scholarly journals Effects of Metformin Combined with Lactoferrin on Lipid Accumulation and Metabolism in Mice Fed with High-Fat Diet

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1628 ◽  
Author(s):  
Qing-Qing Min ◽  
Li-Qiang Qin ◽  
Zhen-Zhen Sun ◽  
Wen-Ting Zuo ◽  
Lin Zhao ◽  
...  
Keyword(s):  
Body Weight ◽  
Lipid Metabolism ◽  
Protein Expression ◽  
Visceral Fat ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Control Group ◽  
Lipolytic Enzyme ◽  
High Fat ◽  
Hepatic Lipid

Metformin (Met) and lactoferrin (Lf) both exhibit beneficial effects on body weight management and lipid accumulation. However, the synergistical action of Met and Lf remains unclear. In this study, 64 mice were divided into five groups, namely, the control group, high-fat diet (HFD group), HFD with Met (Met group), Lf (Lf group), and a combination of Met and Lf (Met + Lf group). Met (200 mg/kg body weight) and Lf (2 g/100 mL) were administrated in drinking water. The experiment lasted for 12 weeks. Body weight, serum, and hepatic lipids were determined. Histology of the liver and perirenal fat was observed. Protein expression related to hepatic lipid metabolism was also measured. HFD significantly increased body weight, visceral fat weight, and lipid profiles, which lead to obesity and dyslipidemia in mice. Compared with the HFD group, the treatments significantly decreased body weight and Lee’s index (body mass index of mice) with the lowest values in the Met + Lf group. The treatments also decreased the weight of visceral fat, and improved circulating lipid profile and the ability for regulating glucose intake. The adipocyte size and serum TC level were significantly lower in the Met + Lf group as compared with those in the Met or Lf group. The treatments alleviated hepatic lipid accumulation, especially in the Met + Lf group. For protein expression, the p-AMPK/AMPK ratio, a key kinase-regulating cellular energy homeostasis, was significantly higher in the Met + Lf group than the ratio in the HFD group. Similarly, the treatments significantly downregulated the protein expression of lipogenic enzymes (FAS, ACC, and SREBP-1) and upregulated the protein expression of lipolytic enzyme (ATGL). The protein expression of HMGCoAR, which is an important rate limiting enzyme in cholesterol biosynthesis, was only significantly lower in the Met + Lf group than in the HFD group. In conclusion, Met and Lf, either alone or in combination, prevented HFD-induced obesity and improved lipid metabolism.

scholarly journals Hepatic Lipid Accumulation Induced by a High-fat Diet Is Regulated by Nrf2 Through Multiple Pathways

2021 ◽  
Author(s):  
sheng Qiu ◽  
Zerong Liang ◽  
Qinan Wu ◽  
Miao Wang ◽  
Mengliu Yang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Underlying Mechanism ◽  
Luciferase Assay ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Abstract BackgroundNuclear factor erythroid 2-related factor 2 (Nrf2) is reportedly involved in hepatic lipid metabolism, but the results are contradictory and the underlying mechanism thus remains unclear. Herein we focused on elucidating the effects of Nrf2 on hepatic adipogenesis and on determining the possible underlying mechanism. We established a metabolic associated fatty liver disease (MAFLD) model in high fat diet (HFD) fed Nrf2 knockout (Nrf2 KO) mice; further, a cell model of lipid accumulation was established using mouse primary hepatocytes (MPHs) treated with free fatty acids (FAs). Using these models, we investigated the relationship between Nrf2 and autophagy and its role in the development of MAFLD.ResultsWe observed that Nrf2 expression levels were up-regulated in patients with MAFLD and diet-induced obese mice. Nrf2 deficiency led to hepatic lipid accumulation in vivo and in vitro, in addition to, promoting lipogenesis mainly by increasing SREBP-1 activity. Moreover, Nrf2 deficiency attenuated autophagic flux and inhibited the fusion of autophagosomes and lysosomes in vivo and in vitro. Weakened autophagy caused reduced lipolysis in the liver. Importantly, Chromatin immunoprecipitation-qPCR (ChIP-qPCR) and dual-luciferase assay results proved that Nrf2 bound to LAMP1 promoter and regulated its transcriptional activity. We accordingly report that Nrf2-LAMP1 interaction has an indispensable role in Nrf2-regulated hepatosteatosis. ConclusionsThese data collectively confirm that Nrf2 deficiency promotes hepatosteatosis by enhancing SREBP-1 activity and attenuating autophagy. To conclude, our data reveal a novel multi-pathway effect of Nrf2 on lipid metabolism in the liver, and we believe that multi-target intervention of Nrf2 signaling is a promising new strategy for the prevention and treatment of MAFLD.

