α-Terpineol induces fatty liver in mice mediated by the AMP-activated kinase and sterol response element binding protein pathway

2013 ◽  
Vol 55 ◽  
pp. 129-136 ◽  
Author(s):  
You-Jin Choi ◽  
Woo-Cheol Sim ◽  
Hyun Kyu Choi ◽  
Seung-Ho Lee ◽  
Byung-Hoon Lee
Keyword(s):  
Fatty Liver ◽  
Binding Protein ◽  
Response Element ◽  
Element Binding Protein

scholarly journals Treatment with Ginger Ameliorates Fructose-Induced Fatty Liver and Hypertriglyceridemia in Rats: Modulation of the Hepatic Carbohydrate Response Element-Binding Protein-Mediated Pathway

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Huanqing Gao ◽  
Tao Guan ◽  
Chunli Li ◽  
Guowei Zuo ◽  
Johji Yamahara ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Liver ◽  
Binding Protein ◽  
Ppar Gamma ◽  
De Novo Lipogenesis ◽  
Nonesterified Fatty Acid ◽  
Alcoholic Extract ◽  
Response Element ◽  
Hepatic Expression ◽  
Element Binding Protein

Ginger has been demonstrated to improve lipid derangements. However, its underlying triglyceride-lowering mechanisms remain unclear. Fructose overconsumption is associated with increase in hepatic de novo lipogenesis, thereby resulting in lipid derangements. Here we found that coadministration of the alcoholic extract of ginger (50 mg/kg/day, oral gavage, once daily) over 5 weeks reversed liquid fructose-induced increase in plasma triglyceride and glucose concentrations and hepatic triglyceride content in rats. Plasma nonesterified fatty acid concentration was also decreased. Attenuation of the increased vacuolization and Oil Red O staining area was evident on histological examination of liver in ginger-treated rats. However, ginger treatment did not affect chow intake and body weight. Further, ginger treatment suppressed fructose-stimulated overexpression of carbohydrate response element-binding protein (ChREBP) at the mRNA and protein levels in the liver. Consequently, hepatic expression of the ChREBP-targeted lipogenic genes responsible for fatty acid biosynthesis was also downregulated. In contrast, expression of neither peroxisome proliferator-activated receptor- (PPAR-) alpha and its downstream genes, nor PPAR-gamma and sterol regulatory element-binding protein 1c was altered. Thus the present findings suggest that in rats, amelioration of fructose-induced fatty liver and hypertriglyceridemia by ginger treatment involves modulation of the hepatic ChREBP-mediated pathway.

scholarly journals The Roles of Carbohydrate Response Element Binding Protein in the Relationship between Carbohydrate Intake and Diseases

2021 ◽  
Vol 22 (21) ◽  
pp. 12058
Author(s):  
Katsumi Iizuka
Keyword(s):  
Fatty Liver ◽  
Binding Protein ◽  
Carbohydrate Intake ◽  
Fibroblast Growth Factor 21 ◽  
High Fructose Corn Syrup ◽  
Response Element ◽  
Corn Syrup ◽  
High Fructose ◽  
Element Binding Protein ◽  
The Relationship

Carbohydrates are macronutrients that serve as energy sources. Many studies have shown that carbohydrate intake is nonlinearly associated with mortality. Moreover, high-fructose corn syrup (HFCS) consumption is positively associated with obesity, cardiovascular disease, and type 2 diabetes mellitus (T2DM). Accordingly, products with equal amounts of glucose and fructose have the worst effects on caloric intake, body weight gain, and glucose intolerance, suggesting that carbohydrate amount, kind, and form determine mortality. Understanding the role of carbohydrate response element binding protein (ChREBP) in glucose and lipid metabolism will be beneficial for elucidating the harmful effects of high-fructose corn syrup (HFCS), as this glucose-activated transcription factor regulates glycolytic and lipogenic gene expression. Glucose and fructose coordinately supply the metabolites necessary for ChREBP activation and de novo lipogenesis. Chrebp overexpression causes fatty liver and lower plasma glucose levels, and ChREBP deletion prevents obesity and fatty liver. Intestinal ChREBP regulates fructose absorption and catabolism, and adipose-specific Chrebp-knockout mice show insulin resistance. ChREBP also regulates the appetite for sweets by controlling fibroblast growth factor 21, which promotes energy expenditure. Thus, ChREBP partly mimics the effects of carbohydrate, especially HFCS. The relationship between carbohydrate intake and diseases partly resembles those between ChREBP activity and diseases.

scholarly journals Correction to: The role of hepatic transcription factor cAMP response element-binding protein (CREB) during the development of experimental nonalcoholic fatty liver: a biochemical and histomorphometric study

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ashraf K. Awaad ◽  
Maher A. Kamel ◽  
Magdy M. Mohamed ◽  
Madiha H. Helmy ◽  
Magda I. Youssef ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Fatty Liver ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Nonalcoholic Fatty Liver ◽  
Histomorphometric Study ◽  
Element Binding Protein

