scholarly journals Malus toringoides (Rehd.) Hughes Improves Metabolic Syndrome and Liver Injury in High-Fructose-Induced Mice

2020 ◽  
Author(s):  
Xiang Hua Quan ◽  
Qie Guo ◽  
Xiang-Peng Li ◽  
Yu Liang ◽  
Meng-Na Cui ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Injury ◽  
Glucose Tolerance ◽  
Lipid Accumulation ◽  
Liver Lipid ◽  
Ethanol Extract ◽  
Edible Plant ◽  
Apo B ◽  
High Fructose

Abstract Background: Malus toringoides (Rehd.) Hughes, as a traditional medicinal and edible plant used in Tibet, China, is used to treat hypertension, hyperlipemia and liver diseases. This present study was designed to investigate the effects of ethanol extract of M. toringoides (EMT) on metabolic syndrome (MS) and liver injury in high-fructose-induced mice. Methods: The C57BL/6J male mice were divided into five groups (n=8). Con group was drunk with standard water, Fru group and the other three with 30% high-fructose water for 8 weeks. EMT (195 mg/kg, 390 mg/kg, 780 mg/kg) was administered to each of high fructose groups simultaneously. Glucose tolerance tests (GTT) were performed. Blood samples were collected from eyeball. The mice were euthanized. Liver and epididymal fat were weighed. The palmitic acid (PA)-induced HepG2 cells were used to evaluate the protective effect of EMT on liver lipid accumulation. Results: The administration of EMT is helpful to maintain near normal body weight, blood glucose, insulin, organ index, glucose tolerance, and serum levels of TC, TG, LDL-C, HDL-C, Apo-B, and Apo-A1 (P < 0.05 or P < 0.01). EMT treatment significantly improved liver injury by the down-regulation of liver lipid accumulation, oxidative stress and inflammatory mediators in high-fructose-induced mice (P < 0.05 or P < 0.01). In vitro, EMT (25 µg/mL-200 µg/mL) significantly decreased lipid droplet accumulation and TG content in PA-induced HepG2 (P < 0.05 or P < 0.01).Conclusion: EMT can obviously improve high fructose-induced MS in mice. In vitro, EMT can inhibit PA-induced lipid accumulation in HepG2 cells.which may emphasizes the use of M. toringoides supplementation in everyday life of over-weighted persons and opens perspectives for clinical trials.

scholarly journals Gastrodia elataAmeliorates High-Fructose Diet-Induced Lipid Metabolism and Endothelial Dysfunction

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Min Chul Kho ◽  
Yun Jung Lee ◽  
Jeong Dan Cha ◽  
Kyung Min Choi ◽  
Dae Gill Kang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Endothelial Dysfunction ◽  
Glucose Tolerance ◽  
Ethanol Extract ◽  
Oral Glucose ◽  
Gastrodia Elata ◽  
High Fructose ◽  
Amp Activated Protein Kinase ◽  
Endothelial Nitric Oxide

Overconsumption of fructose results in dyslipidemia, hypertension, and impaired glucose tolerance, which have documented correlation with metabolic syndrome.Gastrodia elata, a widely used traditional herbal medicine, was reported with anti-inflammatory and antidiabetes activities. Thus, this study examined whether ethanol extract ofGastrodia elataBlume (EGB) attenuate lipid metabolism and endothelial dysfunction in a high-fructose (HF) diet animal model. Rats were fed the 65% HF diet with/without EGB 100 mg/kg/day for 8 weeks. Treatment with EGB significantly suppressed the increments of epididymal fat weight, blood pressure, plasma triglyceride, total cholesterol levels, and oral glucose tolerance, respectively. In addition, EGB markedly prevented increase of adipocyte size and hepatic accumulation of triglycerides. EGB ameliorated endothelial dysfunction by downregulation of endothelin-1 (ET-1) and adhesion molecules in the aorta. Moreover, EGB significantly recovered the impairment of vasorelaxation to acetylcholine and levels of endothelial nitric oxide synthase (eNOS) expression and induced markedly upregulation of phosphorylation AMP-activated protein kinase (AMPK)αin the liver, muscle, and fat. These results indicate that EGB ameliorates dyslipidemia, hypertension, and insulin resistance as well as impaired vascular endothelial function in HF diet rats. Taken together, EGB may be a beneficial therapeutic approach for metabolic syndrome.

