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.

The effect of maternal intake of sucrose or high-fructose corn syrup (HFCS)-55 during gestation and lactation on lipogenic gene expression in rat offspring at 3 and 12 weeks of age

2018 ◽  
Vol 9 (5) ◽  
pp. 481-486 ◽  
Author(s):  
H. Kaur ◽  
C. R. Toop ◽  
B. S. Muhlhausler ◽  
S. Gentili
Keyword(s):  
Messenger Rna ◽  
Binding Protein ◽  
Hepatic Metabolism ◽  
Perinatal Exposure ◽  
High Fructose Corn Syrup ◽  
Corn Syrup ◽  
Hepatic Expression ◽  
Lipogenic Genes ◽  
High Fructose ◽  
Element Binding Protein

AbstractPerinatal exposure to sucrose or high-fructose corn syrup-55 (HFCS-55) in rats has previously been associated with altered hepatic fat content and composition post-weaning, although the effects on hepatic metabolism are unknown. The current study aimed to determine the sex-specific effects of maternal consumption of sucrose or HFCS-55 on the expression of hepatic lipogenic genes in the offspring. Liver samples were collected from offspring of albino Wistar rats provided with ad libitum access to either water (control), 10% sucrose or 10% HFCS-55 solution during pregnancy and lactation at 3 weeks (control n=16, sucrose n=22, HFCS-55 n=16) and 12 weeks (control n=16, sucrose n=10, HFCS-55 n=16) of age. Hepatic expression of the transcription factors such as carbohydrate response element-binding protein, sterol regulatory element-binding protein-1c and downstream genes was determined by quantitative real-time PCR. Sucrose-exposed offspring had higher hepatic SREBP-1c messenger RNA expression compared with control and HFCS-55 groups at both 3 weeks (P=0.01) and 12 weeks (P=0.03) of age. There were no differences in the expression of other hepatic lipogenic genes between groups at either 3 or 12 weeks. Thus, perinatal exposure to sucrose may be more detrimental to offspring hepatic metabolism compared with HFCS-55, independent of sex, and it will be important to evaluate the longer-term effects of perinatal sucrose exposure in future studies.

scholarly journals Effect of Restriction of Foods with High Fructose Corn Syrup Content on Metabolic Indices and Fatty Liver in Obese Children

Obesity Facts ◽  
2017 ◽  
Vol 10 (4) ◽  
pp. 332-340 ◽  
Author(s):  
Lorena del Rocio Ibarra-Reynoso ◽  
Hilda Lissette López-Lemus ◽  
Ma Eugenia Garay-Sevilla ◽  
Juan Manuel Malacara
Keyword(s):  
Fatty Liver ◽  
High Fructose Corn Syrup ◽  
Obese Children ◽  
Corn Syrup ◽  
High Fructose ◽  
Metabolic Indices

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.

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
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