Journal
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
Volume 306, Issue 1, Pages G1-G12Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpgi.00263.2013
Keywords
calbindin; fructose; glucose; glucose transporter 5; metabolism; nutrition
Categories
Funding
- National Science Foundation [IOS-1121049]
- Program Strategic Scholarships for Frontier Research Network for the Joint Ph.D. Program Thai Doctoral Degree
- Office of the Higher Education Commission, Thailand
- Division Of Integrative Organismal Systems
- Direct For Biological Sciences [1121049] Funding Source: National Science Foundation
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Fructose consumption by Americans has increased markedly, whereas Ca2+ intake has decreased below recommended levels. Because fructose metabolism decreases enterocyte ATP concentrations, we tested the hypothesis that luminal fructose acutely reduces active, diet-inducible Ca2+ transport in the small intestine. We confirmed that the decrease in ATP concentrations was indeed greater in fructose- compared with glucose-incubated mucosal homogenates from wild-type and was prevented in fructose-incubated homogenates from ketohexokinase (KHK)(-/-) mice. We then induced active Ca2+ transport by chronically feeding wild-type, fructose transporter glucose transporter 5 (GLUT5)(-/-), as well as KHK-/- mice a low Ca2+ diet and measured transepithelial Ca2+ transport in everted duodenal sacs incubated in solutions containing glucose, fructose, or their nonmetabolizable analogs. The diet-induced increase in active Ca2+ transport was proportional to dramatic increases in expression of the Ca2+ -selective channel transient receptor potential vanilloid family calcium channel 6 as well as of the Ca2+ -binding protein 9k (CaBP9k) but not that of the voltage-dependent L-type channel Ca(v)1.3. Crypt-villus distribution of CaBP9k seems heterogeneous, but low Ca2+ diets induce expression in more cells. In contrast, KHK distribution is homogeneous, suggesting that fructose metabolism can occur in all enterocytes. Diet-induced Ca2+ transport was not enhanced by addition of the enterocyte fuel glutamine and was always greater in sacs of wild-type, GLUT5(-/-), and KHK-/- mice incubated with fructose or nonmetabolizable sugars than those incubated with glucose. Thus duodenal Ca2+ transport is not affected by fructose and enterocyte ATP concentrations but instead may decrease with glucose metabolism, as Ca2+ transport remains high with 3-O-methylglucose that is also transported by sodium-glucose cotransporter 1 but cannot be metabolized.
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