scholarly journals Fast Induction of Hcc in Nash Rodent Model: A Simple Diet Associated with A Chemical Carcinogen

2020 ◽  
Vol 4 (2) ◽  
Keyword(s):  
High Fat Diet ◽  
Tumor Development ◽  
Immunohistochemical Analysis ◽  
Experimental Models ◽  
Rodent Model ◽  
New Drugs ◽  
Sprague Dawley ◽  
High Fat ◽  
Deficient Diet ◽  
Alcoholic Fatty Liver

Introduction: Non-alcoholic fatty liver disease (NAFLD) have been increasing as an important cause of hepatocellular carcinoma (HCC). Experimental models are crucial to identify some pathways in the pathogenesis of HCC secondary to NAFLD. Objective: To systematize an experimental hybrid rodent model of HCC secondary to NAFLD. Material and Methods: Fourteen male Sprague-Dawley rats, weighting 350-500g, were fed with choline-deficient high-fat diet and diethylnitrosamine (DEN) in the drinking water for 16 weeks. The animals were separated into two groups: 7 received DEN in water (100mg/ml) associated to choline-deficient high-fat diet and 7 received only cholinedeficient high-fat diet. Histological and immunohistochemical analysis were also performed. Results: All animals had definitive diagnosis of NASH in both groups with hepatocellular ballooning, steatosis and inflammation. In the group that received high-fat choline deficient diet, only two animals had micro nodular cirrhosis. However, in DEN group with high-fat choline deficient diet, all animals had gross lesions, major nodulations and fibrosis, visible in macroscopy. Besides, according of Edmondson-Steiner classification, 71% of the animals that received DEN + Diet with positive CK19 and oval cells and developed some grades of dysplastic and tumoral lesions. Moreover, in this model we could identify beyond NASH progression, some tumor-development stages, which means this model shows different treatment and study targets. Conclusion: The model is accomplishable, promotes fast induction of HCC in NAFLD context without much complexity to be executed and will be implemented as an interesting model to study new drugs to HCC secondary a NASH.

scholarly journals Fast Induction of Hcc in Nash Rodent Model: A Simple Diet Associated with A Chemical Carcinogen

2020 ◽  
Vol 4 (2) ◽  
Keyword(s):  
High Fat Diet ◽  
Tumor Development ◽  
Immunohistochemical Analysis ◽  
Experimental Models ◽  
Rodent Model ◽  
New Drugs ◽  
Sprague Dawley ◽  
High Fat ◽  
Deficient Diet ◽  
Alcoholic Fatty Liver

Introduction: Non-alcoholic fatty liver disease (NAFLD) have been increasing as an important cause of hepatocellular carcinoma (HCC). Experimental models are crucial to identify some pathways in the pathogenesis of HCC secondary to NAFLD. Objective: To systematize an experimental hybrid rodent model of HCC secondary to NAFLD. Material and Methods: Fourteen male Sprague-Dawley rats, weighting 350-500g, were fed with choline-deficient high-fat diet and diethylnitrosamine (DEN) in the drinking water for 16 weeks. The animals were separated into two groups: 7 received DEN in water (100mg/ml) associated to choline-deficient high-fat diet and 7 received only cholinedeficient high-fat diet. Histological and immunohistochemical analysis were also performed. Results: All animals had definitive diagnosis of NASH in both groups with hepatocellular ballooning, steatosis and inflammation. In the group that received high-fat choline deficient diet, only two animals had micro nodular cirrhosis. However, in DEN group with high-fat choline deficient diet, all animals had gross lesions, major nodulations and fibrosis, visible in macroscopy. Besides, according of Edmondson-Steiner classification, 71% of the animals that received DEN + Diet with positive CK19 and oval cells and developed some grades of dysplastic and tumoral lesions. Moreover, in this model we could identify beyond NASH progression, some tumor-development stages, which means this model shows different treatment and study targets. Conclusion: The model is accomplishable, promotes fast induction of HCC in NAFLD context without much complexity to be executed and will be implemented as an interesting model to study new drugs to HCC secondary a NASH.

scholarly journals Metformin ameliorates maternal high-fat diet-induced maternal dysbiosis and fetal liver apoptosis

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Szu-Wei Huang ◽  
Yu-Che Ou ◽  
Kuo-Shu Tang ◽  
Hong-Ren Yu ◽  
Li-Tung Huang ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Fetal Liver ◽  
Liver Steatosis ◽  
Chow Diet ◽  
Obese Women ◽  
Sprague Dawley ◽  
Maternal Weight ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Beneficial Effects

