scholarly journals Supplementation of concentrated Kurozu, a Japanese black vinegar, reduces the onset of hepatic steatosis in mice fed with a high-fat diet

2019 ◽  
Vol 9 (4) ◽  
pp. 276
Author(s):  
Yoshihiko Shibayama ◽  
Masanobu Nagano ◽  
Kazunori Hashiguchi ◽  
Akira Fujii ◽  
Ken Iseki
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Serum Levels ◽  
Standard Diet ◽  
Chronic Liver Diseases ◽  
High Fat ◽  
Body Weights ◽  
Common Causes ◽  
All Cause Mortality ◽  
Lipid Metabolism Genes

Background: Hepatic steatosis is among the most common causes of chronic liver diseases, although established effective treatments are not evident.  Previous studies reported that Kurozu improved hypercholesterolemia and carbohydrate metabolism. However, the effect of Kurozu on the incidence of hepatic steatosis is not clear.Objective: The effect of Kurozu on the onset of hepatic steatosis by administering a high-fat diet (HFD) for 110 weeks was evaluated in C57BL/6J mice. Methods: HFD treatment for 110 weeks accelerated the onset of hepatic steatosis more than a standard diet, whereas concentrated Kurozu (CK) supplementation ameliorated the effect of an HFD feeding. The effect of supplementation with resveratrol in an HFD on the onset of hepatic steatosis was also evaluated. To elucidate the mechanism of the effect of Kurozu on the expression of lipid metabolism genes, acute treatment for 10 days with Kurozu was also examined.Results: Supplementation with resveratrol in HFD-fed mice did not ameliorate hepatic steatosis. Body weights were significantly lower in the CK + HFD and Resveratrol + HFD groups than in the control HFD group in middle age. No significant differences in all-cause mortality were observed following supplementation with CK or resveratrol. CK and resveratrol supplements significantly inhibited decreases in dehydroepiandrosterone sulphate serum levels at postnatal week 120. CK and resveratrol supplements did not affect the survival of mice. The ingestion of Kurozu for 10 days significantly elevated the expression levels of Sirt1, Pgc-1α, Lpin1, and Igfbp1 in the liver. Conclusion: These results suggest that ingesting CK may delay the onset of hepatic steatosis HFD feeding causes.Keywords: Kurozu, steatosis, Sirt1, Igfbp1, Lpin1, Pgc-1α, resveratrol

scholarly journals Palmitoleic Acid (N-7) Attenuates the Immunometabolic Disturbances Caused by a High-Fat Diet Independently of PPARα

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Camila O. Souza ◽  
Alexandre A. S. Teixeira ◽  
Edson A. Lima ◽  
Helena A. P. Batatinha ◽  
Lara M. Gomes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Oleic Acid ◽  
High Fat Diet ◽  
Palmitoleic Acid ◽  
Serum Levels ◽  
Standard Diet ◽  
Liver Inflammation ◽  
Wild Type ◽  
High Fat

Palmitoleic acid (PMA) has anti-inflammatory and antidiabetic activities. Here we tested whether these effects of PMA on glucose homeostasis and liver inflammation, in mice fed with high-fat diet (HFD), are PPAR-αdependent. C57BL6 wild-type (WT) and PPAR-α-knockout (KO) mice fed with a standard diet (SD) or HFD for 12 weeks were treated after the 10th week with oleic acid (OLA, 300 mg/kg of b.w.) or PMA 300 mg/kg of b.w. Steatosis induced by HFD was associated with liver inflammation only in the KO mice, as shown by the increased hepatic levels of IL1-beta, IL-12, and TNF-α; however, the HFD increased the expression of TLR4 and decreased the expression of IL1-Ra in both genotypes. Treatment with palmitoleate markedly attenuated the insulin resistance induced by the HFD, increased glucose uptake and incorporation into muscle in vitro, reduced the serum levels of AST in WT mice, decreased the hepatic levels of IL1-beta and IL-12 in KO mice, reduced the expression of TLR-4 and increased the expression of IL-1Ra in WT mice, and reduced the phosphorylation of NF𝜅B (p65) in the livers of KO mice. We conclude that palmitoleate attenuates diet-induced insulin resistance, liver inflammation, and damage through mechanisms that do not depend on PPAR-α.

