Literature summary for 2.7.1.3 extracted from

Herman, M.A.; Samuel, V.T.
The sweet path to metabolic demise fructose and lipid synthesis (2016), Trends Endocrinol. Metab., 27, 719-730 .

Search for more literature for 2.7.1.3

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	P50053	-	-

Synonyms

Synonyms	Comment	Organism
KHK	-	Homo sapiens

General Information

General Information	Comment	Organism
drug target	ketohexokinase may be a therapeutic target. Complete knockout of all ketohexokinase isoforms prevents fructose-induced disease. In contrast, selective knockout of the ubiquitous, low-activity KHK-A isoform exacerbates fructose-induced disease, possibly by increasing flux through the KHK-C isoform expressed in key metabolic tissues, like liver	Homo sapiens
metabolism	fructose increases de novo lipogenesis through the efficient and uninhibited action of ketohexokinase and aldolase B, which yields substrates for fatty-acid synthesis. Chronic fructose consumption further enhances the capacity for hepatic fructose metabolism via activation of several key transcription factors (i.e. SREBP1c and ChREBP), which augment expression of lipogenic enzymes, increasing lipogenesis, further compounding hypertriglyceridemia, and hepatic steatosis. Hepatic insulin resistance develops from diacylglycerol-PKCe mediated impairment of insulin signaling and possibly additional mechanisms	Homo sapiens

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Release 2023.1 (January 2023)