Abstract Background The deleterious effect of maternal high-fat diet (HFD) on the fetal rat liver may cause later development of non-alcoholic fatty liver disease (NAFLD). The aim of this study was to evaluate the effect of maternal HFD-induced maternal hepatic steatosis and dysbiosis on the fetal liver and intestines, and the effect of prenatal metformin in a rat model. Methods Sprague–Dawley rats were assigned to three groups (N = 6 in each group). Before mating, the rats were randomly assigned to HFD or normal-chow diet (NCD) group for 7 weeks. After mating, the HFD group rats were continued with high-fat diet during pregnancy and some of the HFD group rats were co-treated with metformin (HFMf) via drinking water during pregnancy. All maternal rats and their fetuses were sacrificed on gestational day 21. The liver and intestinal tissues of both maternal and fetal rats were analyzed. In addition, microbial deoxyribonucleic acid extracted from the maternal fecal samples was analyzed. Results HFD resulted in maternal weight gain during pregnancy, intrahepatic lipid accumulation, and change in the serum short-chain fatty acid profile, intestinal tight junctions, and dysbiosis in maternal rats. The effect of HFD on maternal rats was alleviated by prenatal metformin, which also ameliorated inflammation and apoptosis in the fetal liver and intestines. Conclusions This study demonstrated the beneficial effects of prenatal metformin on maternal liver steatosis, focusing on the gut-liver axis. In addition, the present study indicates that prenatal metformin could ameliorate maternal HFD-induced inflammation and apoptosis in the fetal liver and intestines. This beneficial effect of in-utero exposure of metformin on fetal liver and intestines has not been reported. This study supports the use of prenatal metformin for pregnant obese women.

scholarly journals Hepatic Response of Magnesium-Restricted Wild Type Mice

Metabolites ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 762
Author(s):  
Vera H. Fengler ◽  
Tanja Macheiner ◽  
Walter Goessler ◽  
Maria Ratzer ◽  
Johannes Haybaeck ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Magnesium Deficiency ◽  
Serum Magnesium ◽  
Cholesterol Content ◽  
High Fat ◽  
Deficient Diet ◽  
Metabolic Markers ◽  
Alcoholic Fatty Liver ◽  
Markers Of Inflammation ◽  
And Control

Magnesium-deficiency is implicated in many metabolic disorders, e.g., type 2 diabetes and metabolic syndrome, representing risk factors for non-alcoholic fatty liver disease (NAFLD). This study aims to investigate the contribution of magnesium-restriction to the development of NAFLD. Magnesium-deficiency was induced in C57BL/6 mice by feeding a magnesium-deficient-diet. Metabolic markers as well as markers of inflammation and liver function were assessed. Furthermore, liver tissue was examined histopathologically and compared with specimens from high-fat-diet fed and control mice. Finally, the hepatic inflammatory response was quantified by determining hepatic IL-6, TNFα, and MCP-1. Magnesium-restriction resulted in at least a 2-fold significant reduction of serum magnesium levels compared to the high-fat-diet fed and control mice, whereas the hepatic magnesium content was decreased due to high-fat-diet feeding. No changes in metabolic markers in magnesium-restricted mice were observed, while the cholesterol content was elevated in high-fat-diet fed mice. Magnesium-restricted mice additionally featured inflammation and enlarged hepatocytes in liver histology. Furthermore, magnesium-restricted and high-fat-diet fed mice exhibited elevated hepatic TNFα levels compared to control mice. Accordingly, our data suggest that magnesium is involved in hepatic inflammatory processes and hepatocyte enlargement, key histological features of human NAFLD, and may therefore contribute to development and progression of the disease.

Trans-palmitoleic Acid Reduces Adiposity via Increased Lipolysis in a Rodent Model of Diet-Induced Obesity

2021 ◽  
pp. 1-24
Author(s):  
L. Irasema Chávaro-Ortiz ◽  
Brenda D. Tapia-Vargas ◽  
Mariel Rico-Hidalgo ◽  
Ruth Gutiérrez-Aguilar ◽  
María E. Frigolet
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
Palmitoleic Acid ◽  
Rodent Model ◽  
Adipocyte Size ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Visceral Adipose

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.

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.

