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1000 Titel
  • The Role of Carbohydrate Response Element Binding Protein in Intestinal and Hepatic Fructose Metabolism
1000 Autor/in
  1. Iizuka, Katsumi |
1000 Erscheinungsjahr 2017
1000 Art der Datei
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2017-02-22
1000 Erschienen in
1000 Quellenangabe
  • 9(2):181
1000 Copyrightjahr
  • 2017
1000 Lizenz
1000 Verlagsversion
  • https://dx.doi.org/10.3390/nu9020181 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5331612/ |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • Many articles have discussed the relationship between fructose consumption and the incidence of obesity and related diseases. Fructose is absorbed in the intestine and metabolized in the liver to glucose, lactate, glycogen, and, to a lesser extent, lipids. Unabsorbed fructose causes bacterial fermentation, resulting in irritable bowl syndrome. Therefore, understanding the mechanisms underlying intestinal and hepatic fructose metabolism is important for the treatment of metabolic syndrome and fructose malabsorption. Carbohydrate response element binding protein (ChREBP) is a glucose-activated transcription factor that controls approximately 50% of de novo lipogenesis in the liver. ChREBP target genes are involved in glycolysis (Glut2, liver pyruvate kinase), fructolysis (Glut5, ketohexokinase), and lipogenesis (acetyl CoA carboxylase, fatty acid synthase). ChREBP gene deletion protects against high sucrose diet-induced and leptin-deficient obesity, because Chrebp−/− mice cannot consume fructose or sucrose. Moreover, ChREBP contributes to some of the physiological effects of fructose on sweet taste preference and glucose production through regulation of ChREBP target genes, such as fibroblast growth factor-21 and glucose-6-phosphatase catalytic subunits. Thus, ChREBP might play roles in fructose metabolism. Restriction of excess fructose intake will be beneficial for preventing not only metabolic syndrome but also irritable bowl syndrome.
1000 Sacherschließung
lokal ChREBP
lokal glycolysis
lokal fructose
lokal ketohexokinase
lokal Glut5/SLC2A5
lokal carbohydrate response element binding protein
lokal fructolysis
1000 Fachgruppe
  1. Ernährungswissenschaften |
1000 Fächerklassifikation (DDC)
1000 Liste der Beteiligten
  1. http://orcid.org/0000-0002-9837-6238
1000 Label
1000 Förderer
  1. Japan Society for the Promotion of Science
1000 Fördernummer
  1. 26500005
1000 Förderprogramm
  1. Grant-in-Aid for Scientific Research
1000 Dateien
1000 Objektart article
1000 Beschrieben durch
1000 @id frl:6411746.rdf
1000 Erstellt am 2018-12-12T09:49:39.988+0100
1000 Erstellt von 122
1000 beschreibt frl:6411746
1000 Bearbeitet von 122
1000 Zuletzt bearbeitet Thu Jan 30 22:09:10 CET 2020
1000 Objekt bearb. Wed Dec 12 09:50:20 CET 2018
1000 Vgl. frl:6411746
1000 Oai Id
  1. oai:frl.publisso.de:frl:6411746 |
1000 Sichtbarkeit Metadaten public
1000 Sichtbarkeit Daten public
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