Decabromodiphenyl ether-induced PRKACA Hypermethylation Contributed to Glycolipid Metabolism Disorder via Regulating PKA/AMPK Pathway in Rat and L-02 Cells

2022 ◽  
pp. 103808
Author(s):  
Yupeng Zhu ◽  
Li Jing ◽  
Xiangyang Li ◽  
Guiqing Zhou ◽  
Yue Zhang ◽  
...  
Keyword(s):  
Decabromodiphenyl Ether ◽  
Glycolipid Metabolism ◽  
Ampk Pathway ◽  
Metabolism Disorder

scholarly journals miR-125a-5p ameliorates hepatic glycolipid metabolism disorder in type 2 diabetes mellitus through targeting of STAT3

Theranostics ◽  
2018 ◽  
Vol 8 (20) ◽  
pp. 5593-5609 ◽  
Author(s):  
Lina Xu ◽  
Yue Li ◽  
Lianhong Yin ◽  
Yan Qi ◽  
Huijun Sun ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder

scholarly journals Glycolipid Metabolism Disorder in the Liver of Obese Mice Is Improved by TUDCA via the Restoration of Defective Hepatic Autophagy

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Qinyue Guo ◽  
Qindong Shi ◽  
Huixia Li ◽  
Jiali Liu ◽  
Shufang Wu ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Body Weight Gain ◽  
Obese Mice ◽  
Lower Blood Glucose ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder ◽  
Reduced Body ◽  
Lower Blood ◽  
Important Regulator

Objective.Tauroursodeoxycholic acid (TUDCA) has been considered an important regulator of energy metabolism in obesity. However, the mechanism underlying how TUDCA is involved in insulin resistance is not fully understood. We tested the effects of TUDCA on autophagic dysfunction in obese mice.Material and Methods.500 mg/kg of TUDCA was injected into obese mice, and metabolic parameters, autophagy markers, and insulin signaling molecular were assessed by Western blotting and real-time PCR.Results.The TUDCA injections in the obese mice resulted in a reduced body weight gain, lower blood glucose, and improved insulin sensitivity compared with obese mice that were injected with vehicle. Meanwhile, TUDCA treatment not only reversed autophagic dysfunction and endoplasmic reticulum stress, but also improved the impaired insulin signaling in the liver of obese mice. Additionally, the same results obtained with TUDCA were evident in obese mice treated with the adenoviral Atg7.Conclusions.We found that TUDCA reversed abnormal autophagy, reduced ER stress, and restored insulin sensitivity in the liver of obese mice and that glycolipid metabolism disorder was also improved via the restoration of defective hepatic autophagy.

scholarly journals Rhus chinensis Mill. Fruits Ameliorate Hepatic Glycolipid Metabolism Disorder in Rats Induced by High Fat/High Sugar Diet

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4480
Author(s):  
Zihuan Wu ◽  
Qingqing Ma ◽  
Shengbao Cai ◽  
Yilin Sun ◽  
Yuanyue Zhang ◽  
...  
Keyword(s):  
Chronic Diseases ◽  
Metabolic Disorders ◽  
Ethanol Extract ◽  
Key Factors ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
High Sugar ◽  
Metabolism Disorder ◽  
Rhus Chinensis ◽  
Underlying Mechanisms

Hepatic glycolipid metabolism disorder is considered as one of the key factors in the pathogenesis of many chronic diseases. The objective of this study was to investigate the protective effect and underlying mechanisms of Rhus chinensis Mill. fruits against hepatic glycolipid metabolic disorders in rats induced by a high fat/high sugar diet. Results showed that ethanol extract, especially at a dose of 600 mg/kg b.w., could effectively ameliorate glycolipid metabolic disorders in rats. The biochemical indexes, including CAT, GSH and HOMA-IR, were significantly improved by the administration of ethanol extract. Immunohistochemistry and Western blot analysis revealed that ethanol extract up-regulated the expression levels of PI3K/AKT, PPAR-α, and the phosphorylation of IRS1 and AMPK proteins, and down-regulated the expressions of SREBP-1 and FAS proteins in the liver, which are closely related to hepatic glycolipid metabolism. Those findings suggested that R. chinensis Mill. fruits could be developed as functional foods and/or nutraceuticals for preventing or controlling some chronic diseases related to hepatic glycolipid metabolism disorder.

scholarly journals Citrus reticulatae pericarpium Extract Decreases the Susceptibility to HFD-Induced Glycolipid Metabolism Disorder in Mice Exposed to Azithromycin in Early Life