scholarly journals Prenatal hyperandrogenism induces alterations that affect liver lipid metabolism

2016 ◽  
Vol 230 (1) ◽  
pp. 67-79 ◽  
Author(s):  
Giselle Adriana Abruzzese ◽  
Maria Florencia Heber ◽  
Silvana Rocio Ferreira ◽  
Leandro Martin Velez ◽  
Roxana Reynoso ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Glucose Tolerance ◽  
Fatty Liver ◽  
Lipid Content ◽  
Liver Lipid ◽  
Acid Oxidation ◽  
Liver Lipid Content ◽  
Increased Risk ◽  
Liver Lipid Metabolism

Prenatal hyperandrogenism is hypothesized as one of the main factors contributing to the development of polycystic ovary syndrome (PCOS). PCOS patients have high risk of developing fatty liver and steatosis. This study aimed to evaluate the role of prenatal hyperandrogenism in liver lipid metabolism and fatty liver development. Pregnant rats were hyperandrogenized with testosterone. At pubertal age, the prenatally hyperandrogenized (PH) female offspring displayed both ovulatory (PHov) and anovulatory (PHanov) phenotypes that mimic human PCOS features. We evaluated hepatic transferases, liver lipid content, the balance between lipogenesis and fatty acid oxidation pathway, oxidant/antioxidant balance and proinflammatory status. We also evaluated the general metabolic status through growth rate curve, basal glucose and insulin levels, glucose tolerance test, HOMA-IR index and serum lipid profile. Although neither PH group showed signs of liver lipid content, the lipogenesis and fatty oxidation pathways were altered. The PH groups also showed impaired oxidant/antioxidant balance, a decrease in the proinflammatory pathway (measured by prostaglandin E2 and cyclooxygenase-2 levels), decreased glucose tolerance, imbalance of circulating lipids and increased risk of metabolic syndrome. We conclude that prenatal hyperandrogenism generates both PHov and PHanov phenotypes with signs of liver alterations, imbalance in lipid metabolism and increased risk of developing metabolic syndrome. The anovulatory phenotype showed more alterations in liver lipogenesis and a more impaired balance of insulin and glucose metabolism, being more susceptible to the development of steatosis.

Abstract 037: Role of Pro-opiomelanocortin (POMC) Specific PTP1B in Differential Regulation of Blood Pressure, Liver Lipid Accumulation and Glucose Tolerance in Response to a High Fat Diet

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Nicola Aberdein ◽  
Jussara M do Carmo ◽  
Zhen Wang ◽  
Taolin Fang ◽  
Cecilia P de Lara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Glucose Tolerance ◽  
Fat Mass ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Acute Stress ◽  
Liver Lipid ◽  
Liver Weight ◽  
Metabolic Effects ◽  
High Fat

