Replacing dietary glucose with fructose increases ChREBP activity and SREBP-1 protein in rat liver nucleus

Hyun Young Koo, Michio Miyashita, B. H. Simon Cho, Manabu T. Nakamura

Research output: Contribution to journalArticlepeer-review


Diets high in fructose cause hypertriglyceridemia and insulin resistance in part due to simultaneous induction of gluconeogenic and lipogenic genes in liver. We investigated the mechanism underlying the unique pattern of gene induction by dietary fructose. Male Sprague-Dawley rats (n = 6 per group) were meal-fed (4 h/d) either 63% (w/w) glucose or 63% fructose diet. After two weeks, animals were killed at the end of the last meal. Nuclear SREBP-1 was 2.2 times higher in fructose-fed rats than glucose-fed rats. Nuclear FoxO1 was elevated 1.7 times in fructose group, but did not reach significance (P = 0.08). Unexpectedly, no difference was observed in nuclear ChREBP between two groups. However, ChREBP DNA binding was 3.9× higher in fructose-fed animals without an increase in xylulose-5-phospate, a proposed ChREBP activator. In conclusion, the gene induction by dietary fructose is likely to be mediated in part by simultaneously increased ChREBP activity, SREBP-1 and possibly FoxO1 protein in nucleus.

Original languageEnglish (US)
Pages (from-to)285-289
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - Dec 11 2009


  • Carbohydrate response element-binding protein
  • Forkhead box O1
  • Fructose
  • Glucose-6-phosphatase
  • Phosphoenolpyruvate carboxykinase
  • Sterol regulatory element-binding protein-1

ASJC Scopus subject areas

  • Molecular Biology
  • Biophysics
  • Biochemistry
  • Cell Biology


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