scholarly journals Regular Intake of Pistachio Mitigates the Deleterious Effects of a High Fat-Diet in the Brain of Obese Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 317 ◽  
Author(s):  
Domenico Nuzzo ◽  
Giacoma Galizzi ◽  
Antonella Amato ◽  
Simona Terzo ◽  
Pasquale Picone ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Serum Levels ◽  
Standard Diet ◽  
High Fat ◽  
Neuroprotective Effects ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
The Brain ◽  
Superoxide Dismutase 2 ◽  
Regular Intake

Obesity has been associated with neurodegeneration and cognitive dysfunctions. Recent data showed that pistachio consumption is able to prevent and ameliorate dyslipidemia, hepatic steatosis, systemic and adipose tissue inflammation in mice fed a high-fat diet (HFD). The present study investigated the neuroprotective effects of pistachio intake in HFD mice. Three groups of mice were fed a standard diet (STD), HFD, or HFD supplemented with pistachio (HFD-P) for 16 weeks. Metabolic parameters (oxidative stress, apoptosis, and mitochondrial dysfunction) were analyzed by using specific assays and biomarkers. The pistachio diet significantly reduced the serum levels of triglycerides and cholesterol in the HFD model. No difference was observed in the index of insulin resistance between HFD and HFD-P. A higher number of fragmented nuclei were found in HFD cerebral cortex compared to STD and HFD-P. A decrease in reactive oxygen species, singlet oxygen and phosphorylated extracellular signal-regulated kinase, and an increase of superoxide dismutase 2 and heme oxygenase expression were found in the brains of the HFD-P samples compared to HFD. Furthermore, the impaired mitochondrial function found in HFD brain was partially recovered in HFD-P mice. These results suggest that the regular intake of pistachio may be useful in preventing obesity-related neurodegeneration, being able to reduce both metabolic and cellular dysfunctions.

scholarly journals Time course of changes in in vitro lipolysis of intra-abdominal fat depots in relation to high-fat diet-induced hepatic steatosis in rats

2006 ◽  
Vol 96 (2) ◽  
pp. 268-275 ◽  
Author(s):  
Pascal Collin ◽  
Natalie Chapados ◽  
Elise Dufresne ◽  
Pierre Corriveau ◽  
Pascal Imbeault ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Time Course ◽  
Liver Lipid ◽  
Abdominal Fat ◽  
Standard Diet ◽  
High Fat ◽  
Fat Depots ◽  
Fat Accretion

The purpose of the present study was to determine the time course of changes in in vitro lipolysis and in perilipin content (Western blot) in the mesenteric and/or the retroperitoneal fat depots in relation to the development of hepatic steatosis in high-fat diet-fed rats. Female Sprague-Dawley rats were submitted to a high-fat diet (HF diet; 42% as kJ) or a standard diet (SD diet) for 1, 2, 3 or 8 weeks. Fat accretion in the mesenteric and retroperitoneal tissues was higher (P<0·01) in HF diet-fed than in SD diet-fed rats as soon as 1 week after the beginning of the diet. Liver triacylglycerol concentrations were significantly (P<0·01) higher in HF diet-fed than in SD diet-fed rats throughout the experiment, the highest values being reached at week 2 of the diet. Basal and stimulated lipolysis (10−4 to 10−7m-isoproterienol) in the mesenteric and retroperitoneal fat depots was not changed during the first 3 weeks, regardless of the diet. Lipolysis in the mesenteric adipose tissue in the basal and stimulated states was, however, higher (P<0·01) in HF diet-fed than in SD diet-fed rats after 8 weeks of the diets. There were no significant (P>0·05) effects of diet and time on perilipin content of mesenteric tissue. In spite of a rapid fat accretion, the present results do not provide any evidence of a rapid (3 weeks) increase in in vitro lipolysis in intra-abdominal fat depots upon the undertaking of an HF diet at a time where liver lipid infiltration is the most significant.

