HISTOPATHOLOGICAL STUDY OF THE PROTECTIVE EFFECT OF SPIRULINA PLATENSIS ON FETAL LIVER OF MICE WITH ACUTE FATTY LIVER OF PREGNANCY

Objective: The protective effect of Spirulina platensis on the fetal liver of mice with acute fatty liver of pregnancy was investigated. Methods: Small female mice were divided into four groups: A control group with a standard diet, a high-fat diet to induce liver steatosis, a high-fat diet plus Spirulina, and a high-fat diet plus Simvastatin given through gavage to protect the liver against steatosis. After 2 months, the female mice became pregnant by polygamy method at the same time they were treated by different diets. On day 17, the fetuses were removed by C-section, and histological studies were carried out on their livers. Results: The results showed a significant decrease in liver steatosis in the group treated by Spirulina compared with the other groups (p<0.05). The fatty liver of pregnancy could lead to liver failure and death in both mother and fetus, and medications like Simvastatin that is used for the treatment of fatty liver are harmful to the fetus. However, Spirulina shows a positive effect on the treatment of both fetus and mother. Conclusions: The results of this study show that Spirulina is an effective medical supplement in the treatment of fatty liver of pregnancy.

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Baicalin Attenuates High Fat Diet-Induced Obesity and Liver Dysfunction: Dose-Response and Potential Role of CaMKKβ/AMPK/ACC Pathway

Cellular Physiology and Biochemistry ◽

10.1159/000374037 ◽

2015 ◽

Vol 35 (6) ◽

pp. 2349-2359 ◽

Cited By ~ 42

Author(s):

Youli Xi ◽

Miaozong Wu ◽

Hongxia Li ◽

Siqi Dong ◽

Erfei Luo ◽

...

Keyword(s):

Protein Kinase ◽

Fatty Liver ◽

High Fat Diet ◽

Molecular Mechanisms ◽

Liver Steatosis ◽

Serum Levels ◽

Whole Body ◽

Therapeutic Effects ◽

High Fat ◽

Dependent Protein

Background/Aims: Obesity-associated fatty liver disease affects millions of individuals. This study aimed to evaluate the therapeutic effects of baicalin to treat obesity and fatty liver in high fat diet-induced obese mice, and to study the potential molecular mechanisms. Methods: High fat diet-induced obese animals were treated with different doses of baicalin (100, 200 and 400 mg/kg/d). Whole body, fat pad and liver were weighed. Hyperlipidemia, liver steatosis, liver function, and hepatic Ca2+/CaM-dependent protein kinase kinase β (CaMKKβ) / AMP-activated protein kinase (AMPK) / acetyl-CoA carboxylase (ACC) were further evaluated. Results: Baicalin significantly decreased liver, epididymal fat and body weights in high fat diet-fed mice, which were associated with decreased serum levels of triglycerides, total cholesterol, LDL, alanine transaminase and aspartate transaminase, but increased serum HDL level. Pathological analysis revealed baicalin dose-dependently decreased the degree of hepatic steatosis, with predominantly diminished macrovesicular steatosis at lower dose but both macrovesicular and microvesicular steatoses at higher dose of baicalin. Baicalin dose-dependently inhibited hepatic CaMKKβ/AMPK/ACC pathway. Conclusion: These data suggest that baicalin up to 400 mg/kg/d is safe and able to decrease the degree of obesity and fatty liver diseases. Hepatic CaMKKβ/AMPK/ACC pathway may mediate the therapeutic effects of baicalin in high fat diet animal model.

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Ethanol Extract of Crataegus Oxyacantha L. Ameliorate Dietary Non-Alcoholic Fatty Liver Disease in Rat

Drug Research ◽

10.1055/a-0579-7532 ◽

2018 ◽

Vol 68 (10) ◽

pp. 553-559

Author(s):

Golbahar Saeedi ◽

Fereshteh Jeivad ◽

Mohammadhadi Goharbari ◽

Gholamreza Gheshlaghi ◽

Omid Sabzevari

Keyword(s):