Obese subjects are often resistant to leptin’s metabolic effects although blood pressure (BP) and sympathetic nervous system responses appear to be preserved. Protein tyrosine phosphatase 1B (PTP1B), a negative regulator of leptin signaling, may play a role in promoting this selective leptin resistance and causing metabolic dysfunction in obesity. Our previous studies suggest that the chronic BP responses to leptin are mediated via activation of pro-opiomelanocortin (POMC) neurons. The goal of this study was to determine if PTP1B in POMC neurons differentially controls metabolic functions and BP in mice fed a high fat diet (HFD). Male mice with POMC specific PTP1B deletion (POMC/PTP1B -/- ) and littermate controls (PTP1B flox/flox ) were fed a HFD from 6 to 22 wks of age. Baseline BP after 16 weeks of a HFD (95±2 vs. 95±3 mmHg) and BP responses to acute stress (Δ32±0 vs. Δ32±6 mmHg), measured by telemetry, were not different in POMC/PTP1B -/- compared to control mice, respectively. Heart rate (HR) was not different in POMC/PTP1B -/- and control mice during acute stress (699±4 vs. 697±15 bpm, respectively). Total body weight (TBW) and fat mass were reduced at 20 weeks of age in POMC/PTP1B -/- compared to controls (36.7±0.1 vs. 42.0±1 g TBW and 12.7±0.4 vs. 16.1±1.0 g fat mass, respectively). Liver weight of POMC/PTP1B -/- mice was less than in controls, and this was evident even when liver weight was normalized as % of TBW (4.5±0.2 vs. 5.0±0.2 %). POMC/PTP1B -/- males had reduced liver lipid accumulation compared to controls as measured by EchoMRI (0.08±0.03 vs. 0.15±0.03 g/g liver weight). Glucose tolerance was also improved by 46% in POMC/PTP1B -/- compared to controls as measured by AUC, 25856±1683 vs. 47267±5616 mg/dLx120min, respectively. These findings indicate that PTP1B signaling in POMC neurons plays a crucial role in regulating liver lipid accumulation and glucose tolerance but does not appear to mediate changes in BP or BP responses to acute stress in mice fed a high HFD (supported by NHLBI-PO1HL51971 and NIGMS P20GM104357)

Cardiac and metabolic changes in long-term high fructose-fat fed rats with severe obesity and extensive intramyocardial lipid accumulation

2010 ◽  
Vol 298 (6) ◽  
pp. R1560-R1570 ◽  
Author(s):  
Lene N. Axelsen ◽  
Jacob B. Lademann ◽  
Jørgen S. Petersen ◽  
Niels-Henrik Holstein-Rathlou ◽  
Thorkil Ploug ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Animal Model ◽  
Glucose Tolerance ◽  
Lipid Accumulation ◽  
Severe Obesity ◽  
Ischemia Reperfusion ◽  
Western World ◽  
Cardiac Complications ◽  
The Metabolic Syndrome

Metabolic syndrome and obesity-related diseases are affecting more and more people in the Western world. The basis for an effective treatment of these patients is a better understanding of the underlying pathophysiology. Here, we characterize fructose- and fat-fed rats (FFFRs) as a new animal model of metabolic syndrome. Sprague-Dawley rats were fed a 60 kcal/100 kcal fat diet with 10% fructose in the drinking water. After 6, 12, 18, 24, 36, and 48 wk of feeding, blood pressure, glucose tolerance, plasma insulin, glucose, and lipid levels were measured. Cardiac function was examined by in vivo pressure volume measurements, and intramyocardial lipid accumulation was analyzed by confocal microscopy. Cardiac AMP-activated kinase (AMPK) and hepatic phospho enolpyruvate carboxykinase (PEPCK) levels were measured by Western blotting. Finally, an ischemia-reperfusion study was performed after 56 wk of feeding. FFFRs developed severe obesity, decreased glucose tolerance, increased serum insulin and triglyceride levels, and an initial increased fasting glucose, which returned to control levels after 24 wk of feeding. The diet had no effect on blood pressure but decreased hepatic PEPCK levels. FFFRs showed significant intramyocardial lipid accumulation, and cardiac hypertrophy became pronounced between 24 and 36 wk of feeding. FFFRs showed no signs of cardiac dysfunction during unstressed conditions, but their hearts were much more vulnerable to ischemia-reperfusion and had a decreased level of phosphorylated AMPK at 6 wk of feeding. This study characterizes a new animal model of the metabolic syndrome that could be beneficial in future studies of metabolic syndrome and cardiac complications.

