Long-term fructose consumption prolongs hepatic stearoyl-CoA desaturase 1 activity independent of upstream regulation in rats

Autor: Ling Yao, Jianwei Wang, Lirong Jiang, Shang Wang, Jinxiu Li, Peng Ma, Li Liu, Yong-quan Pan, Dazhi Ke
Rok vydání: 2016
Předmět:
Male
0301 basic medicine
medicine.medical_specialty
Biophysics
Fructose
Oxidative phosphorylation
Biology
Biochemistry
Rats
Sprague-Dawley
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Internal medicine
Dietary Carbohydrates
medicine
Animals
RNA
Messenger
Carbohydrate-responsive element-binding protein
Molecular Biology
Triglycerides
Basic Helix-Loop-Helix Leucine Zipper Transcription Factors
Lipogenesis
Body Weight
Fatty liver
Lipid metabolism
Fasting
Organ Size
Cell Biology
medicine.disease
Rats
Sterol regulatory element-binding protein
Fatty Liver
030104 developmental biology
Endocrinology
Gene Expression Regulation
Liver
chemistry
030220 oncology & carcinogenesis
Fructolysis
lipids (amino acids
peptides
and proteins)
Sterol Regulatory Element Binding Protein 1
Stearoyl-CoA desaturase-1
Stearoyl-CoA Desaturase
Zdroj: Biochemical and Biophysical Research Communications. 479:643-648
ISSN: 0006-291X
Popis: Dietary fructose is considered a risk factor for metabolic disorders, such as fatty liver disease. However, the mechanism underlying the effects of fructose is not well characterized. We investigated the hepatic expression of key regulatory genes related to lipid metabolism following fructose feeding under well-defined conditions. Rats were fed standard chow supplemented with 10% w/v fructose solution for 5 weeks, and killed after chow-fasting and fructose withdrawal (fasting) or chow-fasting and continued fructose (fructose alone) for 14 h. Hepatic deposition of triglycerides was found in rats from both groups. As expected, fructose alone increased mRNA levels of lipogenesis-related genes and correspondingly decreased mRNA levels of lipid oxidative genes in the liver. Interesting, hepatic levels of stearoyl-CoA desaturase (SCD)1 mRNA remained elevated under fructose withdrawn conditions, although expression levels of other genes, including two key transcription factors (carbohydrate response element binding protein (ChREBP) and sterol regulatory element-binding protein (SREBP)-1c) fell to normal levels, indicating that long-term fructose intake increased SCD1 activity, independent of upstream regulatory genes, such as ChREBP and SREBP-1c. In conclusion, SCD1 overexpression in fatty liver disease is not affected by fasting after long-term fructose consumption in rats. Regulation of SCD1 plays an important role in fructose-induced hepatic steatosis.
Databáze: OpenAIRE
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