The Effects of Maternal High Fat Diet on the Lingual CD36 Lipid Sensors of the Offspring Sprague Dawley Rats

Metabolism ◽  
2021 ◽  
Vol 116 ◽  
pp. 154497
Author(s):  
Elif Günalan ◽  
Meyli Ezgi Karagöz ◽  
Bayram Yılmaz ◽  
Burcu Gemici
Keyword(s):  
High Fat Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Lipid Sensors

Lactobacillus plantarum DR7 improved brain health in aging rats via the serotonin, inflammatory and apoptosis pathways

2020 ◽  
Vol 11 (8) ◽  
pp. 753-766
Author(s):  
A.I. Zaydi ◽  
L.-C. Lew ◽  
Y.-Y. Hor ◽  
M.H. Jaafar ◽  
L.-O. Chuah ◽  
...  
Keyword(s):  
Lactobacillus Plantarum ◽  
Cognitive Functions ◽  
High Fat Diet ◽  
Normal Diet ◽  
Sprague Dawley ◽  
Brain Health ◽  
High Fat ◽  
Dietary Strategy ◽  
Apoptosis Pathways ◽  
Insight Into

Aging processes affect the brain in many ways, ranging from cellular to functional levels which lead to cognitive decline and increased oxidative stress. The aim of this study was to investigate the potentials of Lactobacillus plantarum DR7 on brain health including cognitive and memory functions during aging and the impacts of high fat diet during a 12-week period. Male Sprague-Dawley rats were separated into six groups: (1) young animals on normal diet (ND, (2) young animals on a high fat diet (HFD), (3) aged animals on ND, (4) aged animals on HFD, (5) aged animals on HFD and L. plantarum DR7 (109 cfu/day) and (6) aged animals receiving HFD and lovastatin. To induce ageing, all rats in group 3 to 6 were injected sub-cutaneously at 600 mg/kg/day of D-galactose daily. The administration of DR7 has reduced anxiety accompanied by enhanced memory during behavioural assessments in aged-HFD rats (P<0.05). Hippocampal concentration of all three pro-inflammatory cytokines were increased during aging but reduced upon administration of both statin and DR7. Expressions of hippocampal neurotransmitters and apoptosis genes showed reduced expressions of indoleamine dioxygenase and P53 accompanied by increased expression of TPH1 in aged- HFD rats administered with DR7, indicating potential effects of DR7 along the pathways of serotonin and oxidative senescence. This study provided an insight into potentials of L. plantarum DR7 as a prospective dietary strategy to improve cognitive functions during aging. This study provided an insight into potentials of L. plantarum DR7 as a prospective dietary strategy to improve cognitive functions during aging.

High-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and cholecystokinin: implications for circulatory control

2011 ◽  
Vol 300 (3) ◽  
pp. H961-H967 ◽  
Author(s):  
Jackie M. Y. How ◽  
Barbara C. Fam ◽  
Anthony J. M. Verberne ◽  
Daniela M. Sartor
Keyword(s):  
Arterial Pressure ◽  
High Fat Diet ◽  
Cardiovascular Effects ◽  
Vagal Afferents ◽  
Sprague Dawley ◽  
High Fat ◽  
Lower Plasma ◽  
Lower Tertile ◽  
Circulatory Control ◽  
Plasma Leptin

Gastric leptin and cholecystokinin (CCK) act on vagal afferents to induce cardiovascular effects and reflex inhibition of splanchnic sympathetic nerve discharge (SSND) and may act cooperatively in these responses. We sought to determine whether these effects are altered in animals that developed obesity in response to a medium high-fat diet (MHFD). Male Sprague-Dawley rats were placed on a low-fat diet (LFD; n = 8) or a MHFD ( n = 24) for 13 wk, after which the animals were anesthetized and artificially ventilated. Arterial pressure was monitored and blood was collected for the determination of plasma leptin and CCK. SSND responses to leptin (15 μg/kg) and CCK (2 μg/kg) administered close to the coeliac artery were evaluated. Collectively, MHFD animals had significantly higher plasma leptin but lower plasma CCK levels than LFD rats ( P < 0.05), and this corresponded to attenuated or reversed SSND responses to CCK (LFD, −21 ± 2%; and MHFD, −12 ± 2%; P < 0.05) and leptin (LFD, −6 ± 2%; and MHFD, 4 ± 1%; P < 0.001). Alternatively, animals on the MHFD were stratified into obesity-prone (OP; n = 8) or obesity-resistant (OR; n = 8) groups according to their weight gain falling within the upper or lower tertile, respectively. OP rats had significantly higher resting arterial pressure, adiposity, and plasma leptin but lower plasma CCK compared with LFD rats ( P < 0.05). The SSND responses to CCK or leptin were not significantly different between OP and OR animals. These results demonstrate that a high-fat diet is associated with blunted splanchnic sympathoinhibitory responses to gastric leptin and CCK and may impact on sympathetic vasomotor mechanisms involved in circulatory control.

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