scholarly journals Study on the Mechanism of Shugan Xiaozhi Fang on Cells with Non-alcoholic Fatty Liver Disease

2019 ◽  
Vol 17 (1) ◽  
pp. 1328-1338
Author(s):  
Yufeng Xing ◽  
Chuantao Zhang ◽  
Fenfen Zhai ◽  
Tianran Zhou ◽  
Xiang Cui ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver Disease ◽  
Dose Group ◽  
Control Group ◽  
High Dose ◽  
Model Group ◽  
Alcoholic Fatty Liver ◽  
Oil Red O Staining ◽  
Alcoholic Fatty Liver Disease ◽  
Oil Red O

AbstractCells with non-alcoholic fatty liver disease (NAFLD) were studied to determine the mechanism of liver deficiency via the AdipoR2-PPARa pathway. NAFLD cells were randomly divided into a normal control group, blank control group, model group, low dose group, medium dose group, and high dose group. The NAFLD models were established by incubating the cells with linoleic acid (LA) and palmitic acid (PA) (2:1) for 24 h. The test groups were incubated with different doses of Shugan Xiaozhi Fang extract. The pathological changes in cells that accumulated lipids were detected by Oil Red O staining. Malondialdehyde (MDA) and triglyceride (TG) levels were measured. The apoptosis of cells was evaluated by flow cytometry. The levels of AdipoR2, PPARa, CD36, acyl-CoA mRNA, and protein were confirmed by RT- PCR and Western blot. The results of the Oil Red O staining demonstrated that the NAFLD cell model was successfully established. Compared with the model group, the levels of TG and MDA in the groups that received low, medium, and high doses of Shugan Xiaozhi were significantly lower (P<0.01), and a dose effect was evident. In addition, the expression of AdipoR2, PPARa, CD36, acyl-CoA protein, and mRNA in the Shugan Xiaozhi-treated groups was upregulated. Furthermore, the levels of AdipoR2, PPAR, CD36, acyl-CoA protein, and mRNA in all drug treatment groups that were extracted from L-O2 normal human hepatocytes were significantly upregulated (P<0.01). Moreover, the factor pattern of HepG2 human liver carcinoma cells was similar to that of L-O2. The levels of AdipoR, CD36, acyl-CoA, and AdipoR mRNA in the HepG2 low group were increased (P<0.05). AdipoR, PPAR, CD36, and acyl-CoA protein levels and AdipoR mRNA expression were significantly increased in the intermediate dose group and high dose group (P<0.01). Shugan Xiaozhi Fang attenuates hepatic lipid deposition in NAFLD induced by incubating with LA and PA for 24 h, which is associated with the activation of the AdipoR2-PPARα pathway.

scholarly journals A study on the mechanism of adipokine in non-alcoholic fatty liver in rats treated by four herbs decoction

2019 ◽  
Vol 17 ◽  
pp. 205873921985397 ◽  
Author(s):  
Xiao-Hong Sun ◽  
Liang-Deng Zhang ◽  
Wei Wei
Keyword(s):  
Fatty Liver ◽  
Dose Group ◽  
Expression Level ◽  
High Dose Group ◽  
Control Group ◽  
High Dose ◽  
Model Group ◽  
Alcoholic Fatty Liver ◽  
Oil Red O Staining ◽  
Oil Red O

The objective of the study is to determine adipokine-associated mechanism of efficacy of Si He Decoction (SHD) for treating non-alcoholic fatty liver disease (NAFLD). Forty-five Sprague-Dawley (SD) rats were randomly divided into control group, model group, SHD low-dose group, SHD middle-dose group, and SHD high-dose group. Except control group, others were fed with a high-fat diet for 12 weeks to establish model. Then, H&E and oil red O staining were performed, and enzyme-linked immunosorbent assay (ELISA) was used to detect expression level of adipokine-associated molecules. H&E and oil red O staining results revealed that SHD treatment for NAFLD could effectively improve liver pathological conditions compared to that in model group, and the best efficacy was observed in SHD high-dose group. Compared to model group, SHD treatment could effectively downregulate expression level of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), and upregulate expression level of visfatin, adiponectin (APN), leptin (LEP), and resistin in NAFLD rats. SHD can improve NAFLD through multiple means of targeting adipokines.

scholarly journals LncRNA-H19 promotes hepatic lipogenesis by directly regulating miR-130a/PPARγ axis in non-alcoholic fatty liver disease

