Supplementation with Docosahexaenoic Acid and Vitamin E Improves Hepatic Triglyceride Accumulation Induced by High‐Fat Diet in Mice

2020 ◽  
Vol 123 (1) ◽  
pp. 2000224
Author(s):  
Gaofeng Yuan ◽  
Mengmeng Xu ◽  
Meijuan Tan ◽  
Jian Dong ◽  
Xiaoe Chen
Keyword(s):  
Vitamin E ◽  
Docosahexaenoic Acid ◽  
High Fat Diet ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Triglyceride Accumulation

DHA-enriched phospholipids from large yellow croaker roe regulate lipid metabolic disorders and gut microbiota imbalance on SD rats with a high-fat diet

2021 ◽  
Author(s):  
Xiaodan Lu ◽  
Rongbin Zhong ◽  
Ling Hu ◽  
Luyao Huang ◽  
Lijiao Chen ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Docosahexaenoic Acid ◽  
Gut Microbiota ◽  
Polyunsaturated Fatty Acids ◽  
High Fat Diet ◽  
Nutritional Value ◽  
Metabolic Disorders ◽  
Large Yellow Croaker ◽  
High Fat ◽  
Sd Rats

Abstract Large yellow croaker roe phospholipids (LYCRPLs) has great nutritional value because of containing rich docosahexaenoic acid (DHA), which is a kind of n-3 polyunsaturated fatty acids (n-3 PUFAs). In...

Cholate inhibits high-fat diet-induced hyperglycemia and obesity with acyl-CoA synthetase mRNA decrease

1997 ◽  
Vol 273 (1) ◽  
pp. E37-E45 ◽  
Author(s):  
S. Ikemoto ◽  
M. Takahashi ◽  
N. Tsunoda ◽  
K. Maruyama ◽  
H. Itakura ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Skeletal Muscles ◽  
Unsaturation Index ◽  
Sodium Cholate ◽  
Fat Absorption ◽  
High Fat ◽  
Cholesterol Accumulation ◽  
Triglyceride Accumulation ◽  
Responsive Element

The effects of sodium cholate on high-fat diet-induced hyperglycemia and obesity were investigated. Insulin resistance was estimated by measuring 2-deoxyglucose uptake in epitrochlearis muscles incubated in vitro. Addition of 0.5% cholate to high-safflower oil diet completely prevented high fat-induced hyperglycemia and obesity in C57BL/6J mice with a slight decrease of energy intake but with no inhibition of fat absorption. Furthermore, the addition of cholate decreased blood insulin levels and prevented high-fat diet-induced decrease of glucose uptake in epitrochlearis. However, there was no change in the unsaturation index of fatty acids in skeletal muscles and in GLUT-4 levels by cholate. In liver, cholate addition resulted in cholesterol accumulation and completely prevented high-fat diet-induced triglyceride accumulation. The changes of triglyceride level in the liver were paralleled to the changes of acyl-CoA synthetase (ACS) mRNA. ACS catalyzes the formation of acyl-CoA from fatty acid, and acyl-CoA is utilized for triglyceride formation in liver. ACS has a sterol-responsive element 1 in its promoter region. These data indicate that the favorable effects of cholate could be partly the result of downregulation of ACS mRNA.

scholarly journals FoxO3 regulates hepatic triglyceride metabolism via modulation of the expression of sterol regulatory-element binding protein 1c

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Liu Wang ◽  
Xiaopeng Zhu ◽  
Xiaoyang Sun ◽  
Xinyu Yang ◽  
Xinxia Chang ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Hepg2 Cells ◽  
Transcriptional Activity ◽  
Regulatory Element ◽  
Luciferase Reporter ◽  
Chow Diet ◽  
Hepatic Triglyceride ◽  
High Fat ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