Fatty Liver ◽

Protective Effect ◽

High Fat Diet ◽

Normal Diet ◽

Oxidative Stress Marker ◽

Histopathological Study ◽

Potential Candidate ◽

Diet Change ◽

High Fat ◽

Alcoholic Fatty Liver

Abstract Background Non-alcoholic fatty liver (NAFLD) is one the most prevalent disease worldwide which characterized by fat accumulation in liver with no established efficient therapy. We designed this study to investigate protective and therapeutic effect of Crataegus oxyacantha L. (C. oxyacantha) on NAFLD induced by high fat diet in rat models. Methods NAFLD was induced by High Fat Diet+fructose (HFD), 45 Wistar rats were divided to 8 groups including control, HFD, HFD+diet change, HFD+diet change+C. oxyacantha 20 mg/kg, co treatment of HFD+C. oxyacantha 10, 20 and 40 mg/kg, and normal diet+C. oxyacantha 40 mg. C. oxyacantha was administered orally. Effectiveness of the C. oxyacantha was assessed through measuring the biochemical factors, and oxidative stress marker (FRAP, GSH, and MDA). Histopathological study was performed using H & E staining. Results The diet change from high fat to low fat ameliorated liver damage. However, consumption of C. oxyacantha (10 & 20 mg/kg) caused significant reduction in the level of all examined liver biomarkers specially LDH, that showed C. oxyacantha can restore the hepatocyte damage due to HFD. The C. oxyacantha showed a protective effect which was more prominent in the animals treated with the 20 mg/kg C. oxyacantha. The administration of C. oxyacantha caused increased antioxidant status (GSH and FRAP levels) and decreased lipid peroxidation in treated animals. Major Conclusion Accordingly, C. oxyacantha have both therapeutic and protective effect for NAFLD and may be a potential candidate for further assessments in clinical studies.

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Protective Effect of Meretrix meretrix Oligopeptides on High-Fat-Diet-Induced Non-Alcoholic Fatty Liver Disease in Mice

Marine Drugs ◽

10.3390/md16020039 ◽

2018 ◽

Vol 16 (2) ◽

pp. 39 ◽

Cited By ~ 14

Author(s):

Fangfang Huang ◽

Jiajia Wang ◽

Fangmiao Yu ◽

Yunping Tang ◽

Guofang Ding ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Protective Effect ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Meretrix Meretrix ◽

High Fat ◽

Alcoholic Fatty Liver ◽

Alcoholic Fatty Liver Disease

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Crude Extracts fromLycium barbarumSuppress SREBP-1c Expression and Prevent Diet-Induced Fatty Liver through AMPK Activation

BioMed Research International ◽

10.1155/2014/196198 ◽

2014 ◽

Vol 2014 ◽

pp. 1-10 ◽

Cited By ~ 12

Author(s):

Wang Li ◽

Yan Li ◽

Qing Wang ◽

Yi Yang

Keyword(s):

Fatty Liver ◽

High Fat Diet ◽

Uncoupling Protein ◽

Expression Profiles ◽

Liver Steatosis ◽

High Fat ◽

Lycium Barbarum ◽

Brown Adipose

Lycium barbarumpolysaccharide (LBP) is well known in traditional Chinese herbal medicine that, has beneficial effects. Previous study reported that LBP reduced blood glucose and serum lipids. However, the underlying LBP-regulating mechanisms remain largely unknown. The main purpose of this study was to investigate whether LBP prevented fatty liver through activation of adenosine monophosphate-activated protein kinase (AMPK) and suppression of sterol regulatory element-binding protein-1c (SREBP-1c). Male C57BL/6J mice were fed a low-fat diet, high-fat diet, or 100 mg/kg LBP-treatment diet for 24 weeks. HepG2 cells were treated with LBP in the presence of palmitic acid. In our study, LBP can improve body compositions and lipid metabolic profiles in high-fat diet-fed mice. Oil Red O stainingin vivoandin vitroshowed that LBP significantly reduced hepatic intracellular triacylglycerol accumulation. H&E staining also showed that LBP can attenuate liver steatosis. Hepatic genes expression profiles demonstrated that LBP can activate the phosphorylation of AMPK, suppress nuclear expression of SREBP-1c, and decrease protein and mRNA expression of lipogenic genesin vivoorin vitro. Moreover, LBP significantly elevated uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor-γcoactivator-1α(PGC-1α) expression of brown adipose tissue. In summary, LBP possesses a potential novel treatment in preventing diet-induced fatty liver.