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Jun Liu ◽  
Tao Tang ◽  
Guo-Dong Wang ◽  
Bo Liu
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Hepatic Lipogenesis ◽  
Alcoholic Fatty Liver ◽  
Oil Red O Staining ◽  
Alcoholic Fatty Liver Disease ◽  
Oil Red O ◽  
Liver Tissues

Abstract Background: As one of the most common liver disorders worldwide, non-alcoholic fatty liver disease (NAFLD) begins with the abnormal accumulation of triglyceride (TG) in the liver. Long non-coding RNA-H19 was reported to modulate hepatic metabolic homeostasis in NAFLD. However, its molecular mechanism of NAFLD was not fully clear. Methods: In vitro and in vivo models of NAFLD were established by free fatty acid (FFA) treatment of hepatocytes and high-fat feeding mice, respectively. Hematoxylin and Eosin (H&E) and Oil-Red O staining detected liver tissue morphology and lipid accumulation. Immunohistochemistry (IHC) staining examined peroxisome proliferator-activated receptor γ (PPARγ) level in liver tissues. ELISA assay assessed TG secretion. Luciferase assay and RNA pull down were used to validate regulatory mechanism among H19, miR-130a and PPARγ. The gene expression in hepatocytes and liver tissues was detected by quantitative real-time PCR (qRT-PCR) and Western blotting. Results: H19 and PPARγ were up-regulated, while miR-130a was down-regulated in NAFLD mouse and cellular model. H&E and Oil-Red O staining indicated an increased lipid accumulation. Knockdown of H19 inhibited steatosis and TG secretion in FFA-induced hepatocytes. H19 could bind to miR-130a, and miR-130a could directly inhibit PPARγ expression. Meanwhile, miR-130a inhibited lipid accumulation by down-regulating NAFLD-related genes PPARγ, SREBP1, SCD1, ACC1 and FASN. Overexpression of miR-130a and PPARγ antagonist GW9662 inhibited lipogenesis and TG secretion, and PPARγ agonist GW1929 reversed this change induced by miR-130a up-regulation. Conclusion: Knockdown of H19 alleviated hepatic lipogenesis via directly regulating miR-130a/PPARγ axis, which is a novel mechanistic role of H19 in the regulation of NAFLD.

Non-Alcoholic Fatty Liver Disease in Overweight Children and its Relationship with Retinol Serum Levels

2008 ◽  
Vol 78 (1) ◽  
pp. 27-32 ◽  
Author(s):  
Suano de Souza ◽  
Silverio Amancio ◽  
Saccardo Sarni ◽  
Sacchi Pitta ◽  
Fernandes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Lipid Profile ◽  
Fatty Liver Disease ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Control Group ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Objectives: To evaluate the frequency of non-alcoholic fatty liver disease, the retinol serum levels, lipid profile, and insulin resistance in overweight/obese children. To relate these biochemical variables with the risk of this disease in the population studied. Methods: The study was cross-sectional and prospective, with 46 overweight/obese school children (28 female, 18 male; mean age 8.6 years). The control group consisted of 45 children, paired by age and gender. Hepatic steatosis, evaluated by ultrasound, was classified as normal, mild, moderate, or severe. Also evaluated were serum retinol levels; thiobarbituric acid reactive substances; lipid profile; and fasting glucose and serum insulin levels, used for the calculation of the Homeostasis Model Assessment. Results: Hepatic ultrasound alterations were found in 56.5% and 48,9% of the overweight/obese and control group children, respectively. Presence of obesity was associated with high levels of triglycerides (OR = 4.6; P = 0.002). In the studied children, the risk of steatosis was related to a trend to a higher percentage of retinol inadequacy (OR = 2.8; p = 0.051); there was no association with thiobarbituric acid reactive substances, lipid profile, or insulin resistance. Conclusions: The high frequency of non-alcoholic fatty liver disease in both groups, evaluated by hepatic ultrasound, in low-socioeconomic level children, independent of nutritional condition and without significant association with insulin resistance, emphasizes that especially in developing countries, other risk factors such as micronutrient deficiencies (e.g. vitamin A) are involved.

scholarly journals Maternal tadalafil therapy for fetal growth restriction prevents non-alcoholic fatty liver disease and adipocyte hypertrophy in the offspring

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takuya Kawamura ◽  
Hiroaki Tanaka ◽  
Ryota Tachibana ◽  
Kento Yoshikawa ◽  
Shintaro Maki ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fetal Growth ◽  
Fetal Programming ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