Abstract Background Excessive intrahepatic lipid accumulation is the major characteristic of nonalcoholic fatty liver disease (NAFLD). We sought to identify the mechanisms involved in hepatic triglyceride (TG) homeostasis. Forkhead box class O (FoxO) transcription factors have been shown to play an important role in hepatic metabolism. However, little is known about the effect of FoxO3 on hepatic TG metabolism. Methods Liver biopsy samples from patients with NALFD and liver tissues from high glucose and high sucrose (HFHS) fed mice, ob/ob mice and db/db mice were collected for protein and mRNA analysis. HepG2 cells were transfected with small interfering RNA to mediate FoxO3 knockdown, or adenovirus and plasmid to mediate FoxO3 overexpression. FoxO3-cDNA was delivered by adenovirus to the liver of C57BL/6 J male mice on a chow diet or on a high-fat diet, followed by determination of hepatic lipid metabolism. Sterol regulatory element-binding protein 1c (SREBP1c) luciferase reporter gene plasmid was co-transfected into HepG2 cells with FoxO3 overexpression plasmid. Results FoxO3 expression was increased in the livers of HFHS mice, ob/ob mice, db/db mice and patients with NAFLD. Knockdown of FoxO3 reduced whereas overexpression of FoxO3 increased cellular TG concentrations in HepG2 cells. FoxO3 gain-of-function caused hepatic TG deposition in C57BL/6 J mice on a chow diet and aggravated hepatic steatosis when fed a high-fat diet. Analysis of the transcripts established the increased expression of genes related to TG synthesis, including SREBP1c, SCD1, FAS, ACC1, GPAM and DGAT2 in mouse liver. Mechanistically, overexpression of FoxO3 stimulated the expression of SREBP1c, whereas knockdown of FoxO3 inhibited the expression of SREBP1c. Luciferase reporter assays showed that SREBP1c regulated the transcriptional activity of the SREBP1c promoter. Conclusions FoxO3 promotes the transcriptional activity of the SREBP1c promoter, thus leading to increased TG synthesis and hepatic TG accumulation.

scholarly journals Effect of Vitamin E Isoforms on Bone Metabolism in C57BL/6 J Mice Fed a High Fat Diet

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1795-1795
Author(s):  
Chen Du ◽  
Gina Tran ◽  
Victorine Imrhan ◽  
Chandan Prasad ◽  
Parakat Vijayagopal ◽  
...  
Keyword(s):  
Vitamin E ◽  
Bone Loss ◽  
Bone Metabolism ◽  
Bone Mineral ◽  
High Fat Diet ◽  
Alpha Tocopherol ◽  
Type I ◽  
High Fat ◽  
Mineral Density ◽  
Gamma Tocopherol

Abstract Objectives The purpose of this study was to compare the effects of alpha tocopherol, gamma tocopherol, and the combination of alpha and gamma tocopherols on bone mineral density (BMD), bone mineral content (BMC), and bone metabolism in C57BL/6 J mice fed a high-fat diet. Methods A total of 75 male C57BL/6 mice were randomized to either a low fat diet (LFD) with 6% fat, a high fat diet (HFD) with 20% fat, HFD supplemented with alpha tocopherol (AT), gamma tocopherol (GT), or the combination of AT and GT. LFD and HFD were provided to corresponding groups of mice without vitamin E isoform supplements for 15 weeks to induce bone loss. At the end of the 15 weeks, AT, GT, and a combination of AT and GT were added to 3 of the HFD groups and fed for 10 weeks. LFD group and one of the HFD groups were continued on the same diet for another 10 weeks without additional supplements. All mice were euthanized at the end of the 25 weeks period. Left and right fibula bones were excised, cleaned, and scanned using the Lunar PIXImus dual-energy x-ray absorptiometry (DEXA) densitometer to assess BMD, BMC, lean tissue, and fat tissue content. Serum biomarkers of bone metabolism were evaluated post euthanization. Results HFD resulted in significantly lower fibular BMD and higher tibial bone fat content in comparison to LFD. Animals in the HFD supplemented with GT, but not AT, showed significantly reduced effect of HFD in lowering BMD. Additionally, in the group fed HFD supplemented with GT, a significantly higher concentration of alkaline phosphatase (ALP) and N-terminal propeptide of type I procollagen (PINP) were noted, compared to LFD. This may be indicative of increased bone formation resulting from GT incorporated into the HFD diet. Conclusions The findings of the study suggest that different isoforms of vitamin E affect bone density and bone metabolism differently. Within the different isoforms of vitamin E, gamma tocopherol may have protective effects in bone, especially in the situation of high fat diet induced bone loss. Further examination of the mechanistic action of vitamin E isoforms on skeletal health is warranted. Funding Sources Texas Woman's University.