scholarly journals Effect of concentrated Kurozu, a traditional Japanese vinegar, on expression of hepatic miR-34a, -149-3p, and -181a-5p in high-fat diet-fed mice

2020 ◽  
Vol 10 (1) ◽  
pp. 1
Author(s):  
Yoshihiko Shibayama
Keyword(s):  
Lipid Metabolism ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Standard Diet ◽  
High Fat ◽  
Expression Levels ◽  
Small Noncoding Rnas ◽  
Cell Functions ◽  
Micro Rnas

Background: Long-term high-fat diet (HFD) feeding, which can induce obesity, can also induce nonalcoholic steatohepatitis (NASH) and liver tumorigenesis. A previous study reported that concentrated Kurozu (CK) supplementation reduced the incidence of HFD-induced hepatic steatosis in mice. It was showed that CK supplementation improved dyslipidemia in animal and clinical study. Small noncoding RNAs, micro RNAs (miRs), play crucial roles in the biology of cell functions, lipid metabolism and neoplasms. However, the effect of CK treatment on the relationship between HFD and expression of miRs is unclear.Objective: To evaluate changes in the expression of hepatic miRs and lipid metabolism- associated genes on administering a HFD for 60 weeks in C57BL6J mice. The onset of hepatic steatosis induced by HFD treatment was also observed.Methods: The mice received a HFD, HFD with CK, or standard diet (SD) for 60 consecutive weeks. The effect of CK treatment on the expression levels of lipid metabolism-associated genes in the liver was evaluated.Results: HFD feeding significantly increased expression of Tnf, and significantly decreased Adipoq and Mlxipl in the liver. The ingestion of CK elevated the expression levels of Pgc-1α and Igfbp1 in the liver compared with the SD group. HFD feeding significantly increased the expression of miR-488-5p, and significantly decreased miR-29b and -122a-5p in the liver. The ingestion of CK elevated the expression levels of miR-34a, -149-3p, and -181a-5p in the liver compared with the SD group. Expression levels of miR-488-3p in the serum HFD group were significantly higher than in the SD group. The ingestion of CK elevated the expression levels of miR-181a-5p in the serum compared with the SD group.Conclusion: These results suggest that CK supplementation reduced the onset of hepatic hyperplasia, and increased hepatic miR-34a, -149-3p, and -181a-5p. These miRs may function as suppressors of tumors caused by HFD feeding.Key Words:  High-fat diet, carcinogenesis, Kurozu, microRNA, miR-34a, miR-122a-5p, miR-149, miR-181a, miR-488 

scholarly journals High-intensity interval training ameliorates high-fat diet-induced elevation of aminotransferases in male Wistar rats

2021 ◽  
Vol 23 (3) ◽  
pp. 111-115
Author(s):  
Qazaleh Asqari ◽  
Farhad Gholami ◽  
Jabbar Bashiri ◽  
Adel Donyaei
Keyword(s):  
High Fat Diet ◽  
Wistar Rats ◽  
Interval Training ◽  
Serum Levels ◽  
Diet Group ◽  
Standard Diet ◽  
High Intensity Interval Training ◽  
High Fat ◽  
Male Wistar Rats ◽  
High Intensity Interval