AbstractWe aimed to investigate the effects of maternal tadalafil therapy on fetal programming of metabolic function in a mouse model of fetal growth restriction (FGR). Pregnant C57BL6 mice were divided into the control, L-NG-nitroarginine methyl ester (L-NAME), and tadalafil + L-NAME groups. Six weeks after birth, the male pups in each group were given a high-fat diet. A glucose tolerance test (GTT) was performed at 15 weeks and the pups were euthanized at 20 weeks. We then assessed the histological changes in the liver and adipose tissue, and the adipocytokine production. We found that the non-alcoholic fatty liver disease activity score was higher in the L-NAME group than in the control group (p < 0.05). Although the M1 macrophage numbers were significantly higher in the L-NAME/high-fat diet group (p < 0.001), maternal tadalafil administration prevented this change. Moreover, the epididymal adipocyte size was significantly larger in the L-NAME group than in the control group. This was also improved by maternal tadalafil administration (p < 0.05). Further, we found that resistin levels were significantly lower in the L-NAME group compared to the control group (p < 0.05). The combination of exposure to maternal L-NAME and a high-fat diet induced glucose impairment and non-alcoholic fatty liver disease. However, maternal tadalafil administration prevented these complications. Thus, deleterious fetal programming caused by FGR might be modified by in utero intervention with tadalafil.

Efficacy of adjuvant phosphatidylcholine in the management of egyptian patients with non alcoholic fatty liver disease (NAFLD)

2021 ◽  
Vol 6 (8) ◽  
Keyword(s):  
Liver Disease ◽  
Fatty Liver Disease ◽  
Standard Care ◽  
Intervention Group ◽  
Control Group ◽  
Fibrosis Score ◽  
Alcoholic Fatty Liver ◽  
Nafld Fibrosis Score ◽  
Egyptian Patients ◽  
Alcoholic Fatty Liver Disease

Background and Aim: Non-Alcoholic Fatty Liver Disease (NAFLD) has become the most common liver disorder with increased liver related and non-related complications and mortality as a result of increasing obesity, type 2 diabetes and metabolic syndrome (MetS). The current study aims to evaluate the efficacy of adjuvant phosphatidylcholine in treating patients with NAFLD. Methods: This interventional randomized controlled study recruited 100 patients with NAFLD and MetS randomized into: a control group (n=50) that received standard care of life style modifications and an intervention group (n=50) that received phosphatidylcholine (2100 gm/day) plus standard care. Both groups received health education through clinical pharmacist for achieving sustainable weight loss for 6 months. Body mass index (BMI), waist and hip circumference, liver function, lipid profile, homeostasis model of assessment-insulin resistance (HOMA-IR) score, NAFLD-fibrosis score, steatosis score and liver stiffness measurement by transient elastography were recorded at baseline, 3 and 6 months. Results: Intervention group showed significantly (p<0.05) higher number with normalized; alanine aminotransferase, total cholesterol and low density lipoprotein at midpoint and endpoint, aspartate amiontransferase at midpoint and high density lipoproteins and malondaldehyde at endpoint. Intervention group showed a significantly higher participants’ number who shifted to more favorable category of NAFLD-fibrosis score (p=0.02), radiological fibrosis stage (p=0.015) at endpoint, radiological steatosis grades and HOMA-IR score at midpoint and endpoint (p<0.05). Additionally, significant number of participants in intervention group (34%) lost MetS components compared to (10%) in control group at endpoint (p=0.004). Conclusion: Adjuvant phosphatidylcholine has shown laboratory, radiological and clinical benefits in the management of Egyptian patients with NAFLD and ameliorate MetS parameters.

Diet containing dehulled adlay ameliorates hepatic steatosis, inflammation and insulin resistance in rats with non-alcoholic fatty liver disease

2021 ◽  
pp. 1-25
Author(s):  
Wan-Ju Yeh ◽  
Jung Ko ◽  
Wei-Yi Cheng ◽  
Hsin-Yi Yang
Keyword(s):  
Insulin Resistance ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Weight ◽  
Vital Role ◽  
High Dose ◽  
Alcoholic Fatty Liver ◽  
Protein Levels ◽  
Alcoholic Fatty Liver Disease

