Reduced gluconeogenesis and lactate clearance in Huntington's disease
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Reduced gluconeogenesis and lactate clearance in Huntington's disease. / Josefsen, Knud; Nielsen, Signe M B; Campos, André; Seifert, Thomas; Hasholt, Lis; Nielsen, Jørgen E; Nørremølle, Anne; Skotte, Niels H; Secher, Niels H; Quistorff, Bjørn.
In: Neurobiology of Disease, Vol. 40, No. 3, 01.12.2010, p. 656-62.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Reduced gluconeogenesis and lactate clearance in Huntington's disease
AU - Josefsen, Knud
AU - Nielsen, Signe M B
AU - Campos, André
AU - Seifert, Thomas
AU - Hasholt, Lis
AU - Nielsen, Jørgen E
AU - Nørremølle, Anne
AU - Skotte, Niels H
AU - Secher, Niels H
AU - Quistorff, Bjørn
N1 - Copyright © 2010 Elsevier Inc. All rights reserved.
PY - 2010/12/1
Y1 - 2010/12/1
N2 - We studied systemic and brain glucose and lactate metabolism in Huntington's disease (HD) patients in response to ergometer cycling. Following termination of exercise, blood glucose increased abruptly in control subjects, but no peak was seen in any of the HD patients (2.0 ± 0.5 vs. 0.0 ± 0.2mM, P <2 × 10(-6)). No difference was seen in brain metabolism parameters. Reduced hepatic glucose output in the HD mouse model R6/2 following a lactate challenge, combined with reduced phosphoenolpyruvate carboxykinase and increased pyruvate kinase activity in the mouse liver suggest a reduced capacity for gluconeogenesis in HD, possibly contributing to the clinical symptoms of HD. We propose that blood glucose concentration in the recovery from exercise can be applied as a liver function test in HD patients.
AB - We studied systemic and brain glucose and lactate metabolism in Huntington's disease (HD) patients in response to ergometer cycling. Following termination of exercise, blood glucose increased abruptly in control subjects, but no peak was seen in any of the HD patients (2.0 ± 0.5 vs. 0.0 ± 0.2mM, P <2 × 10(-6)). No difference was seen in brain metabolism parameters. Reduced hepatic glucose output in the HD mouse model R6/2 following a lactate challenge, combined with reduced phosphoenolpyruvate carboxykinase and increased pyruvate kinase activity in the mouse liver suggest a reduced capacity for gluconeogenesis in HD, possibly contributing to the clinical symptoms of HD. We propose that blood glucose concentration in the recovery from exercise can be applied as a liver function test in HD patients.
KW - Animals
KW - Blood Glucose
KW - Blotting, Western
KW - Brain
KW - Exercise
KW - Exercise Test
KW - Female
KW - Gluconeogenesis
KW - Humans
KW - Huntington Disease
KW - Lactic Acid
KW - Liver
KW - Liver Function Tests
KW - Male
KW - Mice
KW - Mice, Transgenic
KW - Middle Aged
KW - Reverse Transcriptase Polymerase Chain Reaction
U2 - 10.1016/j.nbd.2010.08.009
DO - 10.1016/j.nbd.2010.08.009
M3 - Journal article
C2 - 20727971
VL - 40
SP - 656
EP - 662
JO - Neurobiology of Disease
JF - Neurobiology of Disease
SN - 0969-9961
IS - 3
ER -
ID: 33601580