Journal
BIOCHEMISTRY AND BIOPHYSICS REPORTS
Volume 18, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.bbrep.2019.100638
Keywords
Fructose; Gluconeogenesis; Insulin; AKT; FoxO1; G6Pase
Categories
Funding
- Council for Science, Technology, and Innovation (CSTI), Cross-ministerial Strategic Innovation Promotion program (SIP) [15J10165]
- Technologies for creating next-generation agriculture, forestry, and fisheries (funding agency: Bio-oriented Technology Research Advancement Institution, National Agriculture and Food Research Organization, NARO)
- Tojuro Iijima Foundation for Food Science and Technology (Chiba, Japan)
- Japanese Ministry of Education, Culture, Sports, Science, and Technology (MEXT, Tokyo) [15J10165, 15K00827]
- Mishima Kaiun Memorial Foundation (Tokyo, Japan)
- University of Shizuoka Grant for Scientific and Educational Research
- Grants-in-Aid for Scientific Research [15J10165, 15K00827] Funding Source: KAKEN
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Excessive intake of fructose increases lipogenesis in the liver, leading to hepatic lipid accumulation and development of fatty liver disease. Metabolic alterations in the liver due to fructose intake have been reported in many studies, but the effect of fructose administration on hepatic gluconeogenesis is not fully understood. The aim of this study was to evaluate the acute effects of fructose administration on fasting-induced hepatic gluconeogenesis. C57BL/6J mice were administered fructose solution after 14 h of fasting and plasma insulin, glucose, free fatty acids, and ketone bodies were analysed. We also measured phosphorylated AKT and forkhead box O (FoxO) 1 protein levels and gene expression related to gluconeogenesis in the liver. Furthermore, we measured glucose production from pyruvate after fructose administration. Glucose-administered mice were used as controls. Fructose administration enhanced phosphorylation of AKT in the liver, without increase of blood insulin levels. Blood free fatty acids and ketone bodies concentrations were as high as those in the fasting group after fructose administration, suggesting that insulin-induced inhibition of lipolysis did not occur in mice administered with fructose. Fructose also enhanced phosphorylation of Fox01 and suppressed gluconeogenic gene expression, glucose-6-phosphatase activity, and glucose production from pyruvate. The present study suggests that acute fructose administration suppresses fasting-induced hepatic gluconeogenesis in an insulin-independent manner.
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