Abstract Dietary modification plays a vital role in the treatment of non-alcoholic liver diseases. We investigated the effects of the consumption of different amount of dehulled adlay, which has hypolipidemic and anti-inflammatory properties, on non-alcoholic fatty liver disease (NAFLD). We fed rats a high-fat-high-fructose liquid diet for 16 weeks to induce NAFLD. The rats were divided into three groups fed the NAFLD diet only (NN) or a diet containing 44.9 g/L or 89.8 g/L of dehulled adlay (group NA and NB, respectively). After 8 weeks, the NA & NB group had lower C-reactive protein levels and improvement in insulin resistance. In addition, the NB group had lower liver weight and hepatic triglyceride and cholesterol concentrations than did the NN group. Compared with the NN group, the high-dose NB group had improved steatosis, lower hepatic TNF-α, IL-1β and IL-6 levels, and lower adipose leptin levels. Our results suggest that a diet containing dehulled adlay can ameliorate NAFLD progression by decreasing of insulin resistance, steatosis and inflammation.

scholarly journals Non alcoholic fatty liver disease is a predictor of subclinical Carotid Atherosclerosis in the presence of Metabolic Syndrome

2019 ◽  
Vol 16 (1) ◽  
pp. 39-45
Author(s):  
Cemal Kemaloglu ◽  
Melek Didem Kemaloglu
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Carotid Atherosclerosis ◽  
Controlled Study ◽  
Control Group ◽  
Alcoholic Fatty Liver ◽  
Increased Risk ◽  
Alcoholic Fatty Liver Disease

Objective: The aim of this study is to identify the relationship between carotid intima-media thickness (c-imt) and non-alcoholic fatty liver disease (NAFLD), and to determine whether NAFLD is an independent predictor for the progression of atherosclerosis.  Method: This is a prospective randomized controlled study. 103 NAFLD patients who have hepatosteatosis with grade II and above were enrolled in this study. Patients were divided into NAFLD with metabolic syndrome (MS) and NAFLD without MS groups and compared with 50 healthy people. Basal demographic characteristics and C-imt of all patients and control group were measured.  Results: C-imt and carotid cross sectional area rates in the NAFLD groups were significantly higher than those in the control group. The mean and max. c-imt levels were significantly higher in the NAFLD group with metabolic syndrome (p<0,001). Homeostatic Model of Assessment-Insulin Resistance (HOMA-IR) levels were increased in the group with metabolic syndrome than those in the group without metabolic syndrome, with statistical significance (p<0.001). There was no difference in c-imt levels between HOMA-IR positive and negative groups (p=0.254) in patients with NAFLD and without metabolic syndrome. There was only a mild positive corelation between c-imt levels and high sensitive C-Reactive protein (hs-CRP) levels in metabolic syndrome positive group (p=0.026 r=0.30).  Conclusion: NAFLD was a significant predictor to determine the increased risk of carotid atherosclerosis. 

Effect of garlic powder supplementation on hepatic steatosis, liver enzymes and lipid profile in patients with non-alcoholic fatty liver disease: a double-blind randomised controlled clinical trial

2020 ◽  
Vol 124 (4) ◽  
pp. 450-456
Author(s):  
Abbas Ali Sangouni ◽  
Mohammad Reza Mohammad Hosseini Azar ◽  
Mohammad Alizadeh
Keyword(s):  
Liver Disease ◽  
Treatment Group ◽  
Lipid Profile ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Liver Enzymes ◽  
Control Group ◽  
Alcoholic Fatty Liver ◽  
Garlic Powder ◽  
Alcoholic Fatty Liver Disease

AbstractNon-alcoholic fatty liver disease (NAFLD) includes a range of disorders from simple steatosis to non-alcoholic steatohepatitis. There is no proven drug treatment for NAFLD, and diet modification is considered part of the main line of treatment for this disease. The aim of this study was to investigate the efficacy of garlic supplementation in NAFLD patients. The effect of garlic powder supplementation on hepatic steatosis, liver enzymes and lipid profile was investigated in NAFLD patients. Ninety NAFLD patients were randomly assigned to take either a garlic powder supplement or a placebo for 12 weeks. The treatment group received four tablets of garlic daily (each tablet contained 400 mg garlic powder). The control group received four tablets of placebo (each placebo contained 400 mg starch). At the end of the study, hepatic steatosis was significantly reduced in the treatment group compared with the control group (P = 0·001). In addition, a significant decrease was seen in the serum concentration of alanine transaminase (P < 0·001), aspartate transaminase (P = 0·002), γ-glutamyltransferase (P = 0·003) as well as total cholesterol (P = 0·009), TAG (P < 0·001), HDL-cholesterol (P < 0·001) and LDL-cholesterol (P = 0·01) in the treatment group compared with the control group. No significant difference was seen between the two groups in serum concentration of alkaline phosphatase. Overall, garlic powder supplementation improved hepatic features and lipid profile among NAFLD patients.