scholarly journals Metabolic syndrome signs in Wistar rats submitted to different high-fructose ingestion protocols

2008 ◽  
Vol 101 (8) ◽  
pp. 1178-1184 ◽  
Author(s):  
Rodrigo Ferreira de Moura ◽  
Carla Ribeiro ◽  
Juliana Aparecida de Oliveira ◽  
Eliane Stevanato ◽  
Maria Alice Rostom de Mello
Keyword(s):  
Metabolic Syndrome ◽  
Drinking Water ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Body Fat ◽  
Wistar Rats ◽  
Control Group ◽  
Adequate Model ◽  
Adult Rat ◽  
High Fructose

In search of an adequate model for the human metabolic syndrome, the metabolic characteristics of Wistar rats were analysed after being submitted to different protocols of high fructose ingestion. First, two adult rat groups (aged 90 d) were studied: a control group (C1;n6) received regular rodent chow (Labina, Purina) and a fructose group (F1;n6) was fed on regular rodent chow. Fructose was administered as a 10 % solution in drinking water. Second, two adult rat groups (aged 90 d) were evaluated: a control group (C2;n6) was fed on a balanced diet (AIN-93G) and a fructose group (F2;n6) was fed on a purified 60 % fructose diet. Finally, two young rat groups (aged 28 d) were analysed: a control group (C3;n6) was fed on the AIN-93G diet and a fructose group (F3;n6) was fed on a 60 % fructose diet. After 4–8 weeks, the animals were evaluated. Glucose tolerance, peripheral insulin sensitivity, blood lipid profile and body fat were analysed. In the fructose groups F2 and F3 glucose tolerance and insulin sensitivity were lower, while triacylglycerolaemia was higher than the respective controls C2 and C3 (P < 0·05). Blood total cholesterol, HDL and LDL as well as body fat showed change only in the second protocol. In conclusion, high fructose intake is more effective at producing the signs of the metabolic syndrome in adult than in young Wistar rats. Additionally, diet seems to be a more effective way of fructose administration than drinking water.

scholarly journals TNF-Like Ligand 1 Aberrance Aggravates Nonalcoholic Steatohepatitis via M1 Macrophage Polarization

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Yuxin Luo ◽  
Jinbo Guo ◽  
Wenxiu Jia ◽  
Mengyao Wu ◽  
Fengrong Yin ◽  
...  
Keyword(s):  
Nonalcoholic Steatohepatitis ◽  
Lipid Accumulation ◽  
Inflammatory Diseases ◽  
Macrophage Polarization ◽  
Primary Biliary Cholangitis ◽  
M2 Macrophage ◽  
Hepatic Lipid Accumulation ◽  
High Fructose ◽  
M1 Macrophage

Nonalcoholic steatohepatitis (NASH) is a progressive, chronic liver disease worldwide which imposes a large economic burden on society. M1/M2 macrophage balance destruction and recruitment of mononuclear immune cells to the liver play critical roles in NASH. Several studies have shown that the expression of TNF-like ligand 1 aberrance (TL1A) increased in macrophages associated with many inflammatory diseases, for example, inflammatory bowel disease, primary biliary cholangitis, and liver fibrosis. One recent research showed that weight, abdominal adipose, and liver leptin, one of the critical fat cytokines, were reduced in TL1A knockout mice. However, the functional and molecular regulatory mechanisms of TL1A on macrophage polarization and recruitment in NASH have yet to be clarified. The authors found that high fructose high fat diet and methionine-choline deficiency diet induced the expression of TL1A in macrophages of liver tissue from murine NASH models. Myeloid-specific TL1A overexpressed mice showed exacerbated steatohepatitis with increased hepatic lipid accumulation, inflammation, liver injury, and apoptosis. M1 macrophages’ infiltration and the production of proinflammatory and chemotactic cytokines increased in liver of NASH mouse models with myeloid-specific TL1A overexpressed. Furthermore, this paper revealed that bone marrow-derived macrophages and Kupffer cells with overexpression of TL1A exacerbated the lipid accumulation and expression of proinflammatory factors in the murine primary hepatocytes after free fatty acid treatment in vitro. In conclusion, TL1A-mediated M1-type macrophage polarization and recruitment into the liver promoted steatohepatitis in murine NASH.

