp. 227-239 ◽  
Author(s):  
Yujie Huang ◽  
Hedong Lang ◽  
Ka Chen ◽  
Yong Zhang ◽  
Yanxiang Gao ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Protein Kinase ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Hepg2 Cells ◽  
Fatty Liver Disease ◽  
Redox Homeostasis ◽  
Nonalcoholic Fatty Liver

Resveratrol (RSV), a well-known bioactive compound, has been reported to exert a broad range of health benefits. Accumulating evidence suggests that RSV is beneficial for many metabolic diseases, including nonalcoholic fatty liver disease (NAFLD). This study investigated the preventive and therapeutic effects of RSV on high-fat diet (HFD)-induced NAFLD in rats and palmitate acid (PA)-induced hepatocyte steatosis in HepG2 cells. Hepatocytes were incubated with inhibitors of peroxisome proliferator-activated receptor α (PPARα) or short interfering RNAs (siRNAs) targeting PPARα, AMP-activated protein kinase (AMPK), and protein kinase A (PKA) to determine the underlying mechanisms. We found that RSV noticeably ameliorated HFD-induced hepatic steatosis in rats and inhibited PA-induced lipid accumulation in HepG2 cells. Moreover, RSV improved lipid metabolism, enhanced antioxidant capacity, and restored mitochondrial respiratory chain activities. Incubation with inhibitors of PPARα or PPARα siRNA abolished the protective effects of RSV on lipid metabolism and redox homeostasis. Furthermore, RSV activated the PKA/AMPK/PPARα signaling pathway. Our results provided direct evidence for a novel, PPARα-mediated mechanism responsible for the beneficial effects of RSV on hepatic steatosis. These findings may have important theoretical and application prospects for the prevention and treatment of NAFLD. Novelty RSV improved lipid metabolism and redox homeostasis and oxidative stress in NAFLD via the PKA/AMPK/PPARα signaling pathway. RSV may have a greater beneficial effect in the early prevention of hepatic steatosis.

scholarly journals Phosphorylation of eIF2α signaling pathway attenuates obesity-induced non-alcoholic fatty liver disease in an ER stress and autophagy-dependent manner

2020 ◽  
Vol 11 (12) ◽  
Author(s):  
Jie Li ◽  
Xinle Li ◽  
Daquan Liu ◽  
Shiqi Zhang ◽  
Nian Tan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Er Stress ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Chow Diet ◽  
Dependent Manner ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

AbstractNon-alcoholic fatty liver disease (NAFLD) is the most common liver disorder and frequently exacerbates in postmenopausal women. In NAFLD, the endoplasmic reticulum (ER) plays an important role in lipid metabolism, in which salubrinal is a selective inhibitor of eIF2α de-phosphorylation in response to ER stress. To determine the potential mechanism of obesity-induced NAFLD, we employed salubrinal and evaluated the effect of ER stress and autophagy on lipid metabolism. Ninety-five female C57BL/6 mice were randomly divided into five groups: standard chow diet, high-fat (HF) diet, HF with salubrinal, HF with ovariectomy, and HF with ovariectomy and salubrinal. All mice except for SC were given HF diet. After the 8-week obesity induction, salubrinal was subcutaneously injected for the next 8 weeks. The expression of ER stress and autophagy markers was evaluated in vivo and in vitro. Compared to the normal mice, the serum lipid level and adipose tissue were increased in obese mice, while salubrinal attenuated obesity by blocking lipid disorder. Also, the histological severity of hepatic steatosis and fibrosis in the liver and lipidosis was suppressed in response to salubrinal. Furthermore, salubrinal inhibited ER stress by increasing the expression of p-eIF2α and ATF4 with a decrease in the level of CHOP. It promoted autophagy by increasing LC3II/I and inhibiting p62. Correlation analysis indicated that lipogenesis in the development of NAFLD was associated with ER stress. Collectively, we demonstrated that eIF2α played a key role in obesity-induced NAFLD, and salubrinal alleviated hepatic steatosis and lipid metabolism by altering ER stress and autophagy through eIF2α signaling.

scholarly journals Human Umbilical Cord-Derived Mesenchymal Stem Cell Therapy Ameliorates Nonalcoholic Fatty Liver Disease in Obese Type 2 Diabetic Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Bing Li ◽  
Yu Cheng ◽  
Songyan Yu ◽  
Li Zang ◽  
Yaqi Yin ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Hepatic Steatosis ◽  
Umbilical Cord ◽  
Fatty Liver Disease ◽  
Human Umbilical Cord ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is increasingly common among patients with type 2 diabetes mellitus (T2DM). The two conditions can act synergistically to produce adverse outcomes. However, the therapeutic options for patients with NAFLD and T2DM are currently limited. Human umbilical cord-derived mesenchymal stem cells (UC-MSCs) have shown therapeutic potential for diabetes and hepatic disorders such as liver cirrhosis and fulminant hepatic failure. The present study is aimed at investigating the effect of human UC-MSCs on a mouse model of NAFLD and T2DM, characterized by obesity-induced hyperglycaemia, dyslipidaemia, hepatic steatosis, and liver dysfunction. Thirty-week-old male C57BL/6 db/db mice were infused with human UC-MSCs or phosphate-buffered saline (PBS) via the tail vein once a week for six weeks. Age-matched male C57BL/6 wild-type db/+ mice were used as controls. Body weight and random blood glucose were measured every week. One week after the sixth infusion, intraperitoneal glucose tolerance tests and insulin tolerance tests were performed and the blood and liver were harvested for biochemical and histopathological examinations. Quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR), immunofluorescence staining, and western blot were performed to monitor the expression of the lipid metabolism- and regulatory pathway-related genes. UC-MSC infusions significantly ameliorated hyperglycaemia, attenuated the elevation of hepatic transaminases, and decreased lipid contents, including triglyceride, total cholesterol, and low-density lipoprotein cholesterol. Moreover, histological lesions in the liver diminished markedly, as evidenced by reduced lipid accumulation and attenuated hepatic steatosis. Mechanistically, UC-MSCs were found to regulate lipid metabolism by increasing the expression of fatty acid oxidation-related genes and inhibiting the expression of lipogenesis-related genes, which were associated with the upregulation of the HNF4α-CES2 pathway. Our results demonstrate that human UC-MSCs can ameliorate NAFLD and reverse metabolic syndrome in db/db mice. Thus, UC-MSCs may serve as a novel therapeutic agent for T2DM patients with NAFLD.

