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Xanthine oxidoreductase activity is correlated with insulin resistance and subclinical inflammation in young humans.

Abstract The enzyme xanthine oxidoreductase (XOR) catalyzes the formation of uric acid (UA) from hypoxanthine and xanthine, which in turn are products of purine metabolism starting from ribose-5-phosphate. Besides the synthesis of UA, basic research has suggested that XOR is involved in the regulation of reactive oxygen species, adipogenesis, and peroxisome proliferator-activated receptor-γ (PPAR-γ). XOR activity has shown to be much lower in humans than in rodents, which makes its accurate measurement difficult. Recently, a novel human plasma XOR activity assay has been established using a combination of liquid chromatography (LC) and triple quadrupole mass spectrometry (TQMS) to detect [(13)C2,(15)N2]UA using [(13)C2,(15)N2]xanthine as a substrate. Using this novel assay, we for the first time determine plasma XOR activity in humans, and evaluate its association with insulin resistance, high-sensitivity C-reactive protein (hsCRP) levels, and other parameters.
PMID
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Authors

Mayor MeshTerms

Insulin Resistance

Keywords

Adiponectin

Inflammation

Insulin resistance

Uric acid

Xanthine oxidoreductase

Journal Title metabolism: clinical and experimental
Publication Year Start




PMID- 28403945
OWN - NLM
STAT- MEDLINE
DA  - 20170413
DCOM- 20170419
LR  - 20170419
IS  - 1532-8600 (Electronic)
IS  - 0026-0495 (Linking)
VI  - 70
DP  - 2017 May
TI  - Xanthine oxidoreductase activity is correlated with insulin resistance and
      subclinical inflammation in young humans.
PG  - 51-56
LID - S0026-0495(17)30044-6 [pii]
LID - 10.1016/j.metabol.2017.01.031 [doi]
AB  - BACKGROUND AND AIMS: The enzyme xanthine oxidoreductase (XOR) catalyzes the
      formation of uric acid (UA) from hypoxanthine and xanthine, which in turn are
      products of purine metabolism starting from ribose-5-phosphate. Besides the
      synthesis of UA, basic research has suggested that XOR is involved in the
      regulation of reactive oxygen species, adipogenesis, and peroxisome
      proliferator-activated receptor-gamma (PPAR-gamma). XOR activity has shown to be 
      much lower in humans than in rodents, which makes its accurate measurement
      difficult. Recently, a novel human plasma XOR activity assay has been established
      using a combination of liquid chromatography (LC) and triple quadrupole mass
      spectrometry (TQMS) to detect [13C2,15N2]UA using [13C2,15N2]xanthine as a
      substrate. Using this novel assay, we for the first time determine plasma XOR
      activity in humans, and evaluate its association with insulin resistance,
      high-sensitivity C-reactive protein (hsCRP) levels, and other parameters.
      METHODS: Of the 29 volunteers who wished to participate in the study, 3 were
      excluded; of the remaining, 11 were female and 15 were male with a mean age of
      25.9+/-3.3years. Blood samples were collected under fasting conditions in the
      early morning to measure XOR activity and other parameters. RESULTS: The natural 
      logarithmic value of XOR activity (ln-XOR) in plasma was 3.4+/-0.8pmol/h/mL.
      Ln-XOR had a positive correlation with UA and body mass index (BMI) and a
      negative correlation with quantitative insulin sensitivity check index (QUICKI)
      and adiponectin. In addition, ln-XOR had a positive correlation with hsCRP
      levels, which serves as a marker of chronic inflammation. CONCLUSIONS: The
      present study has shown that XOR activity is correlated with serum UA levels in
      humans. Furthermore, even in young subjects, XOR activity is correlated with
      insulin resistance, BMI, and subclinical inflammation. Thus, XOR activity may be 
      potentially involved in adiposity and subclinical inflammation in humans.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Washio, Kahori Watanabe
AU  - Washio KW
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Kusunoki, Yoshiki
AU  - Kusunoki Y
AD  - Division of Innovative Diabetes Treatment, Department of Internal Medicine, Hyogo
      College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan.
      Electronic address: [email protected]
FAU - Murase, Takayo
AU  - Murase T
AD  - Radioisotope and Chemical Analysis Center, Laboratory Management Department,
      Sanwa Kagaku Kenkyusho Co. Ltd., 363 Shiosaki Hokusei Town Inabe, Mie 511-0406,
      Japan.
FAU - Nakamura, Takashi
AU  - Nakamura T
AD  - Pharmacological Study Group, Pharmaceutical Research Laboratories, Sanwa Kagaku
      Kenkyusho Co. Ltd., 363 Shiosaki Hokusei Town Inabe, Mie 511-0406, Japan.
FAU - Osugi, Keiko
AU  - Osugi K
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Ohigashi, Mana
AU  - Ohigashi M
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Sukenaga, Tadahiko
AU  - Sukenaga T
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Ochi, Fumihiro
AU  - Ochi F
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Matsuo, Toshihiro
AU  - Matsuo T
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Katsuno, Tomoyuki
AU  - Katsuno T
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Moriwaki, Yuji
AU  - Moriwaki Y
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Yamamoto, Tetsuya
AU  - Yamamoto T
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Namba, Mitsuyoshi
AU  - Namba M
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
FAU - Koyama, Hidenori
AU  - Koyama H
AD  - Division of Diabetes, Endocrinology and Metabolism, Department of Internal
      Medicine, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo
      663-8501, Japan.
LA  - eng
PT  - Journal Article
DEP - 20170204
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (Adiponectin)
RN  - 1AVZ07U9S7 (Xanthine)
RN  - 268B43MJ25 (Uric Acid)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - EC 1.17.1.4 (Xanthine Dehydrogenase)
SB  - IM
MH  - Adiponectin/blood
MH  - Adult
MH  - Body Mass Index
MH  - C-Reactive Protein/analysis
MH  - Chromatography, Liquid
MH  - Female
MH  - Humans
MH  - Inflammation/blood/*enzymology
MH  - *Insulin Resistance
MH  - Male
MH  - Mass Spectrometry
MH  - Uric Acid/metabolism
MH  - Xanthine/metabolism
MH  - Xanthine Dehydrogenase/*metabolism
MH  - Young Adult
OTO - NOTNLM
OT  - Adiponectin
OT  - Inflammation
OT  - Insulin resistance
OT  - Uric acid
OT  - Xanthine oxidoreductase
EDAT- 2017/04/14 06:00
MHDA- 2017/04/20 06:00
CRDT- 2017/04/14 06:00
PHST- 2016/11/08 [received]
PHST- 2017/01/11 [revised]
PHST- 2017/01/30 [accepted]
AID - S0026-0495(17)30044-6 [pii]
AID - 10.1016/j.metabol.2017.01.031 [doi]
PST - ppublish
SO  - Metabolism. 2017 May;70:51-56. doi: 10.1016/j.metabol.2017.01.031. Epub 2017 Feb 
      4.

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