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.
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 -