Effects of Zinc Alpha2 Glycoprotein on Lipid Metabolism of Liver in High-Fat Diet-Induced Obese Mice

2017 ◽  
Vol 49 (10) ◽  
pp. 793-800 ◽  
Author(s):  
Guoqiang Fan ◽  
Yu Qiao ◽  
Shixing Gao ◽  
Jun Guo ◽  
Ruqian Zhao ◽  
...  
Keyword(s):  
Body Weight ◽  
Lipid Metabolism ◽  
High Fat Diet ◽  
Recombinant Plasmid ◽  
Diet Group ◽  
Normal Diet ◽  
Hormone Sensitive Lipase ◽  
High Fat ◽  
Hepatic Lipid ◽  
Protein Levels

AbstractZinc alpha2 glycoprotein (ZAG) is a new type of adipokine involved in adipose tissue mobilization, however, little is known about its lipid metabolism effect in liver. Therefore, we investigated the effects of ZAG in the regulation of hepatic lipid accumulation. Mice were randomly divided into two groups; one was fed a normal diet and another was fed a high-fat diet for eight weeks to establish obesity model. After that, the normal diet group was divided into ND (injection of pcDNA3.1) and NDZ (injection of ZAG recombinant plasmid) and the high-fat diet group was divided into HF (injection of pcDNA3.1) and HFZ (injection of ZAG recombinant plasmid). The mice were weighed once per week and injected with plasmid once every three days for eight times. The results showed that body weight and hepatic TG content were decreased dramatically in HFZ group compared with HF group. The stearoyl-CoAdesaturase1 (SCD1) and Acyl-CoA Synthetase-1 (ACSS1) protein levels in HFZ group were significantly decreased. Furthermore, phosphorylated hormone sensitive lipase (P-HSL) was significantly higher in HFZ group. In HFZ group, hepatic fatty acid translocase (CD36) and fatty acids binding protein-1 (FABP1) protein levels were reduced. In addition, the expression of phosphorylated protein kinase A (PPKA) in HFZ group was higher than the HF group. Meanwhile, NDZ group showed significantly decreased body weight and increased P-HSL level though the hepatic TG content showed no significantly changes compared with the ND group. Therefore, we conclude that ZAG may be beneficial for preventing high-fat-diet-induced hepatic lipid metabolic disorders.

scholarly journals Erchen Decoction Mitigates Lipid Metabolism Disorder by the Regulation of PPARγ and LPL Gene in a High-Fat Diet C57BL/6 Mice Model

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Mengting Zhang ◽  
Yanfei Shao ◽  
Bizhen Gao ◽  
Jicheng Chen ◽  
Ping Zhang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Weight ◽  
Lipid Metabolism ◽  
Visceral Fat ◽  
Protein Level ◽  
High Fat Diet ◽  
Blood Lipid ◽  
Abdominal Circumference ◽  
High Fat ◽  
Gene And Protein Expression

Erchen decoction (ECD) is a common treatment prescribed in traditional Chinese medicine (TCM) clinics, which has remarkable efficacy in the treatment of obesity, fatty liver, hyperlipidemia, diabetes, and other diseases caused by phlegm. In this study, we investigated the effect that ECD had on the lipid metabolism induced by high-fat diet in C57BL/6 mice. Body weight, body length, and abdominal circumference were detected. Blood lipid content was measured via biochemical assay kit. The gene and protein expression of PPARγ and LPL in visceral fat and skeletal muscle of mice was measured by real-time PCR and western blot. The research discovered that the phlegm-resolving effect that ECD had on high-fat diet mice was mainly manifested as reduced body weight, Lee’s index, abdominal circumference, and level of TG and TC. Meanwhile, we observed significantly increased PPARγ mRNA and protein level in visceral fat and PPARγ and LPL protein level in skeletal muscle in the ECD group. Contrarily, a decrease in PPARγ mRNA level in skeletal muscle in the ECD group was observed. Therefore, we speculate that ECD regulates the lipid metabolic disorder by decreasing the blood lipid level. Moreover, the potential molecular mechanism of ECD is to promote the expression of PPARγ in visceral fat and skeletal muscle and the expression of LPL in skeletal muscle.