scholarly journals K27Q/K29Q mutations in sphingosine kinase 1 attenuate high-fat diet induced obesity and altered glucose homeostasis in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jing Xie ◽  
Yong Shao ◽  
Jin Liu ◽  
Meilan Cui ◽  
Xiuxiao Xiao ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Metabolic Diseases ◽  
Sphingosine Kinase ◽  
Protective Role ◽  
Sphingolipid Metabolism ◽  
Acid Oxidation ◽  
Sphingosine Kinase 1 ◽  
High Fat ◽  
Triglyceride Accumulation ◽  
Altered Glucose

AbstractObesity and its associated metabolic disorders are increasingly impacting public health worldwide. Sphingosine kinase 1 (Sphk1) is a critical enzyme in sphingolipid metabolism that has been implicated in various metabolic syndromes. In this study, we developed a mouse model constitutively expressing pseudoacetylated mouse Sphk1 (QSPHK1) to study its role in regulating glucose and lipid metabolism. The results showed that QSPHK1 mice gained less body weight than wide type (WT) mice on a high-fat diet, and QSPHK1 mice had improved glucolipid metabolism and insulin. Moreover, QSPHK1 mice had alleviated hepatic triglyceride accumulation and had high-fat-diet-induced hepatic steatosis that occurred as a result of reduced lipogenesis and enhanced fatty acid oxidation, which were mediated by the AMPK/ACC axis and the FGF21/adiponectin axis. Collectively, this study provided evidence that the K27Q/K29Q mutations of Sphk1 could have a protective role in preventing obesity and the related metabolic diseases. Hence, our results contribute to further understanding of the biological functions of Sphk1, which has great pharmaceutical implications.

scholarly journals Anti-adipogenic and anti-obesity activities of purpurin in 3T3-L1 preadipocyte cells and in mice fed a high-fat diet

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Woo Nam ◽  
Seok Hyun Nam ◽  
Sung Phil Kim ◽  
Carol Levin ◽  
Mendel Friedman
Keyword(s):  
Weight Gain ◽  
High Fat Diet ◽  
Biological Activities ◽  
The Body ◽  
High Fat ◽  
In Vivo Models ◽  
Triglyceride Accumulation ◽  
In Cells