2021 ◽  
Vol 12 ◽  
Author(s):  
Hanqi Lu ◽  
Yanting You ◽  
Xinghong Zhou ◽  
Qiuxing He ◽  
Ming Wang ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
High Fat Diet ◽  
Early Life ◽  
Underlying Mechanism ◽  
Inflammatory Factors ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder ◽  
Adult Mice ◽  
Gut Microbe ◽  
Old Mice

BackgroundStudies have shown that gut microbe disorder in mice due to early-life antibiotic exposure promotes glycolipid metabolism disorder in adulthood. However, the underlying mechanism remains unclear and there is not yet an effective intervention or treatment for this process.PurposeThe study investigated whether early-life azithromycin (AZT) exposure in mice could promote high-fat diet (HFD)-induced glycolipid metabolism disorder in adulthood. Moreover, the effect of citrus reticulata pericarpium (CRP) extract on glycolipid metabolism disorder via regulation of gut microbiome in mice exposed to antibodies early in life were investigated.Methods and ResultsThree-week-old mice were treated with AZT (50 mg/kg/day) via drinking water for two weeks and then were fed a CRP diet (1% CRP extract) for four weeks and an HFD for five weeks. The results showed that early-life AZT exposure promoted HFD-induced glycolipid metabolism disorder, increased the levels of inflammatory factors, promoted the flora metabolism product trimethylamine N-oxide (TMAO), and induced microbial disorder in adult mice. Importantly, CRP extract mitigated these effects.ConclusionTaken together, these findings suggest that early-life AZT exposure increases the susceptibility to HFD-induced glycolipid metabolism disorder in adult mice, and CRP extract can decrease this susceptibility by regulating gut microbiome.

scholarly journals Kaempferide improves glycolipid metabolism disorder by activating PPARγ in high-fat-diet-fed mice

Life Sciences ◽  
2021 ◽  
Vol 270 ◽  
pp. 119133
Author(s):  
Heng Tang ◽  
Qingfu Zeng ◽  
Ting Tang ◽  
Yunjie Wei ◽  
Peng Pu
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Glycolipid Metabolism ◽  
Metabolism Disorder

miR-552-3p modulates transcriptional activities of FXR and LXR to ameliorate hepatic glycolipid metabolism disorder

2021 ◽  
Vol 74 (1) ◽  
pp. 8-19
Author(s):  
Lei Fan ◽  
Rongtao Lai ◽  
Ningning Ma ◽  
Yunxia Dong ◽  
Yu Li ◽  
...  
Keyword(s):  
Glycolipid Metabolism ◽  
Metabolism Disorder

scholarly journals Arrb2 Causes Hepatic Lipid Metabolism Disorder via AMPK Pathway Based on Metabolomics in Alcoholic Fatty Liver

2021 ◽  
Author(s):  
Ying-Yin Sun ◽  
Dong-Qing Wu ◽  
Na-Na Yin ◽  
Lei Yang ◽  
Xin Chen ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Fatty Liver ◽  
Hepatic Lipid Metabolism ◽  
Alcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Ampk Pathway ◽  
Metabolism Disorder ◽  
Lipid Metabolites

Background & Aims: Alcoholic fatty liver (AFL) is an early form of alcoholic liver disease (ALD) that usually manifests as lipid synthesis abnormalities in hepatocytes. Arrb2 is involved in multiple biological processes. This study aimed to explore the role of Arrb2 in the regulation of lipid metabolism in AFL and the underlying mechanism and identify potential targets for the treatment of AFL. Methods: The expression of Arrb2 was detected in liver tissues obtained from AFL patients and Gao-binge AFL model mice. In addition, we specifically knocked down Arrb2 in AFL mouse liver in vivo and used Arrb2-siRNA or pEX3-Arrb2 to silence or overexpress Arrb2 in AML-12 cells in vitro to explore the functional role and underlying regulatory mechanism of Arrb2 in AFL. Finally, we investigated whether Arrb2 could cause changes in hepatic lipid metabolites, thereby leading to dysregulation of lipid metabolism based on liquid chromatography-mass spectrometry (LC-MS) analysis. Results: Arrb2 was upregulated in the livers of AFL patients and AFL mice. The in vivo and in vitro results confirmed that Arrb2 could induce lipid accumulation and metabolism disorders. Mechanistically, Arrb2 induced hepatic metabolism disorder via AMP-activated protein kinase (AMPK) pathway. The results of LC-MS analysis revealed that hepatic lipid metabolites with the most significant differences were primary bile acids. Conclusions: Arrb2 induces hepatic lipid metabolism disorders via AMPK pathway in AFL. On one hand, Arrb2 increases fatty acid synthesis. On the other hand, Arrb2 could increase the cholesterol synthesis, thereby leading to the upregulation of primary bile acid levels.

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