scholarly journals Long-term baicalin administration ameliorates metabolic disorders and hepatic steatosis in rats given a high-fat diet

2009 ◽  
Vol 30 (11) ◽  
pp. 1505-1512 ◽  
Author(s):  
Hong-xia Guo ◽  
Dai-hua Liu ◽  
Ying Ma ◽  
Jin-feng Liu ◽  
Ying Wang ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
High Fat

The beneficial effects of Lactobacillus fermented black barley on high fat diet-induced fatty liver in rats

2021 ◽  
Author(s):  
Qi Guan ◽  
Xinwen Ding ◽  
Lingyue Zhong ◽  
Chuang Zhu ◽  
Pan Nie ◽  
...  
Keyword(s):  
Fatty Liver ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
High Fat ◽  
Beneficial Effects ◽  
Phytochemical Composition

Long term high-fat diet (HF) can cause metabolic disorders, which might induce fatty liver. Fermented whole cereal food exhibit healthy potential due to their unique phytochemical composition and probiotics. In...

scholarly journals Disrupting phosphatase SHP2 in macrophages protects mice from high-fat diet-induced hepatic steatosis and insulin resistance by elevating IL-18 levels

2020 ◽  
Vol 295 (31) ◽  
pp. 10842-10856 ◽  
Author(s):  
Wen Liu ◽  
Ye Yin ◽  
Meijing Wang ◽  
Ting Fan ◽  
Yuyu Zhu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
Metabolic Diseases ◽  
Low Grade ◽  
High Fat ◽  
Caspase 1

Chronic low-grade inflammation plays an important role in the pathogenesis of type 2 diabetes. Src homology 2 domain-containing tyrosine phosphatase-2 (SHP2) has been reported to play diverse roles in different tissues during the development of metabolic disorders. We previously reported that SHP2 inhibition in macrophages results in increased cytokine production. Here, we investigated the association between SHP2 inhibition in macrophages and the development of metabolic diseases. Unexpectedly, we found that mice with a conditional SHP2 knockout in macrophages (cSHP2-KO) have ameliorated metabolic disorders. cSHP2-KO mice fed a high-fat diet (HFD) gained less body weight and exhibited decreased hepatic steatosis, as well as improved glucose intolerance and insulin sensitivity, compared with HFD-fed WT littermates. Further experiments revealed that SHP2 deficiency leads to hyperactivation of caspase-1 and subsequent elevation of interleukin 18 (IL-18) levels, both in vivo and in vitro. Of note, IL-18 neutralization and caspase-1 knockout reversed the amelioration of hepatic steatosis and insulin resistance observed in the cSHP2-KO mice. Administration of two specific SHP2 inhibitors, SHP099 and Phps1, improved HFD-induced hepatic steatosis and insulin resistance. Our findings provide detailed insights into the role of macrophagic SHP2 in metabolic disorders. We conclude that pharmacological inhibition of SHP2 may represent a therapeutic strategy for the management of type 2 diabetes.

scholarly journals Bixin Attenuates High-Fat Diet-Caused Liver Steatosis and Inflammatory Injury through Nrf2/PPARα Signals

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Shasha Tao ◽  
Youjing Yang ◽  
Jianzhong Li ◽  
Hongyan Wang ◽  
Yu Ma
Keyword(s):  
Liver Disease ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Cytoprotective Activity ◽  
Inflammatory Damage

Nonalcoholic fatty liver disease is the most common liver disease worldwide. Hepatic steatosis and oxidative stress are the main characteristics of NAFLD (nonalcoholic fatty liver disease), which also affect its prognosis. Bixin acts as novel Nrf2 (NF-E2 p45-related factor 2) activator with the cytoprotection against oxidative stress and inflammation; this study mainly focused on the mechanism of Nrf2 activation by bixin and explored its potential feasibilities in long-term high-fat diet- (HFD-) caused hepatic steatosis and inflammatory response in vitro and in vivo. Bixin was found to activate Nrf2 signals by the modification of critical Keap1 (Kelch-like ECH-associated protein 1) cystine and competitive interaction with Keap1 with upregulating P62 mRNA and protein expression. In human liver cells exposed to FFA (free fatty acid), bixin displayed a pronounced cytoprotective activity with upregulation of Nrf2-mediated gene expression, such as PPARα and its targets related with fatty acid oxidation. In HFD-fed mice, systemic administration of bixin attenuated lipid accumulation, decreased oxidant inflammatory damage in the liver, and reduced circulating lipid levels through Nrf2. Different from most of other established inducers, bixin activated Nrf2 signals through two different mechanisms with safe administration for protection of oxidant inflammatory damage and attenuation of lipid accumulation in the in vivo long-term HFD-fed mice. Bixin represents a prototype Nrf2 activator that displays cytoprotective activity upon system administration targeting hepatic steatosis and oxidant inflammation originating from long-term HFD-fed mice. And bixin-based Nrf2-directed systemic intervention may also provide therapeutic benefit in protecting other organs in the process of metabolic syndrome.

scholarly journals Structural Characterization of Peptides From Huangjiu and Their Regulation of Hepatic Steatosis and Gut Microbiota Dysbiosis in Hyperlipidemia Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Ying Shi ◽  
Ruixue Feng ◽  
Jieqi Mao ◽  
Shuangping Liu ◽  
Zhilei Zhou ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Bioactive Peptides ◽  
Size Analysis ◽  
High Fat ◽  
Linear Discriminant ◽  
Wide Range ◽  
Gut Microbiota Dysbiosis

