Effects of Chinese herbal medicine Jiangzhi Granule on expressions of liver X receptor α and sterol regulatory element-binding protein-1c in a rat model of non-alcoholic fatty liver disease

2011 ◽  
Vol 9 (9) ◽  
pp. 998-1004 ◽  
Author(s):  
LL Yang
Keyword(s):  
Liver Disease ◽  
Herbal Medicine ◽  
Fatty Liver Disease ◽  
Regulatory Element ◽  
Alcoholic Fatty Liver ◽  
Chinese Herbal ◽  
Liver X Receptor Α ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Alcoholic Fatty Liver Disease

Viral hepatitis and fatty liver disease: how an unwelcome guest makes pâté of the host

2008 ◽  
Vol 416 (2) ◽  
pp. e15-e17 ◽  
Author(s):  
Andrew J. Brown
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Regulatory Element ◽  
Alcoholic Fatty Liver ◽  
Biochemical Journal ◽  
Liver X Receptor Α ◽  
Element Binding Protein ◽  
Sterol Regulatory Element ◽  
Phosphoinositide 3 Kinase

HBV and HCV (hepatitis B and C viruses respectively) affect hundreds of millions of people globally, and are a major cause of chronic liver disease, including NAFLD (non-alcoholic fatty liver disease). Previous work on HCV-associated fatty liver disease has implicated two transcription factors that are important in lipid metabolism, SREBP1c (sterol-regulatory-element-binding protein 1c) and the LXRα (liver X receptor α). HBV-associated fatty liver disease has been less well-studied. New work from Kim and colleagues in this issue of the Biochemical Journal has provided new insight into how HBV causes fatty liver disease. Investigating HBV's so-called X gene product (HBx), they report that this viral protein directly binds to LXRα in the host liver cells to up-regulate the lipogenic transcription factor, SREBP1c. Also discussed in this commentary is another way that viruses such as HBV and HCV could induce SREBP1c-mediated lipogenesis, via the PI3K (phosphoinositide 3-kinase)–Akt signalling pathway.

scholarly journals A Slow-Digesting Carbohydrate Diet during Rat Pregnancy Protects Offspring from Non-Alcoholic Fatty Liver Disease Risk through the Modulation of the Carbohydrate-Response Element and Sterol Regulatory Element Binding Proteins

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 844 ◽  
Author(s):  
Rafael Salto ◽  
Manuel Manzano ◽  
María Dolores Girón ◽  
Ainara Cano ◽  
Azucena Castro ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Regulatory Element ◽  
Liver Lipid ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Sterol Regulatory Element ◽  
Carbohydrate Digestion ◽  
Alcoholic Fatty Liver Disease

High-fat (HF) and rapid digestive (RD) carbohydrate diets during pregnancy promote excessive adipogenesis in offspring. This effect can be corrected by diets with similar glycemic loads, but low rates of carbohydrate digestion. However, the effects of these diets on metabolic programming in the livers of offspring, and the liver metabolism contributions to adipogenesis, remain to be addressed. In this study, pregnant insulin-resistant rats were fed high-fat diets with similar glycemic loads but different rates of carbohydrate digestion, High Fat-Rapid Digestive (HF–RD) diet or High Fat-Slow Digestive (HF–SD) diet. Offspring were fed a standard diet for 10 weeks, and the impact of these diets on the metabolic and signaling pathways involved in liver fat synthesis and storage of offspring were analyzed, including liver lipidomics, glycogen and carbohydrate and lipid metabolism key enzymes and signaling pathways. Livers from animals whose mothers were fed an HF–RD diet showed higher saturated triacylglycerol deposits with lower carbon numbers and double bond contents compared with the HF–SD group. Moreover, the HF–RD group exhibited enhanced glucose transporter 2, pyruvate kinase (PK), acetyl coenzyme A carboxylase (ACC) and fatty acid (FA) synthase expression, and a decrease in pyruvate carboxylase (PyC) expression leading to an altered liver lipid profile. These parameters were normalized in the HF–SD group. The changes in lipogenic enzyme expression were parallel to changes in AktPKB phosphorylation status and nuclear expression in carbohydrate-response element and sterol regulatory element binding proteins. In conclusion, an HF–RD diet during pregnancy translates to changes in liver signaling and metabolic pathways in offspring, enhancing liver lipid storage and synthesis, and therefore non-alcoholic fatty liver disease (NAFLD) risk. These changes can be corrected by feeding an HF–SD diet during pregnancy.

scholarly journals Acupuncture combined with Chinese herbal medicine on non-alcoholic fatty liver disease

Medicine ◽  
2021 ◽  
Vol 100 (51) ◽  
pp. e28083
Author(s):  
Yuan Ma ◽  
Kewei Sun ◽  
Jianzhong Cao ◽  
Xiaowu Qin ◽  
Jiaoling Shi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Herbal Medicine ◽  
Fatty Liver ◽  
Chinese Herbal Medicine ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Chinese Herbal ◽  
Alcoholic Fatty Liver Disease

The Hexane Fraction of Cyperus rotundus Prevents Non-Alcoholic Fatty Liver Disease Through the Inhibition of Liver X Receptor α-Mediated Activation of Sterol Regulatory Element Binding Protein-1c

2015 ◽  
Vol 43 (03) ◽  
pp. 477-494 ◽  
Author(s):  
Gyun-Sik Oh ◽  
Jin Yoon ◽  
Gang Gu Lee ◽  
Jong Hwan Kwak ◽  
Seung-Whan Kim
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Regulatory Element ◽  
Cyperus Rotundus ◽  
Primary Hepatocytes ◽  
Lipogenic Genes ◽  
Liver X Receptor Α ◽  
Element Binding Protein ◽  
Sterol Regulatory Element

The goals of this study were (1) to examine the effects of Cyperus rotundus (CR) rhizome on cellular lipogenesis and non-alcoholic/diet-induced fatty liver disease, and (2) to elucidate the molecular mechanism behind its actions. The present investigation showed that the hexane fraction of CR rhizome (CRHF) reduced the elevated transcription levels of sterol regulatory element binding protein-1c (SREBP-1c) in primary hepatocytes following exposure to the liver X receptor α (LXRα) agonist. The SREBP-1c gene is a master regulator of lipogenesis and a key target of LXRα. CRHF inhibited not only the LXRα-dependent activation of the synthetic LXR response element (LXRE) promoter, but also the activation of the natural SREBP-1c promoter. Moreover, CRHF decreased (a) the recruitment of RNA polymerase II to the LXRE of the SREBP-1c gene; (b) the LXRα-dependent up-regulation of various lipogenic genes; and (c) the LXRα-mediated accumulation of triglycerides in primary hepatocytes. Furthermore, CRHF ameliorated fatty liver disease and reduced the expression levels of hepatic lipogenic genes in high sucrose diet (HSD)-fed mice. Interestingly, CRHF did not affect the expression of ATP-binding cassette transporter A1, another important LXR target gene that is required for reverse cholesterol transport (RCT) and protects against atherosclerosis. Taken together, these results suggest that CRHF might be a novel therapeutic remedy for fatty liver disease through the selective inhibition of the lipogenic pathway.

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