scholarly journals Biochemical changes in Non-alcoholic fatty liver disease (NAFLD): A study in Nepalese Population

2017 ◽  
Vol 2 (2) ◽  
pp. 15-20
Author(s):  
Pooja Maharjan ◽  
Puspa Raj Khanal ◽  
Narayan Prasad Parajuli ◽  
Govardhan Joshi ◽  
Hridaya Parajuli ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Biochemical Parameters ◽  
Developed Countries ◽  
Western World ◽  
Control Group ◽  
P Value ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Background: Non-alcoholic fatty liver disease (NAFLD) has emerged as the most common liver problem in the western world and is a clinicopathologic entity increasingly recognized as a major health burden in developed countries. Different laboratory tests are extremely useful in achieving a better understanding of diseases, and thereby, allow making decision for better management. The examination of different biochemical parameters usually provides excellent clues to the cause of the disease. The present study was conducted with the aim to assess the biochemical markers in Non alcoholic fatty liver disease (NAFLD) patients in Nepalese population.Methods: The biochemical parameters were investigated in 75 NAFLD patients, and 70 normal participants. The diagnosis of hepatic steatosis was established by abdominal ultrasound examination. All patients diagnosed as NAFLD were investigated for biochemical parameters and see the relationship between NAFLD and control was studied.Results: The findings of all biochemical parameters were raised in NAFLD patients in comparison with non-fatty liver control group and the differences were found to be statistically (P value less than 0.005) significant.Conclusions: NAFLD is associated with changes in biochemical parameters in cases of NAFLD. Its early detection will help in modifying the disease course, delaying complications and will also play a major role in preventive cardiology.Ann. Clin. Chem. Lab. Med. 2016:2(2);15-20

scholarly journals Insulin resistance index (HOMA-IR) in the differentiation of patients with non-alcoholic fatty liver disease and healthy individuals

2010 ◽  
Vol 47 (2) ◽  
pp. 165-169 ◽  
Author(s):  
Ana Lúcia Farias de Azevedo Salgado ◽  
Luciana de Carvalho ◽  
Ana Claudia Oliveira ◽  
Virgínia Nascimento dos Santos ◽  
Jose Gilberto Vieira ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Resistance Index ◽  
Control Group ◽  
Oral Glucose ◽  
Healthy Individuals ◽  
Alcoholic Fatty Liver ◽  
Insulin Resistance Index ◽  
Alcoholic Fatty Liver Disease

CONTEXT: Due to its good correlation to glycemic clamp, HOMA-IR has been widely utilized as insulin resistance index in clinical and epidemiological studies involving non-alcoholic fatty liver disease carriers. However, values used for this parameter have shown large variability. OBJECTIVE: To identify the HOMA-IR cut value that best distinguishes non-diabetic non-alcoholic fatty liver disease patients from a control group. METHODS: One hundred sixteen non-alcoholic fatty liver disease patients were studied, diagnosed by clinical, biochemical, and liver image or biopsy criteria, and 88 healthy individuals, without any liver disease and testing for oral glucose tolerance within normality. These groups did not differ in age and gender. All were submitted to oral glucose tolerance test and blood samples were collected for glucose and insulin measurements by immunofluorometric method. HOMA-IR was calculated according to the formula: fasting insulin (µU/L) x fasting glucose (nmol/L)/22.5. RESULTS: NAFLD patients showed higher insulin, glycemia, and HOMA-IR values than control group, even when excluding glucose intolerant and diabetes mellitus patients by their glycemic curves. HOMA-IR 75th percentile for control group was 1.78 and the best area under the curve index was obtained for HOMA-IR values of 2.0 [AUC= 0.840 (0.781-0.899 CI 95%), sensitivity (Se): 85%, specificity (Sp): 83%] while value 2.5 showed best specificity without important loss in sensitivity [AUC=0,831 (0.773-0.888) Se = 72%, Sp = 94%]. CONCLUSION: HOMA-IR values above or equal to 2.0 or 2.5 show enhanced diagnostic value in distinguishing non-alcoholic fatty liver disease carriers from control group individuals.

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