Abstract Background The body responds to overnutrition by converting stem cells to adipocytes. In vitro and in vivo studies have shown polyphenols and other natural compounds to be anti-adipogenic, presumably due in part to their antioxidant properties. Purpurin is a highly antioxidative anthraquinone and previous studies on anthraquinones have reported numerous biological activities in cells and animals. Anthraquinones have also been used to stimulate osteoblast differentiation, an inversely-related process to that of adipocyte differentiation. We propose that due to its high antioxidative properties, purpurin administration might attenuate adipogenesis in cells and in mice. Methods Our study will test the effect purpurin has on adipogenesis using both in vitro and in vivo models. The in vitro model consists of tracking with various biomarkers, the differentiation of pre-adipocyte to adipocytes in cell culture. The compound will then be tested in mice fed a high-fat diet. Murine 3T3-L1 preadipocyte cells were stimulated to differentiate in the presence or absence of purpurin. The following cellular parameters were measured: intracellular reactive oxygen species (ROS), membrane potential of the mitochondria, ATP production, activation of AMPK (adenosine 5′-monophosphate-activated protein kinase), insulin-induced lipid accumulation, triglyceride accumulation, and expression of PPARγ (peroxisome proliferator activated receptor-γ) and C/EBPα (CCAAT enhancer binding protein α). In vivo, mice were fed high fat diets supplemented with various levels of purpurin. Data collected from the animals included anthropometric data, glucose tolerance test results, and postmortem plasma glucose, lipid levels, and organ examinations. Results The administration of purpurin at 50 and 100 μM in 3T3-L1 cells, and at 40 and 80 mg/kg in mice proved to be a sensitive range: the lower concentrations affected several measured parameters, whereas at the higher doses purpurin consistently mitigated biomarkers associated with adipogenesis, and weight gain in mice. Purpurin appears to be an effective antiadipogenic compound. Conclusion The anthraquinone purpurin has potent in vitro anti-adipogenic effects in cells and in vivo anti-obesity effects in mice consuming a high-fat diet. Differentiation of 3T3-L1 cells was dose-dependently inhibited by purpurin, apparently by AMPK activation. Mice on a high-fat diet experienced a dose-dependent reduction in induced weight gain of up to 55%.

scholarly journals Sequestration of Vitamin E by Liver Fat in vivo, in vitro and in Women with Hepato-steatosis

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1696-1696
Author(s):  
Pierre-Christian Violet ◽  
Ifechukwude Ebenuwa ◽  
Stacey Chung ◽  
Jeffrey Atkinson ◽  
Danny Manor ◽  
...  
Keyword(s):  
Liver Disease ◽  
Vitamin E ◽  
High Fat Diet ◽  
Alpha Tocopherol ◽  
Liver Fat ◽  
Slight Reduction ◽  
High Fat ◽  
High Vitamin

Abstract Objectives Hepato-steatosis (HS) due to obesity is now the most common cause of chronic liver disease in the Americas and Western Europe. The only means to prevent disease is avoidance of obesity. α-Tocopherol at doses of 800 I.U. daily was reported to have partial treatment effects for NASH. Because alpha tocopherol is a fat-soluble vitamin, we hypothesized that excess fat in liver, as found in HS, could act unintentionally sequester vitamin E, thereby altering its normal physiology and contributing to development of NASH. Using oral and intravenous deuterated tocopherols, evidence showing HS altered a-tocopherol physiology was reported based on pharmacokinetics studies in obese women with HS. Here we further tested the sequestration hypothesis in vitro, and in vivo. Methods In vitro, we investigated effects of fat on intracellular vitamin E localization. Control human and mouse hepatocytes and hepatocytes pre-loaded with fat were incubated with fluorescent α-tocopherol (BDP-α-tocopherol). In vivo experiments were performed using mice fed a high fat diet with different vitamin E doses. Results Compared to controls, fat- loaded cells contained more a-tocopherol, and BDP-a-tocopherol was specifically localized into intracellular fat droplets. In cells incubated with BDP a-tocopherol, we found that fat loading decreased a-tocopherol release. Induced expression of TPP, which mediates vitamin E intracellular disposition under normal conditions, was not observed in fat loaded cells, further confirming vitamin E was trapped in fat. Livers of mice fed high fat diet had more vitamin E compared to controls. By further increasing vitamin E content of the high fat diet, we observed a reduction in liver size and liver fat in the high vitamin E group. Using a mouse metabolic chamber, we observed a slight reduction of oxygen consumption rate in the high vitamin E group compared to controls. Conclusions Considered together, these findings imply that fat in the liver may produce unrecognized hepatic vitamin E sequestration, which could drive liver disease. These results are consistent with the possibility that increased vitamin E intake might, if begun at an early stage, restore vitamin E physiology, potentially decreasing or preventing progression of HS to NASH. Funding Sources NIH intramural program (DK053213–14).

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