Intestinal-specific ketohexokinase deficiency ameliorates high fructose-induced metabolic dysfunction across the intestinal-liver-kidney axis in mice

Shanshan Song

doi:10.1016/j.jnutbio.2026.110453

Intestinal-specific ketohexokinase deficiency ameliorates high fructose-induced metabolic dysfunction across the intestinal-liver-kidney axis in mice

2026-06-23

0

PRE

AI

S

Shanshan Song

X

Xiaoli Yi

M

Mulan Wang

H

Huiru Yang

W

Wenting Tan

Y

Ying Zhu

J

Jun Yu

C

Chuanming Xu *

DOI：10.1016/j.jnutbio.2026.110453

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Abstract

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• The small intestine is the first gateway for fructose absorption into the body and plays a critical role in fructose-induced pathological processes. • Ketohexokinase (KHK), an initial enzyme for fructose metabolism, is strongly implicated in the development of fructose-associated metabolic syndrome. • Intestinal-specific Khk knockout in fructose-challenged mice is associated with reduced fructose exposure, which likely contributes substantially to the attenuation of metabolic syndrome phenotypes. • Intestinal-specific Khk deletion decreased uric acid production, maintained jejunal Zn2+ homeostasis, and suppressed hepatic triglyceride and fatty acid biosynthesis in fructose-loaded mice. • Our findings highlight intestinal KHK as a critical mediator in high-fructose-induced metabolic syndrome across the intestinal-liver-kidney axis.

Keywords:

Fructose

Ketohexokinase

Metabolic syndrome

Intestinal

Liver

Kidney

Intestinal-specific ketohexokinase deficiency ameliorates high fructose-induced metabolic dysfunction across the intestinal-liver-kidney axis in mice

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