Effects of dietary curcumin on growth, antioxidant capacity, fatty acid composition and expression of lipid metabolism-related genes of large yellow croaker fed a high-fat diet

2020 ◽  
pp. 1-10
Author(s):  
Renlei Ji ◽  
Xiaojun Xiang ◽  
Xueshan Li ◽  
Kangsen Mai ◽  
Qinghui Ai
Keyword(s):  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Antioxidant Capacity ◽  
High Fat Diet ◽  
Control Group ◽  
Large Yellow Croaker ◽  
Lipid Deposition ◽  
High Fat ◽  
Hepatic Lipid

Abstract A 10-week feeding trial was conducted to investigate the effect of dietary curcumin (CC) on growth antioxidant responses, fatty acid composition, and expression of lipid metabolism-related genes of large yellow croaker fed a high-fat diet (HFD). Four diets (lipid level at 18 %) were formulated with different levels of curcumin (0, 0·02, 0·04 and 0·06 %). The best growth performance was found in the 0·04 % curcumin group, with the body and hepatic lipid levels lower than the control group (0 % CC). The content of TAG, total cholesterol and LDL-cholesterol was the least in the 0·06 % curcumin group. The lowest malondialdehyde and the highest superoxide dismutase, catalase and total antioxidant capacity were observed in the 0·04 % curcumin group. The 0·04 % curcumin group had higher expression of Δ6fad, elovl5 and elovl4 and showed higher hepatic n-6 and n-3 PUFA. Expression of ppara, cpt1, and aco was significantly increased, while expression of srebp1 and fas was dramatically decreased in curcumin groups compared with the control group. Overall, 0·04 % curcumin supplementation could mitigate the negative effects caused by HFD and promote growth via reducing hepatic lipid deposition, improving antioxidant activity and increasing PUFA of large yellow croaker. To conclude, abnormal hepatic lipid deposition was probably due to increased fatty acid oxidation and reduced de novo synthesis of fatty acids.

scholarly journals Supplement of bamboo extract lowers serum monocyte chemoattractant protein-1 concentration in mice fed a diet containing a high level of saturated fat

2011 ◽  
Vol 106 (12) ◽  
pp. 1810-1813 ◽  
Author(s):  
Jason K. Higa ◽  
Wanyu Liu ◽  
Marla J. Berry ◽  
Jun Panee
Keyword(s):  
Body Weight ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Water Extract ◽  
Control Group ◽  
Standard Diet ◽  
High Fat ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein

Monocyte chemoattractant protein-1 (MCP-1) is an inflammatory chemokine up-regulated in obese subjects, contributing to the development of type 2 diabetes. The present study investigated the inhibitory effect of an ethanol–water extract from bamboo (BEX,Phyllostachys edulis) on the blood concentration of MCP-1. C57BL/6J mice were fed a standard diet or a high-fat diet with or without the BEX supplement (11 g dry mass/17 000 kJ) for 6 months. A total of ten mice were used in each group. Body weight and food consumption were measured weekly. After euthanisation, the weight of visceral fat and circulating MCP-1 concentration were measured. In comparison with the standard control group, the high-fat control group had increased body weight, abdominal fat storage and serum MCP-1 concentration by 60 % (P < 0·001), 266 % (P < 0·001) and 180 % (P < 0·01), respectively. In comparison with the high-fat control group, the high-fat BEX group showed a 3 % decrease in body weight (P < 0·01), 24 % decrease in mesenteric fat depot (P < 0·01) and 49 % decrease in serum MCP-1 concentration (P < 0·05). The present study suggests that the BEX supplement in the high-fat diet ameliorates elevated MCP-1 concentrations in the blood, and whether this is related to modulated endocrine properties of the visceral fat is to be studied.