Hyperlipidemia is a chronic disorder that is difficult to cure and usually treated with long-term lipid-reducing drugs. Recent trends have led to the use of diet therapies or food-derived strategies in the treatment of such long-term diseases. The Chinese rice wine (huangjiu) contains a wide range of bioactive peptides that are produced during the multi-species fermentation process. To clarify the regulation effects of lipid metabolism and gut microbiota by huangjiu bioactive peptides, three huangjiu peptides were isolated, purified and characterized by hyper-filtration, macroporous resin, gel filtration separation and structural identification. Meanwhile, a mouse model of high-fat diet-induced hyperlipidemia was established to study the effects of huangjiu peptides on serum biomarker, hepatic metabolism and gut microbiota dysbiosis. Experimental results showed that huangjiu peptides T1 and T2 (HpT1, HpT2) treatment alleviated the increase in serum total cholesterol, triglyceride, low-density lipoprotein cholesterol levels and aberrant hepatic lipid accumulation in the high-fat diet-induced hyperlipidemia mice. Furthermore, HpT2 and HpT1 restored the α-diversity and structure of gut microbial community after hyperlipidemia-induced microbiota disturbance compared with simvastatin and HpT3. The administration of HpT2 and HpT1 regulated the microbiota-mediated gut ecology through alterations of characteristic taxa including Lactobacillus, Ileibacterium, Faecalibaculum and Alloprevotella by linear discriminant analysis effect size analysis. Collectively, our results offer new insights into the abilities of food-derived peptides on alleviation of high-fat diet-induced hyperlipidemia, hepatic steatosis and gut dysbiosis in mice.

scholarly journals Luteolin-Enriched Artichoke Leaf Extract Alleviates the Metabolic Syndrome in Mice with High-Fat Diet-Induced Obesity

Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 979 ◽  
Author(s):  
Eun-Young Kwon ◽  
So Kim ◽  
Myung-Sook Choi
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Acid Oxidation ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Diet Induced Obesity ◽  
The Metabolic Syndrome

This current study aimed to elucidate the effects and possible underlying mechanisms of long-term supplementation with dietary luteolin (LU)-enriched artichoke leaf (AR) in high-fat diet (HFD)-induced obesity and its complications (e.g., dyslipidemia, insulin resistance, and non-alcoholic fatty liver disease) in C57BL/6N mice. The mice were fed a normal diet, an HFD, or an HFD plus AR or LU for 16 weeks. In the HFD-fed mice, AR decreased the adiposity and dyslipidemia by decreasing lipogenesis while increasing fatty acid oxidation, which contributed to better hepatic steatosis. LU also prevented adiposity and hepatic steatosis by suppressing lipogenesis while increasing biliary sterol excretion. Moreover, AR and LU prevented insulin sensitivity by decreasing the level of plasma gastric inhibitory polypeptide and activity of hepatic glucogenic enzymes, which may be linked to the lowering of inflammation as evidenced by the reduced plasma interleukin (IL)-6, IL-1β, and plasminogen activator inhibitor-1 levels. Although the anti-metabolic syndrome effects of AR and LU were similar, the anti-adiposity and anti-dyslipidemic effects of AR were more pronounced. These results in mice with diet-induced obesity suggest that long-term supplementation with AR can prevent adiposity and related metabolic disorders such as dyslipidemia, hepatic steatosis, insulin resistance, and inflammation.

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 Long-term Fenretinide treatment prevents high-fat diet-induced obesity, insulin resistance, and hepatic steatosis

2009 ◽  
Vol 297 (6) ◽  
pp. E1420-E1429 ◽  
Author(s):  
Frederic Preitner ◽  
Nimesh Mody ◽  
Timothy E. Graham ◽  
Odile D. Peroni ◽  
Barbara B. Kahn
Keyword(s):  
Insulin Resistance ◽  
Hepatic Steatosis ◽  
Knockout Mice ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Retinol Binding Protein ◽  
Term Therapy ◽  
High Fat ◽  
Diet Induced Obesity

The synthetic retinoid Fenretinide (FEN) increases insulin sensitivity in obese rodents and is in early clinical trials for treatment of insulin resistance in obese humans with hepatic steatosis (46). We aimed to determine the physiological mechanisms for the insulin-sensitizing effects of FEN. Wild-type mice were fed a high-fat diet (HFD) with or without FEN from 4–5 wk to 36–37 wk of age (preventive study) or following 22 wk of HF diet-induced obesity (12 wk intervention study). Retinol-binding protein-4 (RBP4) knockout mice were also fed the HFD with or without FEN in a preventive study. FEN had minimal effects on HFD-induced body weight gain but markedly reduced HFD-induced adiposity and hyperleptinemia in both studies. FEN-HFD mice gained epididymal fat but not subcutaneous or visceral fat mass in contrast to HFD mice without FEN. FEN did not have a measurable effect on energy expenditure, food intake, physical activity, or stool lipid content. Glucose infusion rate during hyperinsulinemic-euglycemic clamp was reduced 86% in HFD mice compared with controls and was improved 3.6-fold in FEN-HFD compared with HFD mice. FEN improved insulin action on glucose uptake and glycogen levels in muscle, insulin-stimulated suppression of hepatic glucose production, and suppression of serum FFA levels in HFD mice. Remarkably, FEN also reduced hepatic steatosis. In RBP4 knockout mice, FEN reduced the HFD-induced increase in adiposity and hyperleptinemia. In conclusion, long-term therapy with FEN partially prevents or reverses obesity, insulin resistance, and hepatic steatosis in mice on HFD. The anti-adiposity effects are independent of the RBP4 lowering effect.

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