Background and aims: A high-fat diet increases triglyceride (TG) accumulations in hepatocytes and results in non-alcoholic fatty liver diseases (NAFLDs). In this regard, this study investigated the effect of high-intensity interval training (HIIT), along with a high-fat diet on the serum levels of aminotransferases in male Wistar rats. Methods: Forty male Wistar rats were randomly assigned to the standard diet, high-fat diet, exercise + standard diet, and exercise + high-fat diet groups (each containing 10 animals). HIIT program consisted of 6-12 repetitions of 2-minute highs-intensity exercise (85-90% of the maximum speed) interspersed with 1-minute low-intensity exercise (45-50% peak speed) with the frequency of 5 sessions a week over 12 weeks. High-fat diet groups received a diet regimen including 58% fat, 25% protein, and 17% carbohydrate, ad libitum. The blood samples were taken from the left ventricle 48 hours following the last intervention to assess TG, alanine aminotransferase (ALT), and aspartate amino-transferase (AST) concentrations. Data were analyzed using one-way ANOVA and Tukey’s post-hoc tests. Results: The findings showed the mean of ALT, AST, and TG in the high-fat diet group was significantly greater compared to the standard diet group (P=0.001). Furthermore, the mean of ALT, AST, and TG in the exercise + high-fat diet group was significantly lower in comparison with the high-fat diet group (P=0.01, P=0.017, and P=0.012, respectively). Conclusion: Although HIIT ameliorated high-fat diet-induced elevations in the serum levels of TG, ALT, and AST, they did not reach the baseline levels. Thus, it may indicate that a diet as the underlying cause of NAFLDs is more important than any other interventions such as exercise.

scholarly journals Krill Oil Ameliorates Mitochondrial Dysfunctions in Rats Treated with High-Fat Diet

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Alessandra Ferramosca ◽  
Annalea Conte ◽  
Vincenzo Zara
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Dietary Fats ◽  
Control Group ◽  
Acid Oxidation ◽  
Standard Diet ◽  
Krill Oil ◽  
High Fat ◽  
Energetic Metabolism ◽  
Respiratory Chain Complexes

In recent years, several studies focused their attention on the role of dietary fats in the pathogenesis of hepatic steatosis. It has been demonstrated that a high-fat diet is able to induce hyperglycemia, hyperinsulinemia, obesity, and nonalcoholic fatty liver disease. On the other hand, krill oil, a novel dietary supplement of n-3 PUFAs, has the ability to improve lipid and glucose metabolism, exerting possible protective effects against hepatic steatosis. In this study we have investigated the effects of krill oil on mitochondrial energetic metabolism in animals fed a high-fat diet. To this end, male Sprague-Dawley rats were divided into three groups and fed for 4 weeks with a standard diet (control group), a diet with 35% fat (HF group), or a high-fat diet supplemented with 2.5% krill oil (HF+KO group). The obtained results suggest that krill oil promotes the burning of fat excess introduced by the high-fat diet. This effect is obtained by stimulating mitochondrial metabolic pathways such as fatty acid oxidation, Krebs cycle, and respiratory chain complexes activity. Modulation of the expression of carrier proteins involved in mitochondrial uncoupling was also observed. Overall, krill oil counteracts the negative effects of a high-fat diet on mitochondrial energetic metabolism.

Niga-ichigoside F1 ameliorates high-fat diet-induced hepatic steatosis in male mice by Nrf2 activation

2018 ◽  
Vol 9 (2) ◽  
pp. 906-916 ◽  
Author(s):  
Shu-Fang Xia ◽  
Jing Shao ◽  
Shu-Ying Zhao ◽  
Yu-Yu Qiu ◽  
Li-Ping Teng ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Nuclear Translocation ◽  
Male Mice ◽  
High Fat ◽  
Genes Expression ◽  
Nrf2 Activation ◽  
Lipid Metabolism Genes ◽  
Regulate Lipid Metabolism

Niga-ichigoside F1 ameliorated high-fat diet-induced hepatic steatosis by increasing Nrf2 nuclear translocation to regulate lipid metabolism genes expression in livers of C57BL/6J mice.

scholarly journals ST2 Deficiency Ameliorates High Fat Diet-Induced Liver Steatosis In BALB/c Mice

2015 ◽  
Vol 16 (1) ◽  
pp. 9-20 ◽  
Author(s):  
Nemanja Jovicic ◽  
Ilija Jeftic ◽  
Marina Miletic Kovacevic ◽  
Irena Tanaskovic ◽  
Nebojsa Arsenijevic ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
Molecular Mechanisms ◽  
Liver Steatosis ◽  
Liver Weight ◽  
Serum Levels ◽  
Immune Reactivity ◽  
High Fat ◽  
Alcoholic Fatty Liver

