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

Authors
  • Koo, Hyun-Young
  • Miyashita, Michio
  • Simon Cho, B.H.
  • Nakamura, Manabu T.
Type
Published Article
Journal
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Publication Date
Jan 01, 2009
Volume
390
Issue
2
Pages
285–289
Identifiers
DOI: 10.1016/j.bbrc.2009.09.109
Source
Elsevier
Keywords
License
Unknown

Abstract

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.

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