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

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• 作者：Li Liu^a ; ¹ ; Shang Wang^a ; ¹ ; Ling Yao^b ; Jin-xiu Li^b ; Peng Ma^a ; Li-rong Jiang^a ; Da-zhi Ke^c ; Yong-quan Pan^d ; ; Jian-wei Wang^b ; ^{wjwcq68@163.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Stearoyl-CoA desaturase (SCD)1 ; Nonalcoholic fatty liver disease (NAFLD) ; Fructose ; Fasting
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2016
• 出版时间：28 October 2016
• 年：2016
• 卷：479
• 期：4
• 页码：643-648
• 全文大小：1091 K

文摘

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 Interesting, hepatic levels of stearoyl-CoA desaturase (SCD)1 mRNA remained elevated under fructose withdrawn conditions, although expression levels of other genes, including two key transcription factors (carbohydrate response element binding protein (ChREBP) and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.