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Low plasma carnosinase activity promotes carnosinemia after carnosine ingestion in humans

Inge Everaert UGent, Youri Taes UGent, Emile de Heer, Hans Baelde, Ana Zutinic, Benito Yard, Sibylle Sauerhöfer, Lander Vanhee UGent, Joris Delanghe UGent and Giancarlo Aldini, et al. (2012) AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY. 302(12). p.F1537-F1544
abstract
A polymorphism in the carnosine dipeptidase-1 gene (CNDP1), resulting in decreased plasma carnosinase activity, is associated with a reduced risk for diabetic nephropathy. Because carnosine, a natural scavenger/suppressor of ROS, advanced glycation end products, and reactive aldehydes, is readily degraded in blood by the highly active carnosinase enzyme, it has been postulated that low serum carnosinase activity might be advantageous to reduce diabetic complications. The aim of this study was to examine whether low carnosinase activity promotes circulating carnosine levels after carnosine supplementation in humans. Blood and urine were sampled in 25 healthy subjects after acute supplementation with 60 mg/kg body wt carnosine. Precooled EDTA-containing tubes were used for blood withdrawal, and plasma samples were immediately deproteinized and analyzed for carnosine and beta-alanine by HPLC. CNDP1 genotype, baseline plasma carnosinase activity, and protein content were assessed. Upon carnosine ingestion, 8 of the 25 subjects (responders) displayed a measurable increase in plasma carnosine up to 1 h after supplementation. Subjects with no measurable increment in plasma carnosine (nonresponders) had approx. 2-fold higher plasma carnosinase protein content and approx. 1.5-fold higher activity compared with responders. Urinary carnosine recovery was 2.6-fold higher in responders versus nonresponders and was negatively dependent on both the activity and protein content of the plasma carnosinase enzyme. In conclusion, low plasma carnosinase activity promotes the presence of circulating carnosine upon an oral challenge. These data may further clarify the link among CNDP1 genotype, carnosinase, and diabetic nephropathy.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
carnosine dipeptidase-1, diabetic nephropathy, beta-alanine
journal title
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
Am. J. Physiol.-Renal Physiol.
volume
302
issue
12
pages
F1537 - F1544
Web of Science type
Article
Web of Science id
000305425300003
JCR category
UROLOGY & NEPHROLOGY
JCR impact factor
3.612 (2012)
JCR rank
12/73 (2012)
JCR quartile
1 (2012)
ISSN
1931-857X
DOI
10.1152/ajprenal.00084.2012
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2941455
handle
http://hdl.handle.net/1854/LU-2941455
date created
2012-06-28 13:25:48
date last changed
2012-09-25 11:10:08
@article{2941455,
  abstract     = {A polymorphism in the carnosine dipeptidase-1 gene (CNDP1), resulting in decreased plasma carnosinase activity, is associated with a reduced risk for diabetic nephropathy. Because carnosine, a natural scavenger/suppressor of ROS, advanced glycation end products, and reactive aldehydes, is readily degraded in blood by the highly active carnosinase enzyme, it has been postulated that low serum carnosinase activity might be advantageous to reduce diabetic complications. The aim of this study was to examine whether low carnosinase activity promotes circulating carnosine levels after carnosine supplementation in humans. Blood and urine were sampled in 25 healthy subjects after acute supplementation with 60 mg/kg body wt carnosine. Precooled EDTA-containing tubes were used for blood withdrawal, and plasma samples were immediately deproteinized and analyzed for carnosine and beta-alanine by HPLC. CNDP1 genotype, baseline plasma carnosinase activity, and protein content were assessed. Upon carnosine ingestion, 8 of the 25 subjects (responders) displayed a measurable increase in plasma carnosine up to 1 h after supplementation. Subjects with no measurable increment in plasma carnosine  (nonresponders) had approx. 2-fold higher plasma carnosinase protein content and approx. 1.5-fold higher activity compared with responders. Urinary carnosine recovery was 2.6-fold higher in responders versus nonresponders and was negatively dependent on both the activity and protein content of the plasma carnosinase enzyme. In conclusion, low plasma carnosinase activity promotes the presence of circulating carnosine upon an oral challenge. These data may further clarify the link among CNDP1 genotype, carnosinase, and diabetic nephropathy.},
  author       = {Everaert, Inge and Taes, Youri and de Heer, Emile and Baelde, Hans and Zutinic, Ana and Yard, Benito and Sauerh{\"o}fer, Sibylle and Vanhee, Lander and Delanghe, Joris and Aldini, Giancarlo and Derave, Wim},
  issn         = {1931-857X},
  journal      = {AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY},
  keyword      = {carnosine dipeptidase-1,diabetic nephropathy,beta-alanine},
  language     = {eng},
  number       = {12},
  pages        = {F1537--F1544},
  title        = {Low plasma carnosinase activity promotes carnosinemia after carnosine ingestion in humans},
  url          = {http://dx.doi.org/10.1152/ajprenal.00084.2012},
  volume       = {302},
  year         = {2012},
}

Chicago
Everaert, Inge, Youri Taes, Emile de Heer, Hans Baelde, Ana Zutinic, Benito Yard, Sibylle Sauerhöfer, et al. 2012. “Low Plasma Carnosinase Activity Promotes Carnosinemia After Carnosine Ingestion in Humans.” American Journal of Physiology-renal Physiology 302 (12): F1537–F1544.
APA
Everaert, I., Taes, Y., de Heer, E., Baelde, H., Zutinic, A., Yard, B., Sauerhöfer, S., et al. (2012). Low plasma carnosinase activity promotes carnosinemia after carnosine ingestion in humans. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 302(12), F1537–F1544.
Vancouver
1.
Everaert I, Taes Y, de Heer E, Baelde H, Zutinic A, Yard B, et al. Low plasma carnosinase activity promotes carnosinemia after carnosine ingestion in humans. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY. 2012;302(12):F1537–F1544.
MLA
Everaert, Inge, Youri Taes, Emile de Heer, et al. “Low Plasma Carnosinase Activity Promotes Carnosinemia After Carnosine Ingestion in Humans.” AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY 302.12 (2012): F1537–F1544. Print.