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Role of GLUT5 and ketohexokinase in fructose‐induced, acute increases in intestinal active Ca transport
Author(s) -
Tharabenjasin Phuntila,
Douard Veronique,
Krishnamra Nateetip,
Zuo Jian,
Johnson Richard J.,
Ferraris Ronaldo P.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1162.5
Subject(s) - fructose , intracellular , enterocyte , glucose transporter , glutamine , chemistry , biochemistry , metabolism , incubation , membrane transport , transporter , biology , small intestine , endocrinology , amino acid , membrane , gene , insulin
Ketohexokinase (KHK) synthesizes fructose (F)‐1‐P and decreases enterocyte intracellular ATP concentrations. We hypothesized that absorption of F by GLUT5 should acutely reduce ATP‐dependent Ca transport. We stimulated Ca transport by chronically feeding mice a low Ca diet, then determined Ca transport in everted sacs incubated in glucose (G, control), F (±ATP donor glutamine), partly metabolizable GLUT5‐substrate 2‐deoxy‐D‐glucose (2‐DG), and nonmetabolizable SGLT1‐substrate 3‐O‐methylglucose (3OMG). In mice fed normal Ca, Ca transport was low and similar in sacs incubated in G or F, suggesting that baseline Ca transport is not acutely modulated by F. Activity and expression of active Ca transporters adaptively increased in all mice fed low Ca. Surprisingly, the adaptive increase in Ca transport was greater in sacs incubated in F‐ and 2‐DG than in G‐ or 3OMG. Glutamine did not modify Ca transport in G‐ or F‐incubated sacs. In KHK −/− and GLUT5 −/− mice, Ca transport was also stimulated by a low Ca diet. However, adaptive Ca transport in these mice was similar in all everted sacs, regardless of incubation solution. Thus, F transport by GLUT5 and metabolism by KHK are required for acutely increasing the component of intestinal Ca transport stimulated by low Ca diets. This adaptive component seems insensitive to acute changes in intracellular ATP concentrations.