scholarly journals Aerobic Exercise Promotes the Expression of ATGL and Attenuates Inflammation to Improve Hepatic Steatosis via lncRNA SRA

2021 ◽  
Author(s):  
Baoai Wu ◽  
Yiming Tian ◽  
Chong Xu ◽  
Yu Zeng ◽  
Feng Yan ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Aerobic Exercise ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Inflammatory Factors ◽  
Control Group ◽  
Inflammatory Factor ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Hepatic Lipid

Abstract The role of aerobic exercise in preventing and improving non-alcoholic fatty liver has been widely established. SRA is a long non-coding RNA, which has received increasing attention due to its important role in lipid metabolism. However, it is unclear whether aerobic exercise can prevent and treat hepatic lipid accumulation via SRA. The mice were randomly divided into three groups as follows, normal control group (NC), high-fat diet group (HFD), and high-fat diet plus aerobic exercise (8weeks, 6 days/ week, 18 m/ min for 50 min, 6% slope) group (HAE). After 8 weeks, the mice in the HAE group showed significant improvement in hepatic steatosis. Body weight as well as blood TC, LDL-C, and liver TG levels were significantly lower in the HAE group than in the HFD group. Compared with the HFD group, the expression of SRA was markedly suppressed and the expression of ATGL was significantly increased in the HAE group. Additionally, the JNK/P38 signaling was inhibited, the pro-inflammatory factors were down-regulated, and the anti-inflammatory factor was increased. The results of this study provided new support for aerobic exercise to improve hepatic lipid metabolism via lncRNA.

Antihyperlipidemic and Hepatoprotective Properties of Vitamin B6 Supplementation in Rats with High-Fat Diet-Induced Hyperlipidemia

2021 ◽  
Vol 21 ◽  
Author(s):  
Qian Zhang ◽  
Da-long Zhang ◽  
Xiao-li Zhou ◽  
Qian Li ◽  
Ning He ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Protein Expression ◽  
High Fat Diet ◽  
Vitamin B6 ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Atherogenic Index ◽  
High Fat ◽  
Hepatic Lipid

Background: The incidence and mortality of hyperlipidemia are increasing year by year, showing a younger trend. At present, the treatment of hyperlipidemia is mainly dependent on western medicine, but its side effects on liver and kidney function are common in clinics. Therefore, it is necessary to study the treatment of hyperlipidemia by augmenting effective dietary nutrition supplements. Vitamin B6 (VitB6), as an essential cofactor for enzymes, participates in lipid metabolism. The effects of VitB6 on hyperlipidemia, however, have not been reported until now. Aim: The present study was to investigate the influence of VitB6 on hepatic lipid metabolism in hyperlipidaemia rats induced by a high-fat diet (HFD). Methods: Male Sprague-Dawley rats were kept on HFD for two weeks to establish the hyperlipidemia model. The rats in low-dosage and high-dosage groups were received 2.00 and 3.00 mg/kg/day of VitB6 for eight weeks, respectively. Results: The results showed that both doses of VitB6 reduced HFD-induced hepatic low-density lipoprotein cholesterol (LDL-C); decreased blood cholesterol (TC), triglycerides, LDL-C, atherogenic index (AI), atherogenic index of plasma (AIP), apolipoprotein B (ApoB) and ApoB/apolipoprotein A-1(ApoA1) ratio; increased liver high-density lipoprotein cholesterol (HDL-C) and serum ApoA1; reduced hepatic steatosis and triglyceride accumulation, lowered fat storage, and recovered heart/body and brain/body ratio to a normal level. In addition, VitB6 supplementation markedly decreased HMGR level, increased the mRNA abundance of LDLR and CYP7A1, and protein expression of SIRT1, following the downregulation of SREBP-1 and PPARγ protein expression in the liver of hyperlipidemia rats. Conclusion: In summary, oral VitB6 supplementation can ameliorate HFD-induced hepatic lipid accumulation and dyslipidemia in SD rats by inhibiting fatty acid and cholesterol synthesis, promoting fatty acid decomposition and cholesterol transport.

