Tags

Type your tag names separated by a space and hit enter

Fructose suppresses uric acid excretion to the intestinal lumen as a result of the induction of oxidative stress by NADPH oxidase activation.
Biochim Biophys Acta Gen Subj. 2017 Mar; 1861(3):559-566.BB

Abstract

BACKGROUND

A high intake of fructose increases the risk for hyperuricemia. It has been reported that long-term fructose consumption suppressed renal uric acid excretion and increased serum uric acid level. However, the effect of single administration of fructose on excretion of uric acid has not been clarified.

METHODS

We used male Wistar rats, which were orally administered fructose (5g/kg). Those rats were used in each experiment at 12h after administration.

RESULTS

Single administration of fructose suppressed the function of ileal uric acid excretion and had no effect on the function of renal uric acid excretion. Breast cancer resistance protein (BCRP) predominantly contributes to intestinal excretion of uric acid as an active homodimer. Single administration of fructose decreased BCRP homodimer level in the ileum. Moreover, diphenyleneiodonium (DPI), an inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox), recovered the suppression of the function of ileal uric acid excretion and the Bcrp homodimer level in the ileum of rats that received single administration of fructose.

CONCLUSIONS

Single administration of fructose decreases in BCRP homodimer level, resulting in the suppression the function of ileal uric acid excretion. The suppression of the function of ileal uric acid excretion by single administration of fructose is caused by the activation of Nox. The results of our study provide a new insight into the mechanism of fructose-induced hyperuricemia.

Authors+Show Affiliations

Laboratory of Clinical Pharmaceutics & Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-12-jo, Nishi-6-chome, Kita-ku, Sapporo 060-0812, Japan.Laboratory of Clinical Pharmaceutics & Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-12-jo, Nishi-6-chome, Kita-ku, Sapporo 060-0812, Japan.Laboratory of Clinical Pharmaceutics & Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-12-jo, Nishi-6-chome, Kita-ku, Sapporo 060-0812, Japan.Laboratory of Clinical Pharmaceutics & Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-12-jo, Nishi-6-chome, Kita-ku, Sapporo 060-0812, Japan.Department of Pharmacy, Hokkaido University Hospital, Kita-14-jo, Nishi-5-chome, Kita-ku, Sapporo 060-8648, Japan. Electronic address: masaki@pharm.hokudai.ac.jp.Laboratory of Clinical Pharmaceutics & Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-12-jo, Nishi-6-chome, Kita-ku, Sapporo 060-0812, Japan.Laboratory of Clinical Pharmaceutics & Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-12-jo, Nishi-6-chome, Kita-ku, Sapporo 060-0812, Japan.Laboratory of Clinical Pharmaceutics & Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University, Kita-12-jo, Nishi-6-chome, Kita-ku, Sapporo 060-0812, Japan; Department of Pharmacy, Hokkaido University Hospital, Kita-14-jo, Nishi-5-chome, Kita-ku, Sapporo 060-8648, Japan. Electronic address: ken-i@pharm.hokudai.ac.jp.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27913188

Citation

Kaneko, Chihiro, et al. "Fructose Suppresses Uric Acid Excretion to the Intestinal Lumen as a Result of the Induction of Oxidative Stress By NADPH Oxidase Activation." Biochimica Et Biophysica Acta. General Subjects, vol. 1861, no. 3, 2017, pp. 559-566.
Kaneko C, Ogura J, Sasaki S, et al. Fructose suppresses uric acid excretion to the intestinal lumen as a result of the induction of oxidative stress by NADPH oxidase activation. Biochim Biophys Acta Gen Subj. 2017;1861(3):559-566.
Kaneko, C., Ogura, J., Sasaki, S., Okamoto, K., Kobayashi, M., Kuwayama, K., Narumi, K., & Iseki, K. (2017). Fructose suppresses uric acid excretion to the intestinal lumen as a result of the induction of oxidative stress by NADPH oxidase activation. Biochimica Et Biophysica Acta. General Subjects, 1861(3), 559-566. https://doi.org/10.1016/j.bbagen.2016.11.042
Kaneko C, et al. Fructose Suppresses Uric Acid Excretion to the Intestinal Lumen as a Result of the Induction of Oxidative Stress By NADPH Oxidase Activation. Biochim Biophys Acta Gen Subj. 2017;1861(3):559-566. PubMed PMID: 27913188.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fructose suppresses uric acid excretion to the intestinal lumen as a result of the induction of oxidative stress by NADPH oxidase activation. AU - Kaneko,Chihiro, AU - Ogura,Jiro, AU - Sasaki,Shunichi, AU - Okamoto,Keisuke, AU - Kobayashi,Masaki, AU - Kuwayama,Kaori, AU - Narumi,Katsuya, AU - Iseki,Ken, Y1 - 2016/11/30/ PY - 2016/08/02/received PY - 2016/11/08/revised PY - 2016/11/28/accepted PY - 2016/12/4/pubmed PY - 2017/10/20/medline PY - 2016/12/4/entrez KW - Breast cancer resistance protein KW - Fructose KW - Hyperuricemia KW - NADPH oxidase KW - Oxidative stress KW - Uric acid excretion SP - 559 EP - 566 JF - Biochimica et biophysica acta. General subjects JO - Biochim Biophys Acta Gen Subj VL - 1861 IS - 3 N2 - BACKGROUND: A high intake of fructose increases the risk for hyperuricemia. It has been reported that long-term fructose consumption suppressed renal uric acid excretion and increased serum uric acid level. However, the effect of single administration of fructose on excretion of uric acid has not been clarified. METHODS: We used male Wistar rats, which were orally administered fructose (5g/kg). Those rats were used in each experiment at 12h after administration. RESULTS: Single administration of fructose suppressed the function of ileal uric acid excretion and had no effect on the function of renal uric acid excretion. Breast cancer resistance protein (BCRP) predominantly contributes to intestinal excretion of uric acid as an active homodimer. Single administration of fructose decreased BCRP homodimer level in the ileum. Moreover, diphenyleneiodonium (DPI), an inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox), recovered the suppression of the function of ileal uric acid excretion and the Bcrp homodimer level in the ileum of rats that received single administration of fructose. CONCLUSIONS: Single administration of fructose decreases in BCRP homodimer level, resulting in the suppression the function of ileal uric acid excretion. The suppression of the function of ileal uric acid excretion by single administration of fructose is caused by the activation of Nox. The results of our study provide a new insight into the mechanism of fructose-induced hyperuricemia. SN - 0304-4165 UR - https://www.unboundmedicine.com/medline/citation/27913188/Fructose_suppresses_uric_acid_excretion_to_the_intestinal_lumen_as_a_result_of_the_induction_of_oxidative_stress_by_NADPH_oxidase_activation_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-4165(16)30481-0 DB - PRIME DP - Unbound Medicine ER -