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High-fat diet overfeeding promotes nondetrimental liver steatosis in female mice

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00022.2018 ◽

2018 ◽

Vol 315 (5) ◽

pp. G772-G780 ◽

Cited By ~ 4

Author(s):

Lino Arisqueta ◽

Hiart Navarro-Imaz ◽

Ibone Labiano ◽

Yuri Rueda ◽

Olatz Fresnedo

Keyword(s):

Liver Disease ◽

Bile Acid ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Enterohepatic Circulation ◽

High Fat ◽

Nonalcoholic Fatty Liver ◽

Female Mice

High-fat diet (HFD) feeding or leptin-deficient mice are extensively used as models resembling features of human nonalcoholic fatty liver disease (NAFLD). The concurrence of experimental factors as fat content and source or total caloric intake leads to prominent differences in the development of the hepatic steatosis and related disturbances. In this work, we characterized the hepatic lipid accumulation induced by HFD in wild-type (WT) and ob/ ob mice with the purpose of differentiating adaptations to HFD from those specific of increased overfeeding due to leptin deficiency-associated hyperphagia. Given that most published works have been done in male models, we used female mice with the aim of increasing the body of evidence regarding NAFLD in female subjects. HFD promoted liver lipid accumulation only in the hyperphagic strain. Nevertheless, a decrease of lipid droplet-associated cholesteryl ester (CE) in both WT and obese animals was observed. These changes were accompanied by an improvement in the profile of lipoproteins that transport cholesterol and liver function markers in plasma from ob/ ob mice and a lower hepatic index. Using primary hepatocytes from female mice, overaccumulation of CE induced by 0.4 mM oleic acid reversed in the presence of a specific Takeda G protein-coupled bile acid receptor agonist. Nevertheless, hepatocytes from male mice were not responsive. This study suggests that enterohepatic circulation of bile acids might be one of the factors that can affect sex dimorphism in NAFLD development, which underlines the importance of including female models in the NAFLD research field. NEW & NOTEWORTHY This work provides new insight into the use of high-fat diet as a model to induce nonalcoholic fatty liver disease in wild-type and ob/ ob female mice. We show that high-fat diet induces steatosis only in ob/ ob mice while, surprisingly, several health indicators improve. Noteworthy, experiments with primary hepatocytes from male and female mice show that they express Takeda G protein-coupled bile acid receptor and that it and bile acid enterohepatic circulation might be accountable for sex dimorphism in nonalcoholic fatty liver disease development.

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Potential protective effect of curcumin in high-fat diet-induced nonalcoholic fatty liver disease in rats

Journal of Current Medical Research and Practice ◽

10.4103/jcmrp.jcmrp_37_20 ◽

2021 ◽

Vol 6 (1) ◽

pp. 92

Author(s):

AhmedM M. Mahmouda ◽

NohaA.-R A. El-Hagag ◽

HusseinI El-Bitar ◽

Abdel-HalimM Afifi

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Protective Effect ◽

Nonalcoholic Fatty Liver Disease ◽

High Fat Diet ◽

Fatty Liver Disease ◽

High Fat ◽

Nonalcoholic Fatty Liver

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Development of nonalcoholic fatty liver disease model by high-fat diet in rats

Journal of Basic and Clinical Physiology and Pharmacology ◽

10.1515/jbcpp-2019-0258 ◽

2019 ◽

Vol 30 (6) ◽

Cited By ~ 1

Author(s):

Hijrawati Ayu Wardani ◽

Mahardian Rahmadi ◽

Chrismawan Ardianto ◽

Santhra Segaran Balan ◽

Norshafarina Shari Kamaruddin ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Liver Steatosis ◽

Serum Triglyceride ◽

High Fat ◽

Serum Triglycerides ◽

Nonalcoholic Fatty Liver

Abstract Background Nonalcoholic fatty liver disease (NAFLD) is indicated by liver steatosis without excessive alcohol use or other liver disease. Several studies have reported that metabolic syndromes such as obesity, type 2 diabetes mellitus, and dyslipidemia have a linear correlation associated with NAFLD pathophysiology. One of the characteristics of dyslipidemia in NAFLD is increase in serum triglycerides. This study aimed to develop a model of NAFLD characterized by an increase in serum triglyceride levels and histological profile of liver steatosis by high-fat diet in rats. Methods Twelve Wistar rats were fed with pellets enriched with 60% fat. They were housed individually, and the remaining pellets were weighted every day for intake evaluation. Blood samples were collected at day 0 and at the end of each trial period at days 7, 14, 21, and 28 for the measurement of triglyceride levels. Every animal from each group was also sacrificed for liver histopathological examination. Results This study has established developing the NAFLD animal model by induction of a high-fat diet. The levels of serum triglycerides were increased from baseline 80.41 ± 12.82 to 1152.00 ± 73.62, 493.66 ± 159.98, 556.00 ± 120.79, and 489.00 ± 156.75 mg/dL at days 7, 14, 21, and 28, respectively. Liver histology also showed liver steatosis development, inflammation, and hepatocellular ballooning, which were associated with the NAFLD state. Conclusions High-fat diet in rats induced hypertriglyceridemia along with NAFLD-like liver histopathology.

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