An amendment to this paper has been published and can be accessed via the original article.

scholarly journals The role of hepatic transcription factor cAMP response element-binding protein (CREB) during the development of experimental nonalcoholic fatty liver: a biochemical and histomorphometric study

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ashraf K. Awaad ◽  
Maher A. Kamel ◽  
Magdy M. Mohamed ◽  
Madiha H. Helmy ◽  
Magda I. Youssef ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Fatty Liver ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Control Group ◽  
Camp Response Element ◽  
Response Element ◽  
Nonalcoholic Fatty Liver ◽  
Element Binding Protein

Abstract Background Several molecular mechanisms contribute to the initiation and progression of nonalcoholic fatty liver disease (NAFLD); however, the exact mechanism is not completely understood. Cyclic adenosine monophosphate (cAMP) is one of the most promising pathways that regulates various cellular functions including lipid and carbohydrate metabolism. cAMP induces gene transcription through phosphorylation of the transcription factor, cAMP response element-binding protein (CREB). The action of cAMP is tightly regulated by its level and repression. Among the repressors, Inducible cAMP Early Repressor (ICER) is the only inducible CRE-binding protein. The present study aimed to evaluate the role of hepatic CREB level in the development of experimental NAFLD model to clarify the pathogenesis of the disease. NAFLD 35 male Wistar rats fed a high fat diet for a period of 14 weeks were studied compared with 35 control rats fed a standard diet. Five fasting rats were sacrificed each 2 weeks intervals for a period of 14 weeks. Results NAFLD group revealed a remarkable duration—dependent elevation in cAMP and CREB levels in the liver tissue compared to control group (P value < 0.004, P value < 0.006, respectively). In contrast, ICER gene expression, as a dominant-negative regulator of CREB, was downregulated in the liver of NAFLD group compared to control group. We also demonstrated that CREB levels were positively correlated with liver function tests, and glucose homeostasis parameters. Conclusions Our results indicate that cAMP/CREB pathway provides an early signal in the progression to NAFLD representing a noninvasive biomarker that can early detect NAFLD and a promising therapeutic target for the treatment of the disease as well.

Scutellarin Mitigates Cancer-Induced Bone Pain by Suppressing CaMKII/CREB Pathway in Rat Models

2019 ◽  
Vol 17 (3) ◽  
pp. 249-253
Author(s):  
Liu Chenglong ◽  
Liu Haihua ◽  
Zhang Fei ◽  
Zheng Jie ◽  
Wei Fang
Keyword(s):  
Protein Kinase ◽  
Bone Pain ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Dependent Protein Kinase ◽  
Response Element ◽  
Protein Kinase Ii ◽  
Element Binding Protein ◽  
Dependent Protein

Cancer-induced bone pain is a severe and complex pain caused by metastases to bone in cancer patients. The aim of this study was to investigate the analgesic effect of scutellarin on cancer-induced bone pain in rat models by intrathecal injection of Walker 256 carcinoma cells. Mechanical allodynia was determined by paw withdrawal threshold in response to mechanical stimulus, and thermal hyperalgesia was indicated by paw withdrawal latency in response to noxious thermal stimulus. The paw withdrawal threshold and paw withdrawal latencies were significantly decreased after inoculation of tumor cells, whereas administration of scutellarin significantly attenuated tumor cell inoculation-induced mechanical and heat hyperalgesia. Tumor cell inoculation-induced tumor growth was also significantly abrogated by scutellarin. Ca2+/calmodulin-dependent protein kinase II is a multifunctional kinase with up-regulated activity in bone pain models. The activation of Ca2+/calmodulin-dependent protein kinase II triggers phosphorylation of cAMP-response element binding protein. Scutellarin significantly reduced the expression of phosphorylated-Ca2+/calmodulin-dependent protein kinase II and phosphorylated-cAMP-response element binding protein in cancer-induced bone pain rats. Collectively, our study demonstrated that scutellarin attenuated tumor cell inoculation-induced bone pain by down-regulating the expression of phosphorylated-Ca2+/calmodulin-dependent protein kinase II and phosphorylated-cAMP-response element binding protein. The suppressive effect of scutellarin on phosphorylated-Ca2+/calmodulin-dependent protein kinase II/phosphorylated-cAMP-response element binding protein activation may serve as a novel therapeutic strategy for CIBP management.

cAMP Response Element Binding Protein Is Expressed and Phosphorylated in the Human Heart

Circulation ◽  
1995 ◽  
Vol 92 (8) ◽  
pp. 2041-2043 ◽  
Author(s):  
Frank Ulrich Müller ◽  
Peter Bokník ◽  
Andreas Horst ◽  
Jörg Knapp ◽  
Bettina Linck ◽  
...  
Keyword(s):  
Human Heart ◽  
Binding Protein ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Response Element ◽  
Element Binding Protein
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