Preventive Effects of Total Flavonoid C-Glycosides from Abrus mollis on Nonalcoholic Fatty Liver Disease through Activating the PPARα Signaling Pathway

Planta Medica ◽  
2019 ◽  
Vol 85 (08) ◽  
pp. 678-688 ◽  
Author(s):  
Xiao-Long Hu ◽  
Ya-Jun Niu ◽  
Mi Chen ◽  
Jia-Hao Feng ◽  
Wei Shen ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Lipid Accumulation ◽  
Fatty Liver Disease ◽  
Total Flavonoid ◽  
Edible Plant ◽  
Nonalcoholic Fatty Liver

Abstract Abrus pulchellus subsp. mollis (Hance) Verdc. (Leguminosae) is a well-known edible plant usually added to soups and beverages. In this study, vicenin-2 (1), isoschaftoside (2), schaftoside (3), and their enrichment fraction, total flavonoid C-glycosides, derived from the extracts of A. mollis, were firstly found to prevent nonalcoholic fatty liver disease both in vitro and in vivo. In the in vitro study, total flavonoid C-glycosides decreased the lipid accumulation in oleic acid-treated HepG2 cells. The mechanisms of total flavonoid C-glycosides are involved in the regulation of peroxisome proliferator-activated receptor α and its downstream, and the reduction of proinflammatory cytokines. In high-fat diet-induced fatty liver rats, total flavonoid C-glycosides decreased the levels of glutamic-oxalacetic transaminease and glutamic-pyruvic transaminase, and decreased the lipid accumulation both in the liver and blood without affecting food intake. In addition, total flavonoid C-glycosides also increased the activities of the antioxidant enzyme system in vivo. In conclusion, total flavonoid C-glycosides are active components of A. mollis on nonalcoholic fatty liver disease, and can be used in functional food and supplements for nonalcoholic fatty liver disease prevention and treatment.

scholarly journals Comparative Study of the Effects of Light Controlled Germination Conditions on Saponarin Content in Barley Sprouts and Lipid Accumulation Suppression in HepG2 Hepatocyte and 3T3-L1 Adipocyte Cells Using Barley Sprout Extracts

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5349
Author(s):  
Jae Sil Kim ◽  
Eunseon Jeong ◽  
So Min Jo ◽  
Joonho Park ◽  
Ji Yeon Kim
Keyword(s):  
Blue Light ◽  
Lipid Accumulation ◽  
Principal Component ◽  
Ethanol Extract ◽  
Growth Conditions ◽  
Total Polyphenol ◽  
Nutrient Supplements ◽  
Physiologically Active Substances ◽  
Active Substances

Barley sprouts (BS) contain physiologically active substances and promote various positive physiological functions in the human body. The levels of the physiologically active substances in plants depend on their growth conditions. In this study, BS were germinated using differently colored LED lights and different nutrient supplements. Overall, there were 238 varied BS samples analyzed for their total polyphenol and flavonoid contents. Principal component analysis (PCA) was performed to determine the relationship between the germinated samples and their total polyphenol and flavonoid contents, and those with high levels were further analyzed for their saponarin content. Based on the PCA plot, the optimal conditions for metabolite production were blue light with 0.1% boric acid supplementation. In vitro experiments using the ethanol extract from the BS cultured in blue light showed that the extract significantly inhibited the total lipid accumulation in 3T3-L1 adipocytes and the lipid droplets in HepG2 hepatocytes. These findings suggest that specific and controlled light source and nutrient conditions for BS growth could increase the production of secondary metabolites associated with inhibited fat accumulation in adipocytes and hepatocytes.

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