ABSTRACTNon-alcoholic fatty liver disease (NAFLD) is strongly associated with obesity, but the molecular mechanisms of liver steatosis and its progression to non-alcoholic steatohepatitis and fibrosis are incompletely understood. Immune reactivity plays an important role in the pathogenesis of NAFLD. The IL-33/ST2 axis has a protective role in adiposity and atherosclerosis, but its role in obesity-associated metabolic disorders requires further clarification. To investigate the unresolved role of IL-33/ST2 signalling in NAFLD, we used ST2-deficient (ST2-/-) and wild type (WT) BALB/c mice maintained on a high-fat diet (HFD) for 24 weeks. HFD-fed ST2-/- mice exhibited increased weight gain, visceral adipose tissue weight and triglyceridaemia and decreased liver weight compared with diet-matched WT mice. Compared with WT mice on an HFD, ST2 deletion significantly reduced hepatic steatosis, liver inflammation and fibrosis and downregulated the expression of genes related to lipid metabolism in the liver. The frequency of innate immune cells in the liver, including CD68+ macrophages and CD11c+ dendritic cells, was lower in HFD-fed ST2-/- mice, accompanied by lower TNFα serum levels compared with diet-matched WT mice. Less collagen deposition in the livers of ST2-/- mice on an HFD was associated with lower numbers of profibrotic CD11b+Ly6clow monocytes and CD4+IL-17+ T cells in the liver, lower hepatic gene expression of procollagen, IL-33 and IL-13, and lower serum levels of IL-33 and IL-13 compared with diet-matched WT mice.Our findings suggest that the IL-33/ST2 axis may have a complex role in obesity-associated metabolic disorders. Although it is protective in HFD-induced adiposity, the IL-33/ST2 pathway promotes hepatic steatosis, inflammation and fibrosis.

scholarly journals Beneficial effects of heat-treated Enterococcus faecalis FK-23 on high-fat diet-induced hepatic steatosis in mice

2014 ◽  
Vol 112 (6) ◽  
pp. 868-875 ◽  
Author(s):  
Masatoshi Kondoh ◽  
Takashi Shimada ◽  
Kazutake Fukada ◽  
Mayuko Morita ◽  
Kazuhiro Katada ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Hepatic Steatosis ◽  
Fatty Acid Oxidation ◽  
Enterococcus Faecalis ◽  
High Fat Diet ◽  
Inhibitory Effect ◽  
Acid Oxidation ◽  
Standard Diet ◽  
High Fat ◽  
Expression Levels

A high-fat diet (HFD) is one of the causes of hepatic steatosis. We previously demonstrated that Enterococcus faecalis FK-23 (FK-23), a type of lactic acid bacteria, exhibits an anti-obesity effect in mice fed a HFD. In the present study, we examined the effects of FK-23 on HFD-induced hepatic steatosis. Male C57BL/6 mice were divided into four groups and given one of four treatments: standard diet (SD); standard diet supplemented with FK-23 (SD+FK); HFD; or HFD supplemented with FK-23 (HFD+FK). For the administration of FK-23, the drinking water was supplemented with FK-23 at a concentration of 2 % (w/w). After 11 weeks, histological findings revealed hepatic steatosis in the liver of HFD-fed mice; however, this effect was attenuated by the administration of FK-23. The expression levels of genes involved in fatty acid oxidation in the liver tissue were significantly reduced in the HFD group compared with the SD group, but FK-23 supplementation tended to up-regulate the expression levels of these genes. Our findings show that the inhibitory effect of FK-23 against hepatic steatosis in HFD-fed mice can be explained by the prevention of fat accumulation in the liver through the modulation of the activities of genes involved in hepatic fatty acid oxidation.

Offspring of high fat diet fed dams develop hepatic steatosis

2014 ◽  
Vol 52 (01) ◽  
Author(s):  
JP Sowa ◽  
L Wingerter ◽  
G Gerken ◽  
M Palmert ◽  
A Canbay ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
High Fat
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