scholarly journals CARF (CDKN2AIP) Regulates Hepatic Lipid Metabolism and Protects Against Development of Non-Alcoholic Fatty Liver Diseases

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A284-A284
Author(s):  
Kamrul M Hasan ◽  
Meher Parveen ◽  
Alondra Pena ◽  
Erick Galdamez Calles ◽  
Marvy Gergis ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Mouse Model ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Hepg2 Cells ◽  
Liver Diseases ◽  
Hepatic Lipid Metabolism ◽  
Alcoholic Fatty Liver ◽  
Hepatic Lipid

Abstract Non-alcoholic fatty liver diseases (NAFLD) is the most common form of liver diseases in the USA with 30–40% of American being affected and about 12% with nonalcoholic steatohepatitis (NASH), a leading cause of end-stage liver diseases. NAFLD has been linked with insulin resistance, type2 diabetes, obesity, and cardiovascular diseases but molecular mechanisms underlying the development of NAFLD and its association with metabolic syndromes are poorly understood. In this study, we explored the role of CARF (collaborator of ARF) also known as CDKN2AIP, a novel gene of ARF-MDM2-p53 pathway in the development of NAFLD. It has been shown that, p53, beyond its tumor suppressor functions, can regulate the cellular glucose and lipid metabolism and its activation has been reported to induce hepatic steatosis in mice. However, as a regulator of p53 pathway, the role of CARF in the lipid metabolism and associated metabolic diseases has not been studied yet. Using high-fat diet (HFD) fed obesity mouse model of NAFLD we found that the expression of CARF along with Sirt1, pAMPK, and pACC was significantly decreased in the HFD induced fatty livers compared to control. Similarly, CARF expression was also down-regulated in palmitate (PA)-treated HepG2 cells, an in vitro model of steatosis. We also observed that shRNA mediated knockdown or lentiviral vector mediated overexpression of CARF induced or reduced the endogenous fat accumulation, respectively, in HepG2 cells, suggesting that CARF expression is negatively regulated in NAFLD. Additionally, we performed RNA seq analysis after CARF silencing in HepG2 cells and demonstrated that silencing of CARF altered the expression of genes regulating hepatic de novo lipogenesis, beta-oxidation, and lipid secretion all of which favor the accumulation of fat in the hepatocytes. Furthermore, genes associated with mitochondrial functions such as the TCA cycle and oxidative phosphorylation were also altered which could play a role in the development of NAFLD. Finally, we demonstrated that AAV mediated hepatic overexpression of CARF in HFD fed mouse model significantly reduced the fat accumulation in the liver as evident by H&E staining of liver sections and intrahepatic triglyceride level. Altogether we conclude that CARF plays a vital role in hepatic lipid metabolism and its downregulation perturbs lipid homeostasis leading to hepatic steatosis and the development of NAFLD.

scholarly journals Alleviating Effect of Quinoa and Underlying Mechanism on Hepatic Steatosis in High Fat Diet Fed Rat

2021 ◽  
Author(s):  
Chenwei Song ◽  
Wei Lv ◽  
Yahui Li ◽  
Pan Nie ◽  
Jun Lu ◽  
...  
Keyword(s):  
Immune Response ◽  
Lipid Metabolism ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Hepatic Tissue ◽  
Circulation System ◽  
Rna Seq ◽  
Rt Pcr ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome

Abstract Background: HF diet-associated fatty liver (is also known as non-alcoholic fatty liver disease, NAFLD) is considered the hepatic component of the metabolic syndrome and has attracted widespread attention due to the increase in its prevalence. Daily dietary management, is considered to be one of the effective strategies for the prevention of NAFLD. In the present study, the effect of quinoa on the hepatic steatosis and the metabolism mechanism were investigated.Methods: Male SD rats simultaneously administered an HF diet and different amounts of quinoa (equivalent to 100 g/day and 300 g/day of human intake, respectively). After 12 weeks of the intervention, Hepatic TG and TC as well as serum anti-oxidative parameters were determined, H&E staining evaluated the hepatic steatosis. Differential metabolite in serum and hepatic tissue were analyzed using UPLC-QTOF-MSE. mRNA expression profile were investigated using RNA-Seq and further verified using real-time RT-PCR.Results: It showed that quinoa effectively controlled the weight of rats, mitigated hepatic steatosis and oxidative stress, which exhibited the beneficial effect of quinoa on prevention of NAFLD. These beneficial effects could be attributed to the regulation of the production of certain metabolites in the circulation system or liver such as LysoPC and PC. The RNA-Seq analysis and RT-PCR verification revealed that an intake of a high amount of quinoa more effectively up-regulated the genes related to lipid metabolism [Apoa (apolipoprotein)5, Apoa4, Apoc2) and down-regulated the genes related immune response [lrf (interferon regulatory factor)5, Tlr6 (Toll like receptor), Tlr10, Tlr11, Tlr12]. Conclusions: Quinoa could alleviate hepatic steatosis due to the regulation of metabolism and the expression of genes related with lipid metabolism and immune response.

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