scholarly journals Anti-Obesity Effects of Matoa (Pometia pinnata) Fruit Peel Powder in High-Fat Diet-Fed Rats

Molecules ◽  
2021 ◽  
Vol 26 (21) ◽  
pp. 6733
Author(s):  
Toshikazu Suzuki ◽  
Mayumi Nagata ◽  
Natsuko Kagawa ◽  
Shiori Takano ◽  
Nahrowi ◽  
...  
Keyword(s):  
Body Weight ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Antioxidant Properties ◽  
Serum Triglyceride ◽  
Inhibitory Effect ◽  
The Body ◽  
High Fat ◽  
Fruit Peel ◽  
Hepatic Lipid

Fruit peels, pericarps, or rinds are rich in phenolic/polyphenolic compounds with antioxidant properties and potentially beneficial effects against obesity and obesity-related non-communicable diseases. This study investigated the anti-obesity effects of matoa (Pometia pinnata) and salak (Salacca zalacca) fruit peel. Neither matoa peel powder (MPP) nor salak peel powder (SPP) affected the body weight, visceral fat weight, or serum glucose or lipid levels of Sprague–Dawley rats when included as 1% (w/w) of a high-fat diet (HFD). However, MPP significantly decreased the hepatic lipid level. MPP at a dose of 3% (w/w) of the HFD decreased body weight, visceral fat, and serum triglyceride levels as well as the hepatic lipid content. The inhibitory effect of MPP on hepatic lipid accumulation was not enhanced when its concentration was increased from 1% to 3% of the HFD. The anti-obesity effect of matoa was partly explained by the inhibitory effect of the matoa peel extract on fatty acid-induced secretion of ApoB-48 protein, a marker of intestinal chylomicrons, in differentiated Caco-2 cell monolayers. We identified hederagenin saponins that are abundant in MPP as potential anti-obesity substances. These results will contribute towards the development of functional foods with anti-obesity effects using the matoa fruit peel.

scholarly journals Effect of High Fat Diet on Body Weight, Visceral Fat Weight, and PPARG Expressions on Visceral Fat in Mice

2021 ◽  
Vol 57 (3) ◽  
pp. 186
Author(s):  
Cantika Putri Melyana ◽  
Sony Wibisono Mudjanarko ◽  
Lilik Herawati ◽  
Mohammad Anam Al-Arif ◽  
Purwo Sri Rejeki
Keyword(s):  
Body Weight ◽  
Visceral Fat ◽  
High Fat Diet ◽  
Alternative Therapy ◽  
The Body ◽  
Control Group ◽  
Standard Diet ◽  
High Fat ◽  
Control Group Design ◽  
Global Epidemic

Obesity becomes a global epidemic nowadays. The high-fat diet is used as an alternative therapy for obesity. The optimal composition of a high-fat diet to reduce body weight is still unknown. This study aimed to determine which components of a high-fat diet can decrease body weight, visceral fat, and PPARG expression of visceral fat. This study was conducted at the Faculty of Veterinary Medicine, Universitas Airlangga, for three months by using a randomized post-test only control group design. Fifty male mice, 2-3 months old, 18-30 grams were adapted for one week given standard diet AIN93-M, then mice were divided into five groups, namely K1 (control group, 12% fat, 20% protein, 62% carbs); K2 (30% fat, 60% proteins, 0% carbs); K3 (45% fat, 45% protein, 0% carbs);  K4 (60% fat, 30% protein, 0% carbs); and K5 (75% fat, 15% protein, 0% carbs). Bodyweight was measured before and after treatment, then the visceral fat and PPARG expressions were evaluated. Statistical comparisons were performed using Statistical Package for the Social Sciences (SPSS) software. After treatment, there were forty-three mice. The body weight and visceral fat weight of the mice with a high-fat diet were decreased. The most significant changes in body weight were in K4 with -9,60 ± 3,806 grams reduction. The bodyweight of mice in K5, slightly increased than K2-K4. This could be caused by the hormesis phenomenon. PPARG expressions decreased in groups with a high-fat diet but increased in K5. The composition of a high-fat diet in group K4 was the most optimal to decrease the body weight, visceral